An octapeptide that is a potent but labile vasoconstrictor. It is produced from angiotensin I after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME. The amino acid in position 5 varies in different species. To block VASOCONSTRICTION and HYPERTENSION effect of angiotensin II, patients are often treated with ACE INHIBITORS or with ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS.
An angiotensin receptor subtype that is expressed at high levels in a variety of adult tissues including the CARDIOVASCULAR SYSTEM, the KIDNEY, the ENDOCRINE SYSTEM and the NERVOUS SYSTEM. Activation of the type 1 angiotensin receptor causes VASOCONSTRICTION and sodium retention.
Cell surface proteins that bind ANGIOTENSINS and trigger intracellular changes influencing the behavior of cells.
Agents that antagonize ANGIOTENSIN II TYPE 1 RECEPTOR. Included are ANGIOTENSIN II analogs such as SARALASIN and biphenylimidazoles such as LOSARTAN. Some are used as ANTIHYPERTENSIVE AGENTS.
An angiotensin receptor subtype that is expressed at high levels in fetal tissues. Many effects of the angiotensin type 2 receptor such as VASODILATION and sodium loss are the opposite of that of the ANGIOTENSIN TYPE 1 RECEPTOR.
Agents that antagonize ANGIOTENSIN RECEPTORS. Many drugs in this class specifically target the ANGIOTENSIN TYPE 1 RECEPTOR.
A decapeptide that is cleaved from precursor angiotensinogen by RENIN. Angiotensin I has limited biological activity. It is converted to angiotensin II, a potent vasoconstrictor, after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME.
An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.
Agents that antagonize the ANGIOTENSIN II TYPE 2 RECEPTOR.
A heptapeptide formed from ANGIOTENSIN II after the removal of an amino acid at the N-terminal by AMINOPEPTIDASE A. Angiotensin III has the same efficacy as ANGIOTENSIN II in promoting ALDOSTERONE secretion and modifying renal blood flow, but less vasopressor activity (about 40%).
A class of drugs whose main indications are the treatment of hypertension and heart failure. They exert their hemodynamic effect mainly by inhibiting the renin-angiotensin system. They also modulate sympathetic nervous system activity and increase prostaglandin synthesis. They cause mainly vasodilation and mild natriuresis without affecting heart rate and contractility.
An octapeptide analog of angiotensin II (bovine) with amino acids 1 and 8 replaced with sarcosine and alanine, respectively. It is a highly specific competitive inhibitor of angiotensin II that is used in the diagnosis of HYPERTENSION.
An ANGIOTENSIN II analog which acts as a highly specific inhibitor of ANGIOTENSIN TYPE 1 RECEPTOR.
A peptidyl-dipeptidase that catalyzes the release of a C-terminal dipeptide, -Xaa-*-Xbb-Xcc, when neither Xaa nor Xbb is Pro. It is a Cl(-)-dependent, zinc glycoprotein that is generally membrane-bound and active at neutral pH. It may also have endopeptidase activity on some substrates. (From Enzyme Nomenclature, 1992) EC
Compounds containing 1,3-diazole, a five membered aromatic ring containing two nitrogen atoms separated by one of the carbons. Chemically reduced ones include IMIDAZOLINES and IMIDAZOLIDINES. Distinguish from 1,2-diazole (PYRAZOLES).
A highly specific (Leu-Leu) endopeptidase that generates ANGIOTENSIN I from its precursor ANGIOTENSINOGEN, leading to a cascade of reactions which elevate BLOOD PRESSURE and increase sodium retention by the kidney in the RENIN-ANGIOTENSIN SYSTEM. The enzyme was formerly listed as EC
Compounds with a BENZENE fused to IMIDAZOLES.
Drugs used to cause constriction of the blood vessels.
Oligopeptides which are important in the regulation of blood pressure (VASOCONSTRICTION) and fluid homeostasis via the RENIN-ANGIOTENSIN SYSTEM. These include angiotensins derived naturally from precursor ANGIOTENSINOGEN, and those synthesized.
A hormone secreted by the ADRENAL CORTEX that regulates electrolyte and water balance by increasing the renal retention of sodium and the excretion of potassium.
Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
An alpha-globulin of about 453 amino acids, depending on the species. It is produced by the liver and secreted into blood circulation. Angiotensinogen is the inactive precursor of natural angiotensins. Upon successive enzyme cleavages, angiotensinogen yields angiotensin I, II, and III with amino acids numbered at 10, 8, and 7, respectively.
A BLOOD PRESSURE regulating system of interacting components that include RENIN; ANGIOTENSINOGEN; ANGIOTENSIN CONVERTING ENZYME; ANGIOTENSIN I; ANGIOTENSIN II; and angiotensinase. Renin, an enzyme produced in the kidney, acts on angiotensinogen, an alpha-2 globulin produced by the liver, forming ANGIOTENSIN I. Angiotensin-converting enzyme, contained in the lung, acts on angiotensin I in the plasma converting it to ANGIOTENSIN II, an extremely powerful vasoconstrictor. Angiotensin II causes contraction of the arteriolar and renal VASCULAR SMOOTH MUSCLE, leading to retention of salt and water in the KIDNEY and increased arterial blood pressure. In addition, angiotensin II stimulates the release of ALDOSTERONE from the ADRENAL CORTEX, which in turn also increases salt and water retention in the kidney. Angiotensin-converting enzyme also breaks down BRADYKININ, a powerful vasodilator and component of the KALLIKREIN-KININ SYSTEM.
Compounds with a six membered aromatic ring containing NITROGEN. The saturated version is PIPERIDINES.
An angiotensin-converting enzyme inhibitor that is used to treat HYPERTENSION and HEART FAILURE.
The nonstriated involuntary muscle tissue of blood vessels.
A strain of Rattus norvegicus with elevated blood pressure used as a model for studying hypertension and stroke.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
A strain of Rattus norvegicus used as a normotensive control for the spontaneous hypertensive rats (SHR).
The physiological narrowing of BLOOD VESSELS by contraction of the VASCULAR SMOOTH MUSCLE.
The circulation of the BLOOD through the vessels of the KIDNEY.
The relationship between the dose of an administered drug and the response of the organism to the drug.
A synthetic nonapeptide (Pyr-Trp-Pro-Arg-Pro-Gln-Ile-Pro-Pro) which is identical to the peptide from the venom of the snake, Bothrops jararaca. It inhibits kininase II and ANGIOTENSIN I and has been proposed as an antihypertensive agent.
Persistent high BLOOD PRESSURE due to KIDNEY DISEASES, such as those involving the renal parenchyma, the renal vasculature, or tumors that secrete RENIN.
The active metabolite of ENALAPRIL and a potent intravenously administered angiotensin-converting enzyme inhibitor. It is an effective agent for the treatment of essential hypertension and has beneficial hemodynamic effects in heart failure. The drug produces renal vasodilation with an increase in sodium excretion.
A branched-chain essential amino acid that has stimulant activity. It promotes muscle growth and tissue repair. It is a precursor in the penicillin biosynthetic pathway.
A potent and specific inhibitor of PEPTIDYL-DIPEPTIDASE A. It blocks the conversion of ANGIOTENSIN I to ANGIOTENSIN II, a vasoconstrictor and important regulator of arterial blood pressure. Captopril acts to suppress the RENIN-ANGIOTENSIN SYSTEM and inhibits pressure responses to exogenous angiotensin.
Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
A family of neutral serine proteases with CHYMOTRYPSIN-like activity. Chymases are primarily found in the SECRETORY GRANULES of MAST CELLS and are released during mast cell degranulation.
The octapeptide amide of bovine angiotensin II used to increase blood pressure by vasoconstriction.
The main trunk of the systemic arteries.
Derivatives of BENZOIC ACID. Included under this heading are a broad variety of acid forms, salts, esters, and amides that contain the carboxybenzene structure.
The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow.
A nonapeptide messenger that is enzymatically produced from KALLIDIN in the blood where it is a potent but short-lived agent of arteriolar dilation and increased capillary permeability. Bradykinin is also released from MAST CELLS during asthma attacks, from gut walls as a gastrointestinal vasodilator, from damaged tissues as a pain signal, and may be a neurotransmitter.
Enlargement of the HEART, usually indicated by a cardiothoracic ratio above 0.50. Heart enlargement may involve the right, the left, or both HEART VENTRICLES or HEART ATRIA. Cardiomegaly is a nonspecific symptom seen in patients with chronic systolic heart failure (HEART FAILURE) or several forms of CARDIOMYOPATHIES.
One of the ANGIOTENSIN-CONVERTING ENZYME INHIBITORS (ACE inhibitors), orally active, that has been used in the treatment of hypertension and congestive heart failure.
A diet which contains very little sodium chloride. It is prescribed by some for hypertension and for edematous states. (Dorland, 27th ed)
A pair of glands located at the cranial pole of each of the two KIDNEYS. Each adrenal gland is composed of two distinct endocrine tissues with separate embryonic origins, the ADRENAL CORTEX producing STEROIDS and the ADRENAL MEDULLA producing NEUROTRANSMITTERS.
A flavoprotein enzyme that catalyzes the univalent reduction of OXYGEN using NADPH as an electron donor to create SUPEROXIDE ANION. The enzyme is dependent on a variety of CYTOCHROMES. Defects in the production of superoxide ions by enzymes such as NADPH oxidase result in GRANULOMATOUS DISEASE, CHRONIC.
A structure, situated close to the intraventricular foramen, which induces DRINKING BEHAVIOR after stimulation with ANGIOTENSIN II.
The consumption of liquids.
Antidiuretic hormones released by the NEUROHYPOPHYSIS of all vertebrates (structure varies with species) to regulate water balance and OSMOLARITY. In general, vasopressin is a nonapeptide consisting of a six-amino-acid ring with a cysteine 1 to cysteine 6 disulfide bridge or an octapeptide containing a CYSTINE. All mammals have arginine vasopressin except the pig with a lysine at position 8. Vasopressin, a vasoconstrictor, acts on the KIDNEY COLLECTING DUCTS to increase water reabsorption, increase blood volume and blood pressure.
General increase in bulk of a part or organ due to CELL ENLARGEMENT and accumulation of FLUIDS AND SECRETIONS, not due to tumor formation, nor to an increase in the number of cells (HYPERPLASIA).
The movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM.
Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury.
Hypertension due to RENAL ARTERY OBSTRUCTION or compression.
A direct-acting vasodilator that is used as an antihypertensive agent.
A member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
The force that opposes the flow of BLOOD through a vascular bed. It is equal to the difference in BLOOD PRESSURE across the vascular bed divided by the CARDIAC OUTPUT.
The predominant form of mammalian antidiuretic hormone. It is a nonapeptide containing an ARGININE at residue 8 and two disulfide-linked cysteines at residues of 1 and 6. Arg-vasopressin is used to treat DIABETES INSIPIDUS or to improve vasomotor tone and BLOOD PRESSURE.
The number of times the HEART VENTRICLES contract per unit of time, usually per minute.
Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.
The thoracolumbar division of the autonomic nervous system. Sympathetic preganglionic fibers originate in neurons of the intermediolateral column of the spinal cord and project to the paravertebral and prevertebral ganglia, which in turn project to target organs. The sympathetic nervous system mediates the body's response to stressful situations, i.e., the fight or flight reactions. It often acts reciprocally to the parasympathetic system.
The renal tubule portion that extends from the BOWMAN CAPSULE in the KIDNEY CORTEX into the KIDNEY MEDULLA. The proximal tubule consists of a convoluted proximal segment in the cortex, and a distal straight segment descending into the medulla where it forms the U-shaped LOOP OF HENLE.
The narrow subcapsular outer zone of the adrenal cortex. This zone produces a series of enzymes that convert PREGNENOLONE to ALDOSTERONE. The final steps involve three successive oxidations by CYTOCHROME P-450 CYP11B2.
The portion of the descending aorta proceeding from the arch of the aorta and extending to the DIAPHRAGM, eventually connecting to the ABDOMINAL AORTA.
Sodium chloride used in foods.
An alpha-1 adrenergic agonist used as a mydriatic, nasal decongestant, and cardiotonic agent.
A free radical gas produced endogenously by a variety of mammalian cells, synthesized from ARGININE by NITRIC OXIDE SYNTHASE. Nitric oxide is one of the ENDOTHELIUM-DEPENDENT RELAXING FACTORS released by the vascular endothelium and mediates VASODILATION. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic GUANYLATE CYCLASE and thus elevates intracellular levels of CYCLIC GMP.
Elements of limited time intervals, contributing to particular results or situations.
Peptides composed of between two and twelve amino acids.
Implanted fluid propulsion systems with self-contained power source for providing long-term controlled-rate delivery of drugs such as chemotherapeutic agents or analgesics. Delivery rate may be externally controlled or osmotically or peristatically controlled with the aid of transcutaneous monitoring.
Sodium excretion by URINATION.
A ZINC-dependent membrane-bound aminopeptidase that catalyzes the N-terminal peptide cleavage of GLUTAMATE (and to a lesser extent ASPARTATE). The enzyme appears to play a role in the catabolic pathway of the RENIN-ANGIOTENSIN SYSTEM.
A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.
A long-acting angiotensin-converting enzyme inhibitor. It is a prodrug that is transformed in the liver to its active metabolite ramiprilat.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
Excision of kidney.
The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.
A cluster of convoluted capillaries beginning at each nephric tubule in the kidney and held together by connective tissue.
Arteries which arise from the abdominal aorta and distribute to most of the intestines.
The outer zone of the KIDNEY, beneath the capsule, consisting of KIDNEY GLOMERULUS; KIDNEY TUBULES, DISTAL; and KIDNEY TUBULES, PROXIMAL.
A potent natriuretic and vasodilatory peptide or mixture of different-sized low molecular weight PEPTIDES derived from a common precursor and secreted mainly by the HEART ATRIUM. All these peptides share a sequence of about 20 AMINO ACIDS.
A 21-amino acid peptide produced in a variety of tissues including endothelial and vascular smooth-muscle cells, neurons and astrocytes in the central nervous system, and endometrial cells. It acts as a modulator of vasomotor tone, cell proliferation, and hormone production. (N Eng J Med 1995;333(6):356-63)
A mitochondrial cytochrome P450 enzyme that catalyzes the 18-hydroxylation of steroids in the presence of molecular oxygen and NADPH-specific flavoprotein. This enzyme, encoded by CYP11B2 gene, is important in the conversion of CORTICOSTERONE to 18-hydroxycorticosterone and the subsequent conversion to ALDOSTERONE.
The hollow, muscular organ that maintains the circulation of the blood.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.
The outer layer of the adrenal gland. It is derived from MESODERM and comprised of three zones (outer ZONA GLOMERULOSA, middle ZONA FASCICULATA, and inner ZONA RETICULARIS) with each producing various steroids preferentially, such as ALDOSTERONE; HYDROCORTISONE; DEHYDROEPIANDROSTERONE; and ANDROSTENEDIONE. Adrenal cortex function is regulated by pituitary ADRENOCORTICOTROPIN.
The presence of proteins in the urine, an indicator of KIDNEY DISEASES.
Highly reactive compounds produced when oxygen is reduced by a single electron. In biological systems, they may be generated during the normal catalytic function of a number of enzymes and during the oxidation of hemoglobin to METHEMOGLOBIN. In living organisms, SUPEROXIDE DISMUTASE protects the cell from the deleterious effects of superoxides.
A non-selective inhibitor of nitric oxide synthase. It has been used experimentally to induce hypertension.
A ubiquitous sodium salt that is commonly used to season food.
Sodium or sodium compounds used in foods or as a food. The most frequently used compounds are sodium chloride or sodium glutamate.
The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065)
A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).
The internal portion of the kidney, consisting of striated conical masses, the renal pyramids, whose bases are adjacent to the cortex and whose apices form prominent papillae projecting into the lumen of the minor calyces.
A generic term used to describe a group of polypeptides with related chemical structures and pharmacological properties that are widely distributed in nature. These peptides are AUTACOIDS that act locally to produce pain, vasodilatation, increased vascular permeability, and the synthesis of prostaglandins. Thus, they comprise a subset of the large number of mediators that contribute to the inflammatory response. (From Goodman and Gilman's The Pharmacologic Basis of Therapeutics, 8th ed, p588)
A potassium sparing diuretic that acts by antagonism of aldosterone in the distal renal tubules. It is used mainly in the treatment of refractory edema in patients with congestive heart failure, nephrotic syndrome, or hepatic cirrhosis. Its effects on the endocrine system are utilized in the treatments of hirsutism and acne but they can lead to adverse effects. (From Martindale, The Extra Pharmacopoeia, 30th ed, p827)
21-Amino-acid peptides produced by vascular endothelial cells and functioning as potent vasoconstrictors. The endothelin family consists of three members, ENDOTHELIN-1; ENDOTHELIN-2; and ENDOTHELIN-3. All three peptides contain 21 amino acids, but vary in amino acid composition. The three peptides produce vasoconstrictor and pressor responses in various parts of the body. However, the quantitative profiles of the pharmacological activities are considerably different among the three isopeptides.
The vessels carrying blood away from the heart.
The smallest divisions of the arteries located between the muscular arteries and the capillaries.
Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.
Molecules or ions formed by the incomplete one-electron reduction of oxygen. These reactive oxygen intermediates include SINGLET OXYGEN; SUPEROXIDES; PEROXIDES; HYDROXYL RADICAL; and HYPOCHLOROUS ACID. They contribute to the microbicidal activity of PHAGOCYTES, regulation of signal transduction and gene expression, and the oxidative damage to NUCLEIC ACIDS; PROTEINS; and LIPIDS.
An serine-threonine protein kinase that requires the presence of physiological concentrations of CALCIUM and membrane PHOSPHOLIPIDS. The additional presence of DIACYLGLYCEROLS markedly increases its sensitivity to both calcium and phospholipids. The sensitivity of the enzyme can also be increased by PHORBOL ESTERS and it is believed that protein kinase C is the receptor protein of tumor-promoting phorbol esters.
The physiological widening of BLOOD VESSELS by relaxing the underlying VASCULAR SMOOTH MUSCLE.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
One of the ANGIOTENSIN-CONVERTING ENZYME INHIBITORS (ACE inhibitors) used for hypertension. It is a prodrug that is hydrolyzed after absorption to its main metabolite cilazaprilat.
A benzoic-sulfonamide-furan. It is a diuretic with fast onset and short duration that is used for EDEMA and chronic RENAL INSUFFICIENCY.
A complex of cells consisting of juxtaglomerular cells, extraglomerular mesangium lacis cells, the macula densa of the distal convoluted tubule, and granular epithelial peripolar cells. Juxtaglomerular cells are modified SMOOTH MUSCLE CELLS found in the walls of afferent glomerular arterioles and sometimes the efferent arterioles. Extraglomerular mesangium lacis cells are located in the angle between the afferent and efferent glomerular arterioles. Granular epithelial peripolar cells are located at the angle of reflection of the parietal to visceral angle of the renal corpuscle.
Cell surface receptors that bind BRADYKININ and related KININS with high affinity and trigger intracellular changes which influence the behavior of cells. The identified receptor types (B-1 and B-2, or BK-1 and BK-2) recognize endogenous KALLIDIN; t-kinins; and certain bradykinin fragments as well as bradykinin itself.
Fluid propulsion systems driven mechanically, electrically, or osmotically that are used to inject (or infuse) over time agents into a patient or experimental animal; used routinely in hospitals to maintain a patent intravenous line, to administer antineoplastic agents and other drugs in thromboembolism, heart disease, diabetes mellitus (INSULIN INFUSION SYSTEMS is also available), and other disorders.
Drugs that bind to and block the activation of MINERALOCORTICOID RECEPTORS by MINERALOCORTICOIDS such as ALDOSTERONE.
A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.
Agents that promote the excretion of urine through their effects on kidney function.
Injections into the cerebral ventricles.
The volume of water filtered out of plasma through glomerular capillary walls into Bowman's capsules per unit of time. It is considered to be equivalent to INULIN clearance.
Any of the tubular vessels conveying the blood (arteries, arterioles, capillaries, venules, and veins).
A constitutively expressed subtype of bradykinin receptor that may play a role in the acute phase of the inflammatory and pain response. It has high specificity for intact forms of BRADYKININ and KALLIDIN. The receptor is coupled to G-PROTEIN, GQ-G11 ALPHA FAMILY and G-PROTEIN, GI-GO ALPHA FAMILY signaling proteins.
A drive stemming from a physiological need for WATER.
An increase in the excretion of URINE. (McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
The geometric and structural changes that the HEART VENTRICLES undergo, usually following MYOCARDIAL INFARCTION. It comprises expansion of the infarct and dilatation of the healthy ventricle segments. While most prevalent in the left ventricle, it can also occur in the right ventricle.
Behaviors associated with the ingesting of water and other liquids; includes rhythmic patterns of drinking (time intervals - onset and duration), frequency and satiety.
Treatment process involving the injection of fluid into an organ or tissue.
Receptors in the vascular system, particularly the aorta and carotid sinus, which are sensitive to stretch of the vessel walls.
Drugs used to cause dilation of the blood vessels.
A branch of the abdominal aorta which supplies the kidneys, adrenal glands and ureters.
The flow of BLOOD through or around an organ or region of the body.
An angiotensin-converting enzyme inhibitor. It is used in patients with hypertension and heart failure.
KIDNEY injuries associated with diabetes mellitus and affecting KIDNEY GLOMERULUS; ARTERIOLES; KIDNEY TUBULES; and the interstitium. Clinical signs include persistent PROTEINURIA, from microalbuminuria progressing to ALBUMINURIA of greater than 300 mg/24 h, leading to reduced GLOMERULAR FILTRATION RATE and END-STAGE RENAL DISEASE.
A group of ISOQUINOLINES in which the nitrogen containing ring is protonated. They derive from the non-enzymatic Pictet-Spengler condensation of CATECHOLAMINES with ALDEHYDES.
A heterogeneous condition in which the heart is unable to pump out sufficient blood to meet the metabolic need of the body. Heart failure can be caused by structural defects, functional abnormalities (VENTRICULAR DYSFUNCTION), or a sudden overload beyond its capacity. Chronic heart failure is more common than acute heart failure which results from sudden insult to cardiac function, such as MYOCARDIAL INFARCTION.
The thin membranous structure supporting the adjoining glomerular capillaries. It is composed of GLOMERULAR MESANGIAL CELLS and their EXTRACELLULAR MATRIX.
Heterocyclic compounds in which an oxygen is attached to a cyclic nitrogen.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
A positive regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.
A steroid metabolite that is the 11-deoxy derivative of CORTICOSTERONE and the 21-hydroxy derivative of PROGESTERONE.
Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.
An element in the alkali group of metals with an atomic symbol K, atomic number 19, and atomic weight 39.10. It is the chief cation in the intracellular fluid of muscle and other cells. Potassium ion is a strong electrolyte that plays a significant role in the regulation of fluid volume and maintenance of the WATER-ELECTROLYTE BALANCE.
Enlargement of the LEFT VENTRICLE of the heart. This increase in ventricular mass is attributed to sustained abnormal pressure or volume loads and is a contributor to cardiovascular morbidity and mortality.
A long-acting dihydropyridine calcium channel blocker. It is effective in the treatment of ANGINA PECTORIS and HYPERTENSION.
The measurement of an organ in volume, mass, or heaviness.
The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
Non-striated, elongated, spindle-shaped cells found lining the digestive tract, uterus, and blood vessels. They are derived from specialized myoblasts (MYOBLASTS, SMOOTH MUSCLE).
An NADPH-dependent enzyme that catalyzes the conversion of L-ARGININE and OXYGEN to produce CITRULLINE and NITRIC OXIDE.
The administration of liquid medication, nutrient, or other fluid through some other route than the alimentary canal, usually over minutes or hours, either by gravity flow or often by infusion pumping.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
Phosphoric acid esters of inositol. They include mono- and polyphosphoric acid esters, with the exception of inositol hexaphosphate which is PHYTIC ACID.
Striated muscle cells found in the heart. They are derived from cardiac myoblasts (MYOBLASTS, CARDIAC).
The rate dynamics in chemical or physical systems.
A non-steroidal anti-inflammatory agent (NSAID) that inhibits the enzyme cyclooxygenase necessary for the formation of prostaglandins and other autacoids. It also inhibits the motility of polymorphonuclear leukocytes.
A class of drugs that act by selective inhibition of calcium influx through cellular membranes.
A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.
An anterior pituitary hormone that stimulates the ADRENAL CORTEX and its production of CORTICOSTEROIDS. ACTH is a 39-amino acid polypeptide of which the N-terminal 24-amino acid segment is identical in all species and contains the adrenocorticotrophic activity. Upon further tissue-specific processing, ACTH can yield ALPHA-MSH and corticotrophin-like intermediate lobe peptide (CLIP).
Pathological processes of the KIDNEY or its component tissues.
Long convoluted tubules in the nephrons. They collect filtrate from blood passing through the KIDNEY GLOMERULUS and process this filtrate into URINE. Each renal tubule consists of a BOWMAN CAPSULE; PROXIMAL KIDNEY TUBULE; LOOP OF HENLE; DISTAL KIDNEY TUBULE; and KIDNEY COLLECTING DUCT leading to the central cavity of the kidney (KIDNEY PELVIS) that connects to the URETER.
The lower right and left chambers of the heart. The right ventricle pumps venous BLOOD into the LUNGS and the left ventricle pumps oxygenated blood into the systemic arterial circulation.
Refers to animals in the period of time just after birth.
2-, 3-, or 4-Pyridinecarboxylic acids. Pyridine derivatives substituted with a carboxy group at the 2-, 3-, or 4-position. The 3-carboxy derivative (NIACIN) is active as a vitamin.
Cell surface proteins that bind ENDOTHELINS with high affinity and trigger intracellular changes which influence the behavior of cells.
A superfamily of PROTEIN-SERINE-THREONINE KINASES that are activated by diverse stimuli via protein kinase cascades. They are the final components of the cascades, activated by phosphorylation by MITOGEN-ACTIVATED PROTEIN KINASE KINASES, which in turn are activated by mitogen-activated protein kinase kinase kinases (MAP KINASE KINASE KINASES).
The HEART and the BLOOD VESSELS by which BLOOD is pumped and circulated through the body.
A CALCIUM-dependent, constitutively-expressed form of nitric oxide synthase found primarily in ENDOTHELIAL CELLS.
Nucleus in the anterior part of the HYPOTHALAMUS.
The presence of albumin in the urine, an indicator of KIDNEY DISEASES.
Rapidly decreasing response to a drug or physiologically active agent after administration of a few doses. In immunology, it is the rapid immunization against the effect of toxic doses of an extract or serum by previous injection of small doses. (Dorland, 28th ed)
A factor synthesized in a wide variety of tissues. It acts synergistically with TGF-alpha in inducing phenotypic transformation and can also act as a negative autocrine growth factor. TGF-beta has a potential role in embryonal development, cellular differentiation, hormone secretion, and immune function. TGF-beta is found mostly as homodimer forms of separate gene products TGF-beta1, TGF-beta2 or TGF-beta3. Heterodimers composed of TGF-beta1 and 2 (TGF-beta1.2) or of TGF-beta2 and 3 (TGF-beta2.3) have been isolated. The TGF-beta proteins are synthesized as precursor proteins.
A response by the BARORECEPTORS to increased BLOOD PRESSURE. Increased pressure stretches BLOOD VESSELS which activates the baroreceptors in the vessel walls. The net response of the CENTRAL NERVOUS SYSTEM is a reduction of central sympathetic outflow. This reduces blood pressure both by decreasing peripheral VASCULAR RESISTANCE and by lowering CARDIAC OUTPUT. Because the baroreceptors are tonically active, the baroreflex can compensate rapidly for both increases and decreases in blood pressure.
The long-term (minutes to hours) administration of a fluid into the vein through venipuncture, either by letting the fluid flow by gravity or by pumping it.
The action of a drug that may affect the activity, metabolism, or toxicity of another drug.
A group of compounds derived from unsaturated 20-carbon fatty acids, primarily arachidonic acid, via the cyclooxygenase pathway. They are extremely potent mediators of a diverse group of physiological processes.
Quantitative determination of receptor (binding) proteins in body fluids or tissue using radioactively labeled binding reagents (e.g., antibodies, intracellular receptors, plasma binders).
Cytoplasmic proteins that specifically bind MINERALOCORTICOIDS and mediate their cellular effects. The receptor with its bound ligand acts in the nucleus to induce transcription of specific segments of DNA.
The action of a drug in promoting or enhancing the effectiveness of another drug.
A powerful vasodilator used in emergencies to lower blood pressure or to improve cardiac function. It is also an indicator for free sulfhydryl groups in proteins.
The balance of fluid in the BODY FLUID COMPARTMENTS; total BODY WATER; BLOOD VOLUME; EXTRACELLULAR SPACE; INTRACELLULAR SPACE, maintained by processes in the body that regulate the intake and excretion of WATER and ELECTROLYTES, particularly SODIUM and POTASSIUM.
A 44-kDa extracellular signal-regulated MAP kinase that may play a role the initiation and regulation of MEIOSIS; MITOSIS; and postmitotic functions in differentiated cells. It phosphorylates a number of TRANSCRIPTION FACTORS; and MICROTUBULE-ASSOCIATED PROTEINS.
The increase in a measurable parameter of a PHYSIOLOGICAL PROCESS, including cellular, microbial, and plant; immunological, cardiovascular, respiratory, reproductive, urinary, digestive, neural, musculoskeletal, ocular, and skin physiological processes; or METABOLIC PROCESS, including enzymatic and other pharmacological processes, by a drug or other chemical.
A polypeptide substance comprising about one third of the total protein in mammalian organisms. It is the main constituent of SKIN; CONNECTIVE TISSUE; and the organic substance of bones (BONE AND BONES) and teeth (TOOTH).
Domesticated bovine animals of the genus Bos, usually kept on a farm or ranch and used for the production of meat or dairy products or for heavy labor.
The lower portion of the BRAIN STEM. It is inferior to the PONS and anterior to the CEREBELLUM. Medulla oblongata serves as a relay station between the brain and the spinal cord, and contains centers for regulating respiratory, vasomotor, cardiac, and reflex activities.
Classic quantitative assay for detection of antigen-antibody reactions using a radioactively labeled substance (radioligand) either directly or indirectly to measure the binding of the unlabeled substance to a specific antibody or other receptor system. Non-immunogenic substances (e.g., haptens) can be measured if coupled to larger carrier proteins (e.g., bovine gamma-globulin or human serum albumin) capable of inducing antibody formation.
Inbred rats derived from Sprague-Dawley rats and used for the study of salt-dependent hypertension. Salt-sensitive and salt-resistant strains have been selectively bred to show the opposite genetically determined blood pressure responses to excess sodium chloride ingestion.
Compounds based on fumaric acid.
A subtype of endothelin receptor found predominantly in the VASCULAR SMOOTH MUSCLE. It has a high affinity for ENDOTHELIN-1 and ENDOTHELIN-2.
The range or frequency distribution of a measurement in a population (of organisms, organs or things) that has not been selected for the presence of disease or abnormality.
The functional units of the kidney, consisting of the glomerulus and the attached tubule.

Quantification of baroreceptor influence on arterial pressure changes seen in primary angiotension-induced hypertension in dogs. (1/7785)

We studied the role of the sino-aortic baroreceptors in the gradual development of hypertension induced by prolonged administration of small amounts of angiotensin II (A II) in intact dogs and dogs with denervated sino-aortic baroreceptors. Short-term 1-hour infusions of A II(1.0-100 ng/kg per min) showed that conscious denervated dogs had twice the pressor sensitivity of intact dogs. Long-term infusions of A II at 5.0 ng/kg per min (2-3 weeks) with continuous 24-hour recordings of arterial pressure showed that intact dogs required 28 hours to reach the same level of pressure attained by denervated dogs during the 1st hour of infusion. At the 28th hour the pressure in both groups was 70% of the maximum value attained by the 7th day of infusion. Both intact and denervated dogs reached nearly the same plateau level of pressure, the magnitude being directly related both the the A II infusion rate and the daily sodium intake. Cardiac output in intact dogs initially decreased after the onset of A II infusion, but by the 5th day of infusion it was 38% above control, whereas blood volume was unchanged. Heart rate returned to normal after a reduction during the 1st day of infusion in intact dogs. Plasma renin activity could not be detected after 24 hours of A II infusion in either intact or denervated dogs. The data indicate that about 35% of the hypertensive effect of A II results from its acute pressor action, and an additional 35% of the gradual increase in arterial pressure is in large measure a result of baroreceptor resetting. We conclude that the final 30% increase in pressure seems to result from increased cardiac output, the cause of which may be decreased vascular compliance. since the blood volume remains unaltered.  (+info)

Acute and chronic dose-response relationships for angiotensin, aldosterone, and arterial pressure at varying levels of sodium intake. (2/7785)

We examined the acute and chronic dose-response relationships between intravenously infused angiotensin II (A II) and the resulting changes in arterial pressure and plasma aldosterone concentration at varying levels of sodium intake. Sequential analysis of plasma aldosterone at each A II infusion rate resulted in an acute dose-related increase in plasma aldosterone which was markedly attenuated after the first 24 hours of infusion, the final level being directly related to the dose of A II and inversely related to sodium intake. A II infused at 5,15, and 23 ng/kg per min was associated with an initial increase (2nd to 8th hour) in plasma aldosterone to 2,6, and 9 times control values, respectively, in dogs receiving 40 mEq Na+/day. But, after the 1st day, aldosterone averaged only 1, 1.7, and 3 times control values for the next 2 weeks at the same rates of A II infusion. Dogs receiving 120 mEq Na+/day during A II infusion exhibited only a transient increase in plasma aldosterone during the 1st day. Sustained hypertension developed over a period of a week at all doses of A II at normal and high sodium intake, but did not occur at any dose of A II in sodium-depleted dogs. Increasing sodium intake from 40 to 120 mEq/day resulted in higher levels of hypertension, 125% compared to 140% of ocntrol values for dogs infused with A II, 5.0 ng/kg per min. We conclude that primary angiotensin-induced hypertension need not be associated with increased levels of plasma aldosterone, which appears to remain elevated only with amounts of A II greater than those required to sustain a significant degree of hypertension.  (+info)

Relaxin is a potent renal vasodilator in conscious rats. (3/7785)

The kidneys and other nonreproductive organs vasodilate during early gestation; however, the "pregnancy hormones" responsible for the profound vasodilation of the renal circulation during pregnancy are unknown. We hypothesized that the ovarian hormone relaxin (RLX) contributes. Therefore, we tested whether the administration of RLX elicits renal vasodilation and hyperfiltration in conscious adult, intact female rats. After several days of treatment with either purified porcine RLX or recombinant human RLX 2 (rhRLX), effective renal plasma flow (ERPF) and glomerular filtration rate (GFR) increased by 20%-40%. Comparable renal vasodilation and hyperfiltration was also observed in ovariectomized rats, suggesting that estrogen and progesterone are unnecessary for the renal response to rhRLX. The nitric oxide synthase inhibitor Nomega-nitro-L-arginine methyl ester completely abrogated the increase in ERPF and GFR elicited by chronic administration of purified porcine RLX. In contrast, the renal vasoconstrictory response to angiotensin II was attenuated by the RLX treatment. Short-term infusion of purified porcine RLX to conscious rats over several hours failed to increase ERPF and GFR. Plasma osmolality was consistently reduced by the chronic administration of both RLX preparations. In conclusion, the renal and osmoregulatory effects of chronic RLX administration to conscious rats resemble the physiological changes of pregnancy in several respects: (a) marked increases in ERPF and GFR with a mediatory role for nitric oxide; (b) attenuation of the renal circulatory response to angiotensin II; and (c) reduction in plasma osmolality.  (+info)

Angiotensin II type 1 receptor-mediated inhibition of K+ channel subunit kv2.2 in brain stem and hypothalamic neurons. (4/7785)

Angiotensin II (Ang II) has powerful modulatory actions on cardiovascular function that are mediated by specific receptors located on neurons within the hypothalamus and brain stem. Incubation of neuronal cocultures of rat hypothalamus and brain stem with Ang II elicits an Ang II type 1 (AT1) receptor-mediated inhibition of total outward K+ current that contributes to an increase in neuronal firing rate. However, the exact K+ conductance(s) that is inhibited by Ang II are not established. Pharmacological manipulation of total neuronal outward K+ current revealed a component of K+ current sensitive to quinine, tetraethylammonium, and 4-aminopyridine, with IC50 values of 21.7 micromol/L, 1.49 mmol/L, and 890 micromol/L, respectively, and insensitive to alpha-dendrotoxin (100 to 500 nmol/L), charybdotoxin (100 to 500 nmol/L), and mast cell degranulating peptide (1 micromol/L). Collectively, these data suggest the presence of Kv2.2 and Kv3.1b. Biophysical examination of the quinine-sensitive neuronal K+ current demonstrated a macroscopic conductance with similar biophysical properties to those of Kv2.2 and Kv3.1b. Ang II (100 nmol/L), in the presence of the AT2 receptor blocker PD123,319, elicited an inhibition of neuronal K+ current that was abolished by quinine (50 micromol/L). Reverse transcriptase-polymerase chain reaction analysis confirmed the presence of Kv2.2 and Kv3.1b mRNA in these neurons. However, Western blot analyses demonstrated that only Kv2.2 protein was present. Coexpression of Kv2.2 and the AT1 receptor in Xenopus oocytes demonstrated an Ang II-induced inhibition of Kv2.2 current. Therefore, these data suggest that inhibition of Kv2.2 contributes to the AT1 receptor-mediated reduction of neuronal K+ current and subsequently to the modulation of cardiovascular function.  (+info)

Recent progress in angiotensin II type 2 receptor research in the cardiovascular system. (5/7785)

Angiotensin II (Ang II) plays an important role in regulating cardiovascular hemodynamics and structure. Multiple lines of evidence have suggested the existence of Ang II receptor subtypes, and at least 2 distinct receptor subtypes have been defined on the basis of their differential pharmacological and biochemical properties and designated as type 1 (AT1) and type 2 (AT2) receptors. To date, most of the known effects of Ang II in adult tissues are attributable to the AT1 receptor. Recent cloning of the AT2 receptor contributes to reveal its physiological functions, but many functions of the AT2 receptor are still an enigma. AT1 and AT2 receptors belong to the 7-transmembrane, G protein-coupled receptor family. However, accumulating evidence demonstrates that the function and signaling mechanisms of these receptor subtypes are quite different, and these receptors may exert opposite effects in terms of cell growth and blood pressure regulation. We will review the role of the AT2 receptor in the cardiovascular system and the molecular and cellular mechanisms of AT2 receptor action.  (+info)

Intracellular sodium modulates the expression of angiotensin II subtype 2 receptor in PC12W cells. (6/7785)

Although the angiotensin II subtype 2 receptor (AT2-R) is expressed abundantly in the adrenal medulla, its physiological significance has not yet been determined. To obtain fundamental knowledge of the regulation of AT2-R expression in the adrenal medulla, we investigated the effects of modulating several ion channels on AT2-R expression in PC12W cells. Experiments were performed after 24 hours of serum depletion under subconfluent conditions. After 48 hours of treatment with various agonists or antagonists, the receptor density and mRNA level of AT2-Rs were quantified by 125I-[Sar1, Ile8]angiotensin II binding and Northern blot analysis. Ouabain (10 to 100 nmol/L) and insulin (10 to 100 nmol/L) dose-dependently increased receptor density and mRNA level. Analysis of the binding characteristics revealed that the ouabain-dependent increase in AT2-R levels was due to an increase in binding capacity without a change in the Kd value. These increases were blocked by lowering the Na+ concentration in the medium. A low concentration of the sodium ionophore monensin (10 nmol/L), the K+-channel blocker quinidine (10 micromol/L), and the ATP-sensitive K+-channel blockers tolbutamide (100 micromol/L) and glybenclamide (10 micromol/L) also significantly increased receptor density, but the ATP-sensitive K+-channel agonist cromakalim (100 micromol/L) decreased receptor density significantly (P<0.01). Nifedipine (10 micromol/L) decreased basal receptor density and completely blocked the increase in receptor density caused by these agents. The increase in receptor density caused by an increase in intracellular Na+ was accompanied by an increase in mRNA level, whereas the ATP-sensitive K+-channel blockers did not change mRNA level. Nifedipine slightly decreased mRNA level. These results suggest that AT2-R expression is sensitively regulated by intracellular cation levels. The change in intracellular Na+ level transcriptionally regulates AT2-R expression, whereas the K+-channel blocker-dependent upregulation appears to be at least in part posttranslational.  (+info)

Kidney aminopeptidase A and hypertension, part II: effects of angiotensin II. (7/7785)

Aminopeptidase A (APA) is the principal enzyme that metabolizes angiotensin II (Ang II) to angiotensin III. Previously, we showed that kidney APA was elevated in spontaneously hypertensive rats and was reduced after angiotensin-converting enzyme inhibition. In the present study, we sought to determine whether kidney APA expression was altered after chronically elevated Ang II, either exogenously delivered via osmotic minipumps or endogenously produced in two-kidney, one clip (2K1C) hypertensive rats. Ang II (200 ng. kg-1. min-1) was infused subcutaneously for 1 or 2 weeks by osmotic minipumps, and 2K1C rats were tested 4 weeks after unilateral renal artery clipping. Blood pressure was not significantly elevated in the Ang II-infused animals but was significantly increased at 3 and 4 weeks in the 2K1C animals. APA was significantly elevated approximately 2-fold in kidney cortical membranes from Ang II-infused animals but was decreased 45% in the clipped kidney and 18% in the nonclipped kidneys from 2K1C animals. Isolated glomeruli from Ang II-infused animals and the nonclipped kidneys from 2K1C animals had markedly higher APA activity and immunoreactivity. Likewise, histochemical and immunohistochemical studies indicated that APA levels were increased in glomeruli from angiotensin-infused animals and in both nonclipped and clipped kidneys from 2K1C animals. In contrast, tubular APA was decreased in tubular elements from 2K1C animals, most markedly in the clipped kidneys. Thus, despite the increase in glomerular APA expression in kidneys from 2K1C animals, the decrease in tubular APA expression is more extensive and accounts for the measured reduction in total APA in cortical homogenates. Because clipped kidneys are not exposed to high blood pressure, these results suggest that glomerular APA expression is positively regulated and tubular APA negatively regulated by Ang II. These results further suggest that changes in kidney APA expression could influence the progression of angiotensin-dependent hypertension.  (+info)

Insulin-like growth factor-1 induces Mdm2 and down-regulates p53, attenuating the myocyte renin-angiotensin system and stretch-mediated apoptosis. (8/7785)

Insulin-like growth factor (IGF)-1 inhibits apoptosis, but its mechanism is unknown. Myocyte stretching activates p53 and p53-dependent genes, leading to the formation of angiotensin II (Ang II) and apoptosis. Therefore, this in vitro system was used to determine whether IGF-1 interfered with p53 function and the local renin-angiotensin system (RAS), decreasing stretch-induced cell death. A single dose of 200 ng/ml IGF-1 at the time of stretching decreased myocyte apoptosis 43% and 61% at 6 and 20 hours. Ang II concentration was reduced 52% at 20 hours. Additionally, p53 DNA binding to angiotensinogen (Aogen), AT1 receptor, and Bax was markedly down-regulated by IGF-1 via the induction of Mdm2 and the formation of Mdm2-p53 complexes. Concurrently, the quantity of p53, Aogen, renin, AT1 receptor, and Bax was reduced in stretched myocytes exposed to IGF-1. Conversely, Bcl-2 and the Bcl-2-to-Bax protein ratio increased. The effects of IGF-1 on cell death, Ang II synthesis, and Bax protein were the consequence of Mdm2-induced down-regulation of p53 function. In conclusion, the anti-apoptotic impact of IGF-1 on stretched myocytes was mediated by its capacity to depress p53 transcriptional activity, which limited Ang II formation and attenuated the susceptibility of myocytes to trigger their endogenous cell death pathway.  (+info)

TY - JOUR. T1 - Regulation of proximal tubule transport by angiotensin II. AU - Quan, Albert. AU - Baum, Michel. PY - 1997. Y1 - 1997. N2 - Angiotensin II maintains extracellular volume homeostasis, in part, by regulating proximal tubule transport. Physiological doses of angiotensin II stimulate volume and solute transport in the proximal tubule independent of changes in the glomerular filtration rate. Stimulation of bicarbonate transport primarily occurs via increasing activity of the sodium/hydrogen exchanger and the sodium/bicarbonate cotransporter. The effects of circulating angiotensin II are mediated by angiotensin II receptors on the basolateral membrane of the proximal tubule. Recently, the proximal tubule was found to synthesize and secrete angiotensin II into the lumen. The luminal membrane contains angiotensin II receptors and luminal angiotensin II levels are 100 to 200-fold higher than that found in plasma. Luminal angiotensin II receptor blockade or luminal inhibition of ...
Over the last 2 decades, it has become clear that angiotensin can be generated not only in the systemic circulation but also in multiple tissue sites, where its production can be regulated by local factors. Given the ability of angiotensin II to influence target cell proliferation, hypertrophy, and apoptosis, tissue angiotensin systems potentially play an important role in a wide variety of physiological processes. In this issue of Hypertension, De Mello and Danser1 review the evidence for the synthesis of angiotensin II in the heart and discuss its possible role in health and disease. Their review complements other recent reviews of this subject, such as that by Dostal and Baker.2 Uniquely, however, the present review discusses the potential role of intracellular angiotensin II, called intracrine angiotensin II, in intercellular signaling and calcium flux in the heart. These findings are based on De Mellos studies1 of renin, angiotensin I, and angiotensin II dialyzed into rat cardiac cells. ...
Angiotensin II receptor type 1 or AT1 receptor is the best characterized angiotensin receptor. It has vasopressor effects and regulates aldosterone secretion. It is an important effector controlling blood pressure and volume in the cardiovascular system. Angiotensin II receptor antagonists are drugs indicated for hypertension, diabetic nephropathy and congestive heart failure. The AT1 receptor mediates the major cardiovascular effects of angiotensin II. Effects include vasoconstriction, aldosterone synthesis and secretion, increased vasopressin secretion, cardiac hypertrophy, augmentation of peripheral noradrenergic activity, vascular smooth muscle cells proliferation, decreased renal blood flow, renal renin inhibition, renal tubular sodium reuptake, modulation of central sympathetic nervous system activity, cardiac contractility, central osmocontrol and extracellular matrix formation. The angiotensin receptor is activated by the vasoconstricting peptide angiotensin II. The activated receptor in ...
Nox2-containing NADPH oxidases are reported to be involved in the development of cardiac fibrosis in response to chronic angiotensin II infusion, but the cellular source(s) of Nox2 involved in fibrosis remains unclear. We investigated the role of endothelial Nox2 in angiotensin II-induced left ventricular hypertrophy (LVH). Male transgenic mice with endothelial-specific overexpression of Nox2 were compared with matched wild-type (wt) littermates after angiotensin II (1.1 mg/kg per day) or saline infusion for 14 days. Basal blood pressure and left ventricular NADPH oxidase activity were similar in wt and transgenic mice. After angiotensin II infusion, both wt and transgenic groups developed similar hypertension (170.2±11.6 vs 170.4±12.3 mm Hg; n=10) and hypertrophy (left ventricular/body weight ratio 4.8±0.2 vs 4.7±0.2 mg/g; and echocardiographic septal thickness increased by 34% wt and 37% transgenic mice; n,10). NADPH oxidase activity was higher in angiotensin II-infused transgenic compared ...
The angiotensin II receptors, (AGTR1) and (AGTR2), are a class of G protein-coupled receptors with angiotensin II as their ligands. They are important in the renin-angiotensin system: they are responsible for the signal transduction of the vasoconstricting stimulus of the main effector hormone, angiotensin II. The AT1 and AT2 receptors share a sequence identity of ~30%, but have a similar affinity for angiotensin II, which is their main ligand. The AT1 receptor is the best elucidated angiotensin receptor. The AT1 subtype is found in the heart, blood vessels, kidney, adrenal cortex, lung and brain and mediates the vasoconstrictor effects. The angiotensin receptor is activated by the vasoconstricting peptide angiotensin II. The activated receptor in turn couples to Gq/11 and Gi/o and thus activates phospholipase C and increases the cytosolic Ca2+ concentrations, which in turn triggers cellular responses such as stimulation of protein kinase C. Activated receptor also inhibits adenylate cyclase and ...
1. Infusion of angiotensin II into dogs at constant dose over 2 weeks caused a progressive rise in arterial pressure.. 2. When the infusion was stopped the pressure dropped slowly from hypertensive levels over 48 h.. 3. Dose-response studies at weekly intervals showed progressive elevation, without steepening, of the plasma angiotensin II-blood pressure curve.. 4. Thus, during prolonged administration of angiotensin II, a given plasma concentration of the peptide can sustain a higher arterial pressure than it can during acute infusions. ...
Ang II infusion induces an immediate vasoconstrictive response that is typically followed by a gradual recovery despite continued infusion of the pressor agent. The buffering effect on Ang II-induced vasoconstriction is at least in part mediated by vasodilatory PGs, including PGE2.14,16-18 In a previous study, we discovered a novel role of mPGES-1-derived PGE2 in modulating Ang II-induced hypertensive response. In extension of this work, the present study demonstrated that the vasculoprotection of PGE2 is mediated by the suppression of oxidative stress.. Ang II-induced hypertension in mPGES-1−/− mice was completely prevented by Tempol treatment and was fully restored on termination of the antioxidant. Treatment with a second antioxidant, apocynin, produced a similar blood pressure-lowering effect. Apocynin is widely used as an inhibitor of NADPH oxidase19 but was recently found to inhibit vascular oxidative stress via an NADPH oxidase-independent mechanism.20 Together, the similar results ...
Background: In humans, infusion of angiotensin II increases erythropoietin (EPO) serum levels in a dose-dependent manner. However, it is not known whether angiotensin II stimulates EPO-producing renal fibroblasts directly via a receptor or by alteration of renal hemodynamics with a consecutive decrease of renal blood flow. The purpose of this study was to investigate EPO secretion and gene expression under direct angiotensin II stimulation in a cell model thereby excluding hemodynamic effects. Methods: In an established EPO-secreting cell line (HepG2), EPO concentrations were measured under various conditions (normoxia and hypoxia) and different angiotensin II concentrations. mRNA levels of EPO were analyzed by LightCycler quantitative PCR after reverse transcription normalized to the housekeeping gene cyclophilin. Results: Angiotensin II did not affect EPO production in any concentration (1 n M or 100 µ M ) under conditions of normoxia. Reduced oxygen tension (1% O|sub|2|/sub|) led to the
1. When the renin-angiotensin system of rats had been suppressed by a high salt diet or by bilateral nephrectomy, large doses of angiotensin II antiserum were required to block the pressor action of exogenous angiotensin II. Infusion of renin profoundly lowered the blocking requirement of such animals.. 2. It is postulated that renin bound to blood vessels generates angiotensin locally which is taken up by vascular receptors. Where such receptors are left unoccupied and free to bind exogenous angiotensin, high doses of blocking antisera are required.. 3. Animals with hypertension produced by renal artery constriction with contralateral nephrectomy were shown to be in positive sodium balance. Nevertheless their blocking requirement was low.. 4. It is suggested that the local generation of angiotensin may play a role in the production of renal hypertension and that this accounts for the development of hypertension even in animals immunized against angiotensin. ...
Background: Under conditions of cardiovascular dysfunction, protease-activated receptor 2 (PAR2) agonists maintain vasodilatation activity, which has been attributed to increased cyclooxygenase-2, nitric oxide synthase and calcium-activated potassium channel (SK3.1) activities. Protease-activated receptor 2 agonist mediated vasodilatation is unknown under conditions of dysfunction caused by angiotensin II. The main purpose of our study was to determine whether PAR2-induced vasodilatation of resistance arteries was attenuated by prolonged angiotensin II treatment in mice. We compared the vasodilatation of resistance-type arteries (mesenteric) from angiotensin II-treated PAR2 wild-type mice (WT) induced by PAR2 agonist 2-furoyl-LIGRLO-amide (2fly) to the responses obtained in controls (saline treatment). We also investigated arterial vasodilatation in angiotensin IItreated PAR2 deficient (PAR2-/-) mice. Results: 2fly-induced relaxations of untreated arteries from angiotensin II-treated WT were not ...
TY - JOUR. T1 - Reactive oxygen species and cyclooxygenase 2-derived thromboxane A2 reduce angiotensin II type 2 receptor vasorelaxation in diabetic rat resistance arteries. AU - Retailleau, Kevin. AU - Belin De Chantemèle, Eric J.. AU - Chanoine, Sébastien. AU - Guihot, Anne Laure. AU - Vessières, Emilie. AU - Toutain, Bertrand. AU - Faure, Sébastien. AU - Bagi, Zsolt. AU - Loufrani, Laurent. AU - Henrion, Daniel. PY - 2010/2. Y1 - 2010/2. N2 - Angiotensin II has a key role in the control of resistance artery tone and local blood flow. Angiotensin II possesses 2 main receptors. Although angiotensin II type 1 receptor is well known and is involved in the vasoconstrictor and growth properties of angiotensin II, the role of the angiotensin II type 2 receptor (AT2R) remains much less understood. Although AT2R stimulation induces vasodilatation in normotensive rats, it induces vasoconstriction in pathological conditions involving oxidative stress and cyclooxygenase 2 expression. Thus, we studied ...
Angiotensin I is converted to angiotensin II (AII) through removal of two C-terminal residues by the enzyme angiotensin-converting enzyme (ACE), primarily through ACE within the lung (but also present in endothelial cells, kidney epithelial cells, and the brain). Angiotensin II acts on the CNS to increase ADH production, and also acts on venous and arterial vessels smooth muscle to cause vasoconstriction. Angiotensin II also increases Aldosterone secretion, therefore, it acts as an endocrine, autocrine/paracrine, and intracrine hormone.. ACE is a target of ACE inhibitor drugs, which decrease the rate of Angiotensin II production. Angiotensin II increases blood pressure by stimulating the Gq protein in vascular smooth muscle cells (which in turn activates an IP3-dependent mechanism leading to a rise in intracellular calcium levels and ultimately causing contraction). In addition, angiotensin II acts at the Na/H+ exchanger in the proximal tubules of the kidney to stimulate Na reabsorption and H+ ...
It is now firmly established that inhibition of ACE does have a markedly beneficial effect in the treatment of heart failure. ACE inhibitor therapy, however, does not completely block angiotensin II production, and in some patients, angiotensin II levels remain elevated, in part, because of the conversion of angiotensin I to angiotensin II by chymase activity.29 Thus, continued AT2 receptor stimulation could occur. This hypothesis is indirectly supported by the relative upregulation of the AT2 receptor in human heart failure,30 31 although this finding is controversial.32 33 Currently, no therapeutic agents that specifically act on the AT2 receptor are approved for clinical trials. However, numerous AT1 receptor blockers are available that could hypothetically shunt the activity of the cardiac RAS toward stimulation of the beneficial AT2 receptor.. Two separate clinical approaches evaluate this hypothesis. First, ACE inhibitor therapy was directly compared with AT1 receptor antagonist therapy in ...
TY - JOUR. T1 - Ionophoric Properties of Angiotensin II Peptides. Nuclear Magnetic Resonance Kinetic Studies of the Hormone-Mediated Transport of Manganese Ions Across Phosphatidylcholine Bilayers. AU - Degani, Hadassa. AU - Lenkinski, Robert E.. PY - 1980/1/1. Y1 - 1980/1/1. N2 - The linear peptide hormones angiotensin II and [Asn1, Val5] angiotensin II are found to mediate the transport of Mn(II) ions across phosphatidylcholine bilayers. Nuclear magnetic resonance spectroscopy (NMR) is applied to monitor the rate of transport of Mn(II) ions by measuring the rate of disappearance of the NMR signal of the choline methyl groups of the inner phospholipid layer. This rate of disappearance is analyzed in terms of a pseudo-first-order rate equation for the transport process. The rate of transport of Mn(II) varies linearly with both the concentrations of Mn(II) and angiotensin II (A-II) present, suggesting that the ions are transported in a complex with 1:1 stoichiometry. An analysis of the ...
Angiotensin II regulation of L-type calcium currents in cardiac muscle is controversial and the underlying signaling events are not completely understood. Moreover, the possible role of auxiliary subunit composition of the channels in Angiotensin II modulation of L-type calcium channels has not yet …
We studied the effects of intravenous infusion of angiotensin II on the circulation of the fetus in lambs in utero through chronically maintained intravascular catheters. Angiotensin II infused in doses of 29-280 ng/min per kg fetal weight resulted in an increase in plasma angiotensin II from a control value of 87 +/- 17 to 341 +/- 129 (mean +/- SE) pg/ml; these levels are similar to those observed following hemorrhage in fetal lambs. Fetal mean arterial blood pressure increased from 46 +/- 2.0 to 56 +/- 2.7 torr and fetal heart rate increased from 172 +/- 6 to 189 +/- 6 beats/min, an effect which was not altered by beta-adrenergic or cholinergic blockade. Fetal cardiac output and its distribution were measured before and during infusion of angiotensin II by the radionuclide-labeled microsphere technique. Combined ventricular output increased significantly from 526 +/- 32 to 616 +/- 24 ml/min per kg fetal body weight. Angiotensin constricted the umbilical-placental circulation as well as the ...
TY - JOUR. T1 - Vasopressor response to angiotensin II infusion in patients with chronic heart failure receiving β-blockers. AU - Vittorio, Timothy J.. AU - Lang, Chim C.. AU - Katz, Stuart D.. AU - Packer, Milton. AU - Mancini, Donna M.. AU - Jorde, Ulrich P.. PY - 2003/1/21. Y1 - 2003/1/21. N2 - Background - A synergistic interaction between the angiotensin II (Ang II) type 1 receptor and α1-adrenergic receptors has been described. We hypothesized that the nonselective β-antagonist carvedilol, through its α1-adrenergic blocking properties, may modulate vascular reactivity to Ang II in patients with chronic heart failure (CHF). Accordingly, we compared the vasopressor response to infused Ang II in patients treated with carvedilol and metoprolol, a selective β-antagonist. Methods and Results - All subjects were treated with carvedilol or metoprolol for at least 3 months. ACE inhibitor therapy was standardized to enalapril 40 mg/d or the maximally tolerated dose. Exogenous Ang II was ...
The rennin-angiotensin II system (RAS) and the insulin-PI3kinase signalling pathways cross-interact with important physiological and pathophysiological consequences for cells and the whole organism. Here, the effect of 24 h pre-incubation of EA.hy926 with two different concentrations of angiotensin II, on insulin-mediated activation of the PI3kinase-AKT-eNOS signalling was investigated. Quiescent EA.hy926 cells were treated with insulin (100 nM, 30 min) following 24 h pre-treatment with or without either 0.1 or 1 µM of angiotensin II. Cell lysates were immunoblotted for phospho AKT Ser-473, phospho eNOS Ser-1177 and normalized with β-actin. Homogenates of EA.hy926 treated with insulin in the presence or absence of 1 µM angiotensin II, were also subjected to nitric oxide synthase (NOS) activity assay using titrated arginine as substrate. To exclude cytotoxicity of the 1 µM angiotensin II concentration, Trypan blue cell viability assay as well as the microscopic examination of
The examination of synthetic valyl-5-angiotensin II-amide in the conscious dog revealed the following:. 1. Both the arterial and the central venous pressure responses exhibit tachyplylaxis when high doses of angiotensin II are administered, althoug not when medium or low doses are given. Cross-tachyphylaxis can be demonstrated between renin and angiotensin II but not between either of these and norepinephrine. These results suggest that tachyphylaxis to renin is due to tachyphylaxis to angiotensin.. 2. Angiotensin II and norepinephrine provoke a dose-dependent increase in central venous pressure. The threshold dose is about 10 times higher than that necessary for the effect on arterial pressure. In doses eliciting the same increase of arterial blood pressure, norepinephrine is about twice as active on the venous pressure as angiotensin II.. 3. Anesthesia and atropinization both reduce or abolish the effect of angiotensin II as well as that of norepinephrine on the venous pressure, indicating the ...
Methods and Results-Mice infused with angiotensin II showed a marked increase in interleukin-12p35 expression in cardiac macrophages. The degree of cardiac fibrosis was significantly enhanced in interleukin-12p35 knockout (p35-KO) mice compared with wild-type (WT) littermates in response to angiotensin II. Fibrotic hearts of p35-KO mice showed increased accumulation of alternatively activated (M2) macrophages and expression of M2 genes such as Arg-1 and Fizz1. Bone marrow-derived macrophages from WT or p35-KO mice did not differ in differentiation in response to angiotensin II treatment; however, in the presence of CD4+ T cells, macrophages from p35-KO mice differentiated into M2 macrophages and showed elevated expression of transforming growth factor-β. Moreover, CD4+ T-cell-treated p35-KO macrophages could stimulate cardiac fibroblasts to differentiate into α-smooth muscle actin-positive and collagen I-positive myofibroblasts in 3-dimensional nanofiber gels. Neutralizing antibodies against ...
1. This study was designed to quantify the role of angiotensin II in determining the chronic relationships between arterial pressure, renal haemodynamics and sodium excretion.. 2. In six control dogs sodium balance was achieved during chronic increases in sodium intake from 5 to 495 mmol/day with small increases in arterial pressure (7mmHg), moderate increases in glomerular filtration rate (19%) and decreases in filtration fraction. Similar increases in sodium intake in dogs whose circulating levels of angiotensin II were fixed, due to a constant intravenous infusion of 4.85 pmol of angiotensin II min−1 kg−1, caused large increases in arterial pressure (42%), glomerular filtration rate (31%), filtration fraction and calculated renal sodium reabsorption above control. In six dogs whose angiotensin II formation was blocked by SQ 14 225, sodium balance at intakes of 5-80 mmol/day occurred at reduced arterial pressure, glomerular filtration rate, filtration fraction and sodium reabsorption ...
1. Competitive or non-competitive inhibition of the myotropic and pressor response of angiotensin II is dependent on the nature of the substituent in position 8 of the antagonist peptide analogue. Substituents in other positions of the molecule, particularly position 1, contribute greatly to the potency of these antagonists.. 2. As is evidenced after adrenalectomy or after blockade with phentolamine and phenoxybenzamine, the initial pressor activity observed with all the antagonistic peptides is partially due to the release of catecholamines and partially to a direct myotropic effect.. 3. [Sar1, Thr8]angiotensin II has been found to possess the lowest agonist to antagonist ratio of all antagonists tested.. 4. [Des-Asp1, Ile8]angiotensin II selectively and specifically inhibits the release of aldosterone from adrenal cortex. Thus, unlike angiotensin II, this heptapeptide has pronounced organ specificity, suggesting that the heptapeptide (angiotensin III) is the aldosterone-releasing ...
Peptides , Angiotensins and Related Peptides , Angiotensin II, human; The octapeptide angiotensin II (Ang II) exerts a wide range of effects on the cardiovascular system. It is also implicated in the regulation of cell proliferation, fibrosis and apoptosis. Ang II is formed by cleavage of Ang I by the angiotensin-converting enzyme (ACE) or chymases. Human heart chymase, a chymotrypsin-like serine proteinase, hydrolyzes the Phe8-His9 bond to yield the octapeptide hormone angiotensin II and His-Leu.; DRVYIHPF; H-Asp-Arg-Val-Tyr-Ile-His-Pro-Phe-OH
TY - JOUR. T1 - Downregulation of vascular angiotensin II type 1 receptor by thyroid hormone. AU - Fukuyama, Kae. AU - Ichiki, Toshihiro. AU - Takeda, Kotaro. AU - Tokunou, Tomotake. AU - Iino, Naoko. AU - Masuda, Satoko. AU - Ishibashi, Minako. AU - Egashira, Kensuke. AU - Shimokawa, Hiroaki. AU - Hirano, Katsuya. AU - Kanaide, Hideo. AU - Takeshita, Akira. PY - 2003/3/1. Y1 - 2003/3/1. N2 - Thyroid hormone has a broad effect on cardiovascular system. 3,3′,5-triiodo-L-thyronine (T3), a biologically active form of thyroid hormone, increases cardiac contractility. T3 causes arterial relaxation and reduction of systemic vascular resistance, resulting in an increase in cardiac output. However, the molecular mechanisms of vascular relaxation by T3 are incompletely characterized. We studied the effect of T3 on the angiotensin (Ang) II type 1 receptor (AT1R) expression in vascular smooth muscle cells. T3 dose-dependently decreased expression levels of AT1R mRNA, with a peak at 6 hours of ...
ABSTRACT. Angiotensin II (Ang II) is a critical component of the renin-angiotensin system that contributes to hypertension. Although platelets in blood from hypertensive subjects have an abnormal biological profile, it is unclear if circulating Ang II influences platelet aggregation or thrombus formation. One of the abnormalities presented to the platelets during hypertension is an elevated plasma concentration of serotonin (5-HT) caused by reduced 5-HT uptake secondary to loss of the 5-HT transporter (SERT) on the platelet plasma membrane. In the current study, we evaluated in vivo platelet function after 7 days of subcutaneous Ang II infusion to establish hypertension in mice and additionally assessed the biology of isolated platelets exposed to Ang II in vitro. The administration of Ang II elevated systolic blood pressure, but markers of platelet activation including P-selectin and PEJon/A staining were not changed. However, the aggregation response to collagen was reduced in isolated ...
Angiotensin I is converted to angiotensin II (AII) through removal of two C-terminal residues by the enzyme angiotensin-converting enzyme (ACE), primarily through ACE within the lung (but also present in endothelial cells, kidney epithelial cells, and the brain). Angiotensin II acts on the CNS to increase vasopressin production, and also acts on venous and arterial smooth muscle to cause vasoconstriction. Angiotensin II also increases aldosterone secretion, therefore, it acts as an endocrine, autocrine/paracrine, and intracrine hormone. ACE is a target of ACE inhibitor drugs, which decrease the rate of angiotensin II production. Angiotensin II increases blood pressure by stimulating the Gq protein in vascular smooth muscle cells (which in turn activates an IP3-dependent mechanism leading to a rise in intracellular calcium levels and ultimately causing contraction). In addition, angiotensin II acts at the Na+/H+ exchanger in the proximal tubules of the kidney to stimulate Na reabsorption and H+ ...
Angiotensin II (Ang II) is a critical component of the reninangiotensin system that contributes to hypertension. Although platelets in blood from hypertensive subjects have an abnormal biological profile, it is unclear if circulating Ang II influences platelet aggregation or thrombus formation. One of the abnormalities presented to the platelets during hypertension is an elevated plasma concentration of serotonin (5-HT) caused by reduced 5-HT uptake secondary to loss of the 5-HT transporter (SERT) on the platelet plasma membrane. In the current study, we evaluated in vivo platelet function after 7 days of subcutaneous Ang II infusion to establish hypertension in mice and additionally assessed the biology of isolated platelets exposed to Ang II in vitro. The administration of Ang II elevated systolic blood pressure, but markers of platelet activation including P-selectin and PEJon/A staining were _disibledevent=font-size:10pt;line-height:1.5;font-family:Verdana;>5-HT in platelets, an event
TY - JOUR. T1 - Angiotensin II relaxes microvessels via the AT 2 receptor and Ca 2+ -activated K + (BK Ca ) channels AU - Dimitropoulou, Christiana. AU - White, Richard E.. AU - Fuchs, Leslie. AU - Zhang, Hanfang. AU - Catravas, John D.. AU - Carrier, Gerald O.. PY - 2001/1/1. Y1 - 2001/1/1. N2 - Angiotensin II (Ang II) is one of the most potent vasoconstrictor substances, yet paradoxically. Ang II may dilate certain vascular beds via an undefined mechanism. Ang II-induced vasoconstriction is mediated by the AT 1 receptor, whereas the relative expression and functional importance of the AT 2 receptor in regulating vascular resistance and blood pressure are unknown. We now report that Ang II induces relaxation of mesenteric microvessels and that this vasodilatory response was unaffected by losartan, an AT 1 receptor antagonist, but was inhibited by PD123.319. a selective antagonist of AT 2 receptors. In addition, reverse transcriptase-polymerase chain reaction studies revealed high amounts of AT ...
TY - JOUR. T1 - Impaired pulmonary conversion of angiotensin I to angiotensin II in rats exposed to chronic hypoxia. AU - Jackson, Robert. AU - Narkates, A. J.. AU - Oparil, S.. PY - 1986/1/1. Y1 - 1986/1/1. N2 - The effects of exposing rats to hypoxia at normal atmospheric pressure for periods of 21-24 days on intrapulmonary conversion of angiotensin I (ANG I) to angiotensin II (ANG II) were examined using an isolated rat lung preparation perfused at constant flow. 125I-ANG I (160 fmol) was injected alone and with graded doses (0.1, 1.0, and 100 nmol) of unlabeled ANG I into the pulmonary artery, and the effluent was collected for measurement of ANG I, ANG II, and metabolites. At low doses of injected ANG I (125I-ANG I alone or with 0.1 to 1.0 nmol unlabeled ANG I), the percent conversion of ANG I to ANG II was 67.5 ± 2.1 (SE), 65.1 ± 2.0, and 62.5 ± 1.6 in 21-day hypoxia-exposed animals and 83.8 ± 2.7, 81.4 ± 3.9, and 79.6 ± 2.3 (P , 0.01) in control rats maintained under normoxic ...
Szekeres, Mária and Nádasy, György László and Turu, Gábor and Soltész-Katona, Eszter and Benyó, Zoltán and Ruisanchez, Éva and Szabó, Eszter and Takáts, Zoltán and Bátkai, Sándor and Tóth, Zsuzsanna E. and Hunyady, László (2015) Endocannabinoid-mediated modulation of G protein-coupled receptor signaling-induced vasoconstriction and hypertension. MOLECULAR AND CELLULAR ENDOCRINOLOGY, 403C. pp. 46-56. ISSN 0303-7207 Gyires, Klára and Rónai, András Z and Zádori, Zoltán S and Tóth, Viktória E and Németh, József and Szekeres, Mária and Hunyady, László (2014) Angiotensin II-induced activation of central AT1 receptors exerts endocannabinoid-mediated gastroprotective effect in rats. Molecular and cellular endocrinology, 382 (2). pp. 971-8. ISSN 1872-8057 Gyires, Klára and Rónai, Z. András and Zádori, Zoltán Sándor and Tóth, Viktória E. and Németh, József and Szekeres, Mária and Hunyady, László (2014) Angiotensin II-induced activation of central AT1 receptors ...
Infusion of angiotensin II continuously into the renal artery of conscious dogs led to a modest increase in arterial pressure that was associated in the steady state with increased total peripheral resistance. The dose of angiotensin II used (0.5 ng ⋅ kg−1 ⋅ min−1) was subpressor acutely (both over the 1st h and at 24 h) and reduced renal blood flow by about 15% during the 1st h of infusion. Onday 7 of the angiotensin II infusion, mean arterial pressure was still close to preinfusion values, and an increase in resting arterial pressure was observed only fromday 14 onward, with the elevation in arterial pressure being well maintained for the rest of the infusion period.. Evidence that the hypertension was due to the intrarenal actions of angiotensin II is provided by comparison with the effects of intravenous angiotensin II infusion at the same dose in the same dogs. Intravenous infusion of angiotensin II did not alter arterial pressure, and there were no significant changes in total ...
Previous findings have shown that hypotensive doses of losartan prevent the excess of apoptosis present in the hypertrophied left ventricle of adult spontaneously hypertensive rats (SHR). This study was designed to determine whether angiotensin II facilitates apoptosis in cardiomyocytes of adult SHR.. Primary cultures of ventricular cardiomyocytes from 30-week-old normotensive Wistar-Kyoto rats (WKY) and SHR with left ventricular hypertrophy were exposed to 10(-)(9) mol/L angiotensin II for 24 hours. Apoptotic cells were assessed by terminal deoxynucleotidyl transferase assay and confirmed by Annexin V detection. The expression of Bax-alpha, Bcl-2, p53, and caspase-3 proteins was assessed by Western blot assays. The expression of BAX gene was assessed by Northern blot. Angiotensin II increased (P,0.01) cardiomyocyte apoptosis, and this effect was higher (P,0.001) in SHR cells than in WKY cells.. Whereas losartan (10(-7) mol/L) blocked the apoptotic effect of the octapeptide in cells from the two ...
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The peptide angiotensin II is the effector molecule of the reninangiotensin system. All the haemodynamic effects of angiotensin II, including vasoconstriction and adrenal aldosterone release, are mediated through a single class of cell-surface receptors known as AT1 (refs 1, 2). These receptors cont …
Anti-ACE-1 (Angiotension Converting Enzyme, Angiotension I-converting enzyme, Peptidyl-dipeptidase-A); Carboxy Catalytic domain Antibody related publications, related pathways and related gentaur products
We identified an angiotensin-generating system in pancreatic islets and found that exogenously administered angiotensin II, after binding to its receptors (angiotensin II type 1 receptor [AT1R]), inhibits insulin release in a manner associated with decreased islet blood flow and (pro)insulin biosynthesis. The present study tested the hypothesis that there is a change in AT1R expression in the pancreatic islets of the obesity-induced type 2 diabetes model, the db/db mouse, which enables endogenous levels of angiotensin II to impair islet function. Islets from 10-week-old db/db and control mice were isolated and investigated. In addition, the AT1R antagonist losartan was administered orally to 4-week-old db/db mice for an 8-week period. We found that AT1R mRNA was upregulated markedly in db/db islets and double immunolabeling confirmed that the AT1R was localized to beta-cells. Losartan selectively improved glucose-induced insulin release and (pro)insulin biosynthesis in db/db islets. Oral ...
Angiotensin II (Ang II) is one of the most potent vasoconstrictor substances, yet paradoxically. Ang II may dilate certain vascular beds via an undefined mechanism. Ang II-induced vasoconstriction is mediated by the AT1 receptor, whereas the relative expression and functional importance of the AT2 receptor in regulating vascular resistance and blood pressure are unknown. We now report that Ang II induces relaxation of mesenteric microvessels and that this vasodilatory response was unaffected by losartan, an AT1 receptor antagonist, but was inhibited by PD123.319. a selective antagonist of AT2 receptors. In addition, reverse transcriptase-polymerase chain reaction studies revealed high amounts of AT2 receptor mRNA in smooth muscle from these same microvessels. Ang II-induced relaxation was inhibited by either tetraethylammonium or iberiotoxin, suggesting involvement of the large-conductance, calcium- and voltage-activated potassium (BKCa) channel. Subsequent whole-cell and single-channel patch-clamp
UNLABELLED Angiotensin II has articularly shown to play a key role in the regulation of inflammatory processes in hypertension. AIM The present study aims to correlate the angiotensin II-induced hypertension 4th systemic inflammation. MATERIAL AND METHODS We conducted an experimental study on Wistar male rats who received Ang II via subcutaneous miniosmotic pumps for 2 weeks. Rats were exposed to a 12h light /12h dark cycle. Sham rats were used as control. Systolic load pressure measurements and a flow cytometric analysis of lymphocyte surface markers were performed. After 14 days, the animals were euthanized under anesthesia with ylazine/ketaniine. RESULTS Systolic BP progressively and significantly increased in rats 4th Ang II chronic infusion. We observed a statistical significant difference (p = 0.00001), in terms of T lymphocytes percentage between control rats plasma and Ang H treated rats lasma, in 14 days. CONCLUSIONS Angiotensin II is an important mediator of hypertension and directly
New Report on Angiotensin II Receptor Type 1 (AT1 Receptor) Inhibitors-Pipeline Insights, 2017 added to store which has 60 pages and available for purchase at US $ 1250.
Approach and Results-We combined an extensive in vivo imaging protocol (high-frequency ultrasound and contrast-enhanced microcomputed tomography at baseline and after 3, 10, 18, and 28 days of angiotensin II infusion) with synchrotron-based ultrahigh resolution ex vivo imaging (phase contrast X-ray tomographic microscopy) in n=47 angiotensin II-infused mice and 6 controls. Aortic regurgitation increased significantly over time, as did the luminal volume of the ascending aorta. In the samples that were scanned ex vivo, we observed one or several focal dissections, with the largest located in the outer convex aspect of the ascending aorta. The volume of the dissections moderately correlated to the volume of the aneurysm as measured in vivo (r2=0.46). After 3 days of angiotensin II infusion, we found an interlaminar hematoma in 7/12 animals, which could be linked to an intimal tear. There was also a significant increase in single laminar ruptures, which may have facilitated a progressive ...
Cardiac hypertrophy increases the risk of morbidity and mortality of cardiovascular disease and thus inhibiting such hypertrophy is beneficial. In the present study, we explored the effect of a bioactive peptide (PAP) on angiotensin II (Ang II)-induced hypertrophy and associated ventricular arrhythmias in in vitro and in vivo models. PAP enhances p21 activated kinase 1 (Pak1) activity by increasing the level of phosphorylated Pak1 in cultured neonatal rat ventricular myocytes (NRVMs). Such PAP-induced Pak1 activation is associated with a significant reduction of Ang II-induced hypertrophy in NRVMs and C57BL/6 mice, in vitro and in vivo, respectively. Furthermore, PAP antagonizes ventricular arrhythmias associated with Ang II-induced hypertrophy in mice. Its antiarrhythmic effect is likely to be involved in multiple mechanisms to affect both substrate and trigger of ventricular arrhythmogenesis. Thus our results suggest that Pak1 activation achieved by specific bioactive peptide represents a potential
TY - JOUR. T1 - Angiotensin II depresses glutamate depolarizations and excitatory postsynaptic potentials in locus coeruleus through angiotensin II subtype 2 receptors. AU - Xiong, H.. AU - Marshall, K. C.. PY - 1994/9. Y1 - 1994/9. N2 - A previously reported depression of glutamate responses by angiotensin II was investigated to define the nature of this neuromodulatory effect. Studies were carried out in an in vitro brain slice preparation containing the locus coeruleus, using intracellular recordings, and iontophoretic, micropressure and bath perfusion methods for application of drugs. The angiotensin action was found to be blocked by a non-peptide antagonist specific for the angiotensin type 2 receptor, and not by an antagonist selective for the type 1 receptor. Excitatory postsynaptic potentials mediated primarily by excitatory amino acids were also depressed by angiotensin II. The angiotensin II depressions of glutamate were shown to be strong and highly specific. The low effectiveness of ...
Angiotensin II blockade with sarcosine1-alanine8-angiotensin II (saralasin, P-113) was done in 40 studies of 20 hypertensive patients. Eleven of 12 patients with a depressor response to angiotensin II blockade had significant renovascular or renal disease, and nine of 10 had renal vein renin measurements that lateralized to the abnormal kidney. In contrast, none of the patients without a depressor response had renovascular abnormalities. Plasma renin activity was usually high in responders to saralasin (18 ng/ml · h) when compared with nonresponders (0.5 ng/ml · h). In these studies a correlation between the fall in blood pressure and the rise in plasma renin activity during angiotensin II blockade was observed while renin was unchanged in the absence of depressor responses. In two renovascular renin-dependent hypertensive patients, treatment with diuretics induced severe hyperreninemia and a rise in blood pressure that was reversed by sodium loading. ...
The bovine adrenal angiotensin II receptor was solubilized with the non-ionic detergent octyl β-D-glucoside following its binding with the high-affinity antagonist 125I-labelled [Sar1,Ile8]angiotensin II. The complex was sufficiently stable to allow the determination of its hydrodynamic properties. The solubilized receptor migrated on a Superose 6 column as a single peak with a Stokes radius of 5.29 nm. Comparison of sedimentation behaviour through a sucrose density gradient in H2O and 2H2O lead to a partial specific volume of 0.751 ml/g and a sedimentation coefficient (S20,w) of 5.17 S. Combination of gel filtration and sedimentation data indicated that the labelled protein-detergent complex has an Mr of 124,000 and a frictional ratio of 1.42. The Mr of the angiotensin II receptor was estimated as 104,000 kDa after correction for the bound detergent. Photoaffinity cross-linking of 125I-[Sar1, (4-N3)Phe8]angiotension II with bovine adrenal membrane receptor followed by SDS/PAGE under reducing ...
Experimental data indicate the existence of a vascular tissue renin-angiotensin system in several different vessels from various animal models. Active renin can be locally synthesized into the vessel wall or taken up from circulating plasma to produce vascular angiotensin II. Using the human forearm technique, we produced evidence indicating the release of active and inactive renin and of angiotensin II from the vessels of hypertensive patients. Moreover, the production of vascular angiotensin II seems to be strictly correlated to the circulating renin profile, suggesting the possibility that vascular renin might be at least partially taken up from plasma. To investigate a possible function of the vascular renin-angiotensin system, we studied its interaction with sympathetic neurotransmission in essential hypertensive patients. In line with animal studies, vascular angiotensin II increases the vasoconstriction induced by the stimulation of the sympathetic nervous system through the potentiation ...
1. Granulocyte colony stimulating factor (G-CSF) is reported to have a beneficial effect on cardiac dysfunction in postinfarction and doxorubicin-induced cardiomyopathy. Thus, the aim of the present study was to investigate the effects of G-CSF on cardiac remodelling in angiotensin (Ang) II-induced hypertrophy. 2. Four groups of mice were investigated. The first group served as a control group. The second group was injected with recombinant human G-CSF (10 microg/kg per day, s.c.) on the first 5 days of each week and treatment was continued for 4 weeks. An osmotic minipump was implanted subcutaneously into each mouse in the third group so that pressor doses of AngII (2.88 mg/kg per day) or saline could be administered over a period of 4 weeks. The fourth group was infused with AngII (2.88 mg/kg per day) and injected with G-CSF (10 microg/kg per day, s.c.) for 4 weeks. 3. Angiotensin II treatment significantly elevated blood pressure and caused cardiac hypertrophy and fibrosis in mice. Treatment ...
TY - JOUR. T1 - A cloned angiotensin receptor isoform from the turkey adrenal gland is pharmacologically distinct from mammalian angiotensin receptors. AU - Murphy, T. J.. AU - Nakamura, Y.. AU - Takeuchi, K.. AU - Alexander, R. W.. PY - 1993. Y1 - 1993. N2 - A 2046-base pair cDNA clone, homologous to mammalian angiotensin (AT) AT1 receptors, was isolated from a library prepared from adrenal glands of the domestic turkey (Meleagris gallopavo). Sequence analysis of the cDNA insert in clone pTAT2 reveals a 1077-base pair open reading frame predicting a 359- amino acid protein ~75% homologous to mammalian AT1 receptors. Saturation radioligand binding studies performed in membranes of COS-7 cells transfected with pTAT2 show high affinity specific binding of 125I-angiotensin II, with a K(d) of 172 pM. The rank order of affinities for a series of ligands determined by competition binding studies is angiotensin II ≥ [Sar1,Ile8]- angiotensin II , angiotensin II ≃ [Sar1,Ala8]-angiotensin II ≃ ...
TY - JOUR. T1 - Angiotensin II increases expression of α1C subunit of L-type calcium channel through a reactive oxygen species and cAMP response element-binding protein-dependent pathway in HL-1 myocytes. AU - Tsai, Chia Ti. AU - Wang, Danny Ling. AU - Chen, Wen Pin. AU - Hwang, Juey Jen. AU - Hsieh, Chia Shan. AU - Hsu, Kuan Lih. AU - Tseng, Chuen Den. AU - Lai, Ling Ping. AU - Tseng, Yung Zu. AU - Chiang, Fu Tien. AU - Lin, Jiunn Lee. PY - 2007/5/1. Y1 - 2007/5/1. N2 - Angiotensin II (Ang II) is involved in the pathogenesis of atrial fibrillation (AF). L-type calcium channel (LCC) expression is altered in AF remodeling. We investigated whether Ang II modulates LCC current through transcriptional regulation, by using murine atrial HL-1 cells, which have a spontaneous calcium transient, and an in vivo rat model. Ang II increased LCC α1C subunit mRNA and protein levels and LCC current density, which resulted in an augmented calcium transient in atrial myocytes. An ≈2-kb promoter region of LCC ...
Renin is regulated by angiotensin subtype 1 (AT1) receptor, but it is unknown whether angiotensin subtype 2 (AT2) receptor contributes to this regulation. We hypothesized that AT2 receptors inhibit angiotensin II (Ang II) through inhibition of renin biosynthesis. We monitored changes in renal Ang II, renin mRNA and protein expression, and plasma renin concentration (PRC) in response to renal cortical administration of the AT1 receptor blocker valsartan or the AT2 receptor blocker PD 123319 (PD) in conscious rats administered low sodium intake (LS). Renal interstitial Ang II increased by 47-fold in response to LS and increased further in response to valsartan or PD by 67-fold and 61-fold from normal sodium diet (NS) and by 41% and 29% from LS, respectively. Renin mRNA increased 63% during LS, and either valsartan or PD increased it further by 600% and 250% from NS and 538% and 187% from LS, respectively. Similarly, renal renin content and PRC increased in response to LS and increased further in response
TY - JOUR. T1 - Functional coupling of human L-type Ca2+ channels and angiotensin AT(1A) receptors coexpressed in Xenopus laevis oocytes. T2 - Involvement of the carboxyl-terminal Ca2+ sensors. AU - Murat, O. Z.. AU - Melia, Michael T.. AU - Soldatov, Nikolai M.. AU - Abernethy, Darrell R.. AU - Morad, Martin. N1 - Copyright: Copyright 2020 Elsevier B.V., All rights reserved.. PY - 1998. Y1 - 1998. N2 - A human recombinant L-type Ca2+ channel (α(1C,77)) was coexpressed with the rat angiotensin AT(1A) receptor in Xenopus laevis oocytes. In oocytes expressing only α(1C,77) channels, application of human angiotensin II (1-10 μM) did not affect the amplitude or kinetics of Ba2+ currents (I(Ba)). In sharp contrast, in oocytes coexpressing α(1C,77) channels and AT(1A) receptors, application of 1 nM to 1 μM angiotensin gradually and reversibly inhibited I(Ba), without significantly changing its kinetics. The inhibitory effect of angiotensin on I(Ba) was abolished in oocytes that had been ...
Myocardial infarction (MI) induces cardiac remodeling. This may increase the susceptibility of the infarcted heart to subsequent ischemic events. While chronic angiotensin II blockade is cardioprotective post-MI, the acute effects of angiotensin II i
Quantitative autoradiography was used to characterize angiotensin AT1 and AT2 receptors, in the rat aorta at three developmental ages; embryonic day 18 (E18), and postnatal weeks 2 and 8. The expression of angiotensin receptors was higher in the aorta of E18 and 2-week-old rat. A major proportion of the angiotensin receptors expressed in the aorta at these two ages was AT2 (84 and 81% respectively). Conversely, in the aorta of 8-week-old rats, AT1 was the predominant angiotensin receptor subtype (71%). In 8-week-old rats, the AT2 subtype was also present (28%). In pre- and postnatal rats, [125I]Sar1-angiotensin II binding to AT1 receptors was sensitive to GTP gamma S whereas binding to AT2 receptors was not. AT2 receptors may serve an important role during stages of rapid growth of the aorta, and also have a significant function in the adult vasculature ...
TY - JOUR. T1 - Hemodynamic effects of direct angiotensin ii blockade compared to converting enzyme inhibition in rat model of heart failure. AU - Raya, Thomas E.. AU - Fonken, Steven J.. AU - Lee, Richard W.. AU - Daugherty, Sherry. AU - Goldman, Steven. AU - Wong, Pancras C.. AU - Timmermans, Pieter B.M.W.M.. AU - Morkin, Eugene. PY - 1991/1/1. Y1 - 1991/1/1. N2 - The purpose of this investigation was to compare the chronic effects of converting enzyme inhibition with captopril to direct blockade of angiotensin II (All) with DuP 753 in the rat model of heart failure. Rats with chronic heart failure postinfarction were treated for 2 weeks with either captopril (2 g/L, N = 9) in their drinking water or with DuP 753 (40 mg/kg/day for two weeks by gastric gavage, N = 10), or placebo (N = 9). At this dose, DuP 753 shifted the log dose-pressor response curve to All parallel to the right by two orders of magnitude in both chronically treated normal and heart failure rats. In rats with heart failure, ...
Animation showing: Physiology of the renin angiotensin aldosteone system (RAAS). Mechanism of action of ACE inhibitors, Angiotensin II receptor blockers (ARBs).
Murine N1E-115 neuroblastoma cells are shown to express a single class of angiotensin II (Ang II) receptors that display all the pharmacological properties defining the Ang II receptor subtype 2 (AT2): high affinity for 125I-labelled AT2-selective agonist CGP 42112 (Kd 91 +/- 19 pM); expected rank order of potency (CGP 42112 = (Sar1,Ile8)Ang II , or = Ang II , PD 123319 ,, DUP 753) for several Ang II analogues; increased binding in the presence of the reducing reagent dithiothreitol (DTT); and insensitivity to analogues of GTP. Molecular cloning of cDNA encoding AT2 receptors from N1E-115 cells reveals nucleotide sequence identity with the AT2 subtype expressed in fetal tissue. Murine AT2 receptors transiently expressed in COS cells display the same pharmacological profile as endogenous Ang II receptors of N1E-115 cells. Taken together, these data reveal the exclusive presence of the AT2 receptor subtype in N1E-115 cells. Incubation of N1E-115 cells with Ang II leads to a marked decrease in the ...
In the injured arteries, chymaselike activity and chymase mRNA level were remarkably increased, whereas a slight increase in ACE activity and no increase in ACE mRNA expression were detected. The current study demonstrated for the first time that tranilast prevented vascular chymase expression and effectively inhibited neointima formation and luminal stenosis. Our previous study showed that the vascular ANG II content doubled in the injured arteries compared with that in the uninjured arteries and that an ANG II receptor antagonist but not an ACE inhibitor prevented the neointima formation.15 In the current study, tranilast treatment did not affect plasma ANG II concentration, plasma ACE activity, or PRA. Vascular ANG II-forming activity of chymase increased 4.8-fold in vehicle-treated dogs, whereas tranilast treatment completely prevented the increase in chymase activity. Therefore, the ANG II-forming rate in local vascular tissues supposedly increased after vascular injury but returned to the ...
The reduced capacity of insulin to stimulate glucose transport into skeletal muscle, termed insulin resistance, is a primary defect leading to the development of prediabetes and overt type 2 diabetes. Although the etiology of this skeletal muscle insulin resistance is multifactorial, there is accumulating evidence that one contributor is overactivity of the renin-angiotensin system (RAS). Angiotensin II (ANG II) produced from this system can act on ANG II type 1 receptors both in the vascular endothelium and in myocytes, with an enhancement of the intracellular production of reactive oxygen species (ROS). Evidence from animal model and cultured skeletal muscle cell line studies indicates ANG II can induce insulin resistance. Chronic ANG II infusion into an insulin-sensitive rat produces a markedly insulin-resistant state that is associated with a negative impact of ROS on the skeletal muscle glucose transport system. ANG II treatment of L6 myocytes causes impaired insulin receptor substrate ...
Azilsartan medoxomil(TAK 491) is an orally administered angiotensin II receptor type 1 antagonist with IC50 of 0.62 nM, which used in the treatment of adults with essential hypertension.
Cardiovascular responses after the central blockade of the brain angiotensin system with peptide or nonpeptide angiotensin II analogs in conscious, freely moving hypertensive Dahl salt-sensitive (DS/JR) rats were measured. Four-week-old animals were maintained on an 8% salt diet until experimentation at 7 weeks of age. At the time of experimentation, mean arterial pressures were 176 +/- 6 mm Hg. The i.c.v. administration of 20 micrograms of the peptide analog sarcosine1, threonine8-angiotensin II (sarthran) resulted in a significant bradycardic response (approximately 17% decrease in H.R. peaking at 8 min after injection) without a significant change in blood pressure. Central administration of the AT1 antagonist losartan (10 micrograms) or of the AT2 antagonist PD 123319 (10 micrograms) was without effect. The peptide and nonpeptide analogs differed in their ability to inhibit central angiotensin II (10 ng)-induced pressor and dipsogenic responses. PD 123319 (10 micrograms) had no effect on the ...
OBJECTIVE: The goal of this study was to determine whether inhibition of transient receptor potential canonical (TRPC) channels underlies attenuation of angiotensin II (Ang II)-induced vasoconstriction by phosphodiesterase (PDE) 3 inhibition. METHODS AND RESULTS: Pretreatment of rat thoracic aorta with cilostazol, a selective PDE3 inhibitor, suppressed vasoconstriction induced by Ang II but not that induced by KCl. The Ang II-induced contraction was largely dependent on Ca(2+) influx via receptor-operated cation channels. Cilostazol specifically suppressed diacylglycerol-activated TRPC channels (TRPC3/TRPC6/TRPC7) through protein kinase A (PKA)-dependent phosphorylation of TRPC channels in HEK293 cells. In contrast, we found that phosphorylation of TRPC6 at Thr69 was essential for the suppression of Ang II-induced Ca(2+) influx by PDE3 inhibition in rat aortic smooth muscle cells (RAoSMCs). Cilostazol specifically induced phosphorylation of endogenous TRPC6 at Thr69. The endogenous TRPC6, but ...
The latest market report published by Credence Research, Inc. Global Angiotensin Converting Enzyme (ACE) Inhibitors Market - Growth, Share, Opportunities, Competitive Analysis, and Forecast, 2016 - 2022, the angiotensin converting enzyme (ACE) inhibitors market was valued at USD 11,477.1 Mn in 2015, and is expected to reach USD 11,094.6 Mn by 2023, expanding at a CAGR of (0.5%) from 2016 to 2023.. Browse the full report Angiotensin Converting Enzyme (ACE) Inhibitors Market - Growth, Share, Opportunities, Competitive Analysis, and Forecast, 2016 - 2023 report at Market Insights. ACE inhibitors are class of drugs (angiotensin-converting enzyme inhibitors) that block the conversion of angiotensin I to angiotensin II, used in the treatment of hypertension and congestive heart failure and in the prevention of microvascular complications of diabetes mellitus. According to World Health Organization (WHO), ...
The importance of beta and gamma epithelial Na(+) channel (ENaC) proteins in vascular smooth muscle cell (VSMC)-mediated pressure-induced constriction in renal interlobar arteries has been demonstrated recently. In renal epithelial tissue, ENaC expre
TY - JOUR. T1 - CAC score as a possible criterion for administration of angiotensin converting enzyme inhibitors and/or angiotensin receptor blockers. T2 - The MultiEthnic Study of Atherosclerosis. AU - Darabian, Sirous. AU - Luo, Yanting. AU - Homat, Arman. AU - Khosraviani, Khashayar. AU - Wong, Nathan. AU - Zeb, Irfan. AU - Nasir, Khurram. AU - Budof, Matthew J.. PY - 2015/11/3. Y1 - 2015/11/3. N2 - Introduction Several trials have demonstrated that angiotensin converting enzyme inhibitors (ACEIs) decrease cardiovascular (CV) mortality rates in patients with heart failure; however, the Prevention of Events with Angiotensin-Converting Enzyme Inhibition (PEACE) and European Trial on Reduction of Cardiac Events with Perindopril in Stable Coronary Artery Disease (EUROPA) trials failed to show significant similar preventive effects in normal ejection fraction patients. We evaluated the baseline coronary artery calcium (CAC) score as a predictor of the effects of ACEIs/angiotensin receptor blockers ...
Cerebral blood vessels are the premier target of the brain damage produced by hypertension, a major risk factor for stroke and dementia (Iadecola and Davisson, 2008; Unverzagt et al., 2011). Chronic hypertension is well known to alter cerebrovascular structure and function (Cipolla, 2007). In particular, hypertension disrupts vital neurovascular mechanisms coupling the local delivery of blood flow with the energetic needs of active brain regions (Kazama et al., 2004; Jennings et al., 2005; Iadecola and Davisson, 2008). The resulting mismatch between blood supply and energy demands is particularly damaging to subcortical white matter regions perfused by poorly collateralized arteriolar networks at the interface between adjacent vascular territories (Markus et al., 2000; Fernando et al., 2006; Iadecola, 2010). Thus, subcortical white matter lesions are closely related to hypertension and are associated with an increased risk of stroke, vascular cognitive impairment and Alzheimers disease (Englund ...
Data from the literature show lights and shadows about the use of angiotensin II (Ang II), for instance as an alternative vasopressor in patients with vasodilatory shock that requires high doses of catecholamines. Recently, an international randomized controlled trial (ATHOS-3) [1] has shown that Ang II can induce a significant increase in mean arterial pressure (MAP) if compared to placebo. Moreover, during the first 48 hours from the randomization, doses of the vasopressors (norepinephrine (NE) and vasopressin) were significantly reduced in the Ang II group but not in the placebo group. Interestingly, no difference in adverse effects was remarkable between the two groups.. However, some important issues need to be clarified before any definitive conclusion about Ang II in vasodilatory shock. Firstly, we do not know exactly the timing for Ang II initiation: is it better to add Ang II only when NE doses jump to 0.2 μg/kg/min or when NE requirements rapidly increase (e.g., 0.5 μg/kg every ...
Please note these generic angiotensin ii receptor antagonists replacementss will also travel to Mc Kees Rocks, Carnegie, Glenshaw, Homestead, Presto, Allison Park, Bethel Park, Braddock, Bridgeville, Coraopolis, Ingomar, Morgan, Oakdale, Sewickley, West Mifflin, Wildwood, Cuddy, Dravosburg, Duquesne, East Pittsburgh, Indianola, Oakmont, Turtle Creek, Verona, Gibsonia, Glassport, Imperial, Library, Mc Keesport, Sturgeon ...
This investigation was performed to study the renin-angiotensin system in the human fetoplacental circulation. Full-term placentas from uncomplicated pregnancies were studied within 30 min of delivery. The umbilical artery and vein to a single placental cotyledon were cannulated and the artery perfused with RPMI media (0.764 ml/min). Angiotensin II caused a dose-dependent increase in perfusion pressure that was blunted by the administration of the competitive angiotensin II receptor antagonist saralasin. The properties of human placental angiotensin II receptors were further defined in binding studies performed on a crude membrane fraction of placental cotyledons. In experiments performed at 22 degrees C, saturable binding reached steady state at 30 min and was linear with protein concentration. Scatchard analysis of binding data indicated a single class of high-affinity binding sites. The potency order to competitive binding of analogues and antagonists of angiotensin II was [Ile5]angiotensin ...
It is a derivative of angiotensin II. Angiotensin. ... Angiotensinamide (INN; BAN and USAN angiotensin amide) is a ...
"Angiotensin II receptor blockers". Proceedings (Baylor University. Medical Center). 16 (1): 123-126. doi:10.1080/08998280.2003. ... Two years after his research on angiotensin blockers at Harvard, Watkins returned to Johns Hopkins and joined the admissions ... Work on angiotensin blockers[edit]. Watkins left Johns Hopkins in 1973 for Harvard University where he researched the use of ... 1911-1994)[4][5] and Lillian Varnado (1917-2013).[6] He grew up with five siblings: two brothers, James Watkins and Donald V. ...
Losartan works by blocking the effects of angiotensin II by preventing it from binding to the angiotensin I receptor while ... However, with coadministration of losartan which is an angiotensin II receptor antagonist, the low levels of potassium are ... an angiotensin II receptor antagonist) and hydrochlorothiazide (a diuretic).[1] It is taken by mouth.[1] ... Losartan works by blocking the effects of angiotensin II while hydrochlorothiazide works by decreasing the ability of the ...
Angiotensin II -> Vasopressin) Increase PAI-1 and PAI-2 also through Angiotensin II Lipid Increase HDL, triglyceride Decrease ... II. Correlation of the extent of conversion of plasma androstenedione to estrone with age". The Journal of Clinical ... 38 (2-3): 103-7. doi:10.1016/0303-7207(84)90108-4. PMID 6510548. S2CID 24198956. Koot RW, Amelink GJ, Blankenstein MA, Bär PR ( ... 92 (2): 169-80. doi:10.1016/S0166-4328(97)00189-7. PMID 9638959. S2CID 28276218. Warnock JK, Swanson SG, Borel RW, Zipfel LM, ...
Angiotensin II receptor blockers (ARBs)[edit]. ARB treatment results in an improvement in diastolic dysfunction and ... Angiotensin converting enzyme (ACE) inhibitors[edit]. Likewise, treatment with angiotensin converting enzyme inhibitors, such ... In fact, in two studies appearing in the New England Journal of Medicine in 2006, evidence was presented to suggest that the ... Grade II diastolic dysfunction is called "pseudonormal filling dynamics". This is considered moderate diastolic dysfunction and ...
Ryan, Una; Ryan, James W (April 1980). "Angiotensin-Converting Enzyme: II. Pulmonary Endothelial Cells in Culture". ... Ryan has two daughters, Tamsin Smith, a poet and social impact innovator, who helped create and served as founding president of ... II. Boca Raton, Florida: CRC Press. ISBN 978-0-8493-4991-1. Ryan, Una S. (1988). Endothelial Cells. III. Boca Raton, Florida: ... Ryan, Una; Ryan, James W; Smith, David S (1975). "Alveolar type II cells: Studies on the mode of release of lamellar bodies". ...
Inagaki K, Iwanaga Y, Sarai N, Onozawa Y, Takenaka H, Mochly-Rosen D, Kihara Y (Oct 2002). "Tissue angiotensin II during ... Paul K, Ball NA, Dorn GW, Walsh RA (Nov 1997). "Left ventricular stretch stimulates angiotensin II--mediated ... angiotensin II and diastolic stretch; adenosine; hypoxia and Akt-induced stem cell factor; ROS generated via pharmacologic ... Initially, PKCε was thought to protect mitochondria from MPT through its association with VDAC1, ANT, and hexokinase II; ...
ARBs block angiotensin II from acting. The patient's diet should also be changed. The patient should restrict salt intake to ... ACEIs will decrease hypertension by preventing the body from creating angiotensin II, which narrows the blood vessels. ... If the DPGN is caused by IgA nephropathy then corticosteroids, angiotensin-converting enzyme inhibitor (ACEIs), angiotensin ... Two common immunosuppressive drugs used to treat DPGN are cyclophosphamide (CYC) and mycophenolate mofetil (MMF) if the DPGN is ...
Angiotensin is involved in regulating aldosterone and is the core regulator. Angiotensin II acts synergistically with potassium ... by increase in the plasma concentration of angiotensin III. by increased plasma angiotensin II, ACTH, or potassium levels. The ... Aldosterone synthase normally is not ACTH sensitive, and only activated by angiotensin II. Aldosterone causes the tubules of ... Control of aldosterone release from the adrenal cortex: The role of the renin-angiotensin system: ...
... is an angiotensin II receptor antagonist. It was withdrawn from FDA review by the manufacturer after phase III ... ISBN 978-0-12-369417-1. Dina R, Jafari M (July 2000). "Angiotensin II-receptor antagonists: an overview". Am J Health Syst ...
Weber KT, Swamynathan SK, Guntaka RV, Sun Y (1999). "Angiotensin II and extracellular matrix homeostasis". The International ... These two proposed mechanisms illustrate therapeutic potential for the reduction of fibrotic remodelling in the hypertensive ... 69 (2): 483-90. doi:10.1161/01.res.69.2.483. PMID 1860186. Tomasek JJ, Gabbiani G, Hinz B, Chaponnier C, Brown RA (May 2002). " ... 102 (2): 437-42. Bibcode:2005PNAS..102..437S. doi:10.1073/pnas.0408704102. PMC 544320. PMID 15625103. Villarreal FJ, Lee AA, ...
Cazaubon S, Deshayes F, Couraud PO, Nahmias C (April 2006). "[Endothelin-1, angiotensin II and cancer]". Médicine/Sciences. 22 ... Ariza AC, Bobadilla NA, Halhali A (2007). "[Endothelin 1 and angiotensin II in preeeclampsia]". Revista de Investigacion ... 68 (2): 357-418. doi:10.1124/pr.115.011833. PMC 4815360. PMID 26956245. Han SG, Ko S, Lee WK, Jung ST, Yu YG (August 2017). " ... 45 (2): 151-4. PMID 12855940. Doggrell SA (June 2004). "The endothelin system and its role in acute myocardial infarction". ...
... angiotensin converting enzyme (ACE) converts angiotensin I to angiotensin II; angiotensin II causes vasoconstriction and ... competitive angiotensin II receptor type 1 (AT1) antagonist, reducing the end organ responses to angiotensin II. Losartan ... angiotensin II, and ultimately decreasing blood pressure. Angiotensin II receptor antagonists include losartan, valsartan, ... It is in the angiotensin receptor blocker family of medication. It works by blocking angiotensin II. Losartan was patented in ...
... fimasartan blocks angiotensin II receptor type 1 (AT1 receptors), reducing pro-hypertensive actions of angiotensin II, such as ... Angiotensin-converting enzyme (ACE) then catalyzes the reaction that forms angiotensin II, which acts on AT1 receptors on the ... Harada K, Sugaya T, Murakami K, Yazaki Y, Komuro I (November 1999). "Angiotensin II type 1A receptor knockout mice display less ... Sun Y, Zhang JQ, Zhang J, Ramires FJ (August 1998). "Angiotensin II, transforming growth factor-beta1 and repair in the ...
This secreted protein catalyzes the cleavage of angiotensin I into angiotensin 1-9, and angiotensin II into the vasodilator ... The virus is able to use Angiotensin-converting enzyme 2 (ACE2) as an entry receptor to bind to and enter target cells. No ... "ACE2 angiotensin I converting enzyme 2 - Gene". NCBI. 2020-02-28. Retrieved 2020-03-21. The protein encoded by this gene ... Recombinant viruses can arise when two viral genomes are present in the same host cell. The first cases of the infection with ...
Ariza AC, Bobadilla NA, Halhali A (2007). "[Endothelin 1 and angiotensin II in preeeclampsia]". Rev. Invest. Clin. 59 (1): 48- ... The B2 receptor forms a complex with angiotensin converting enzyme (ACE), and this is thought to play a role in cross-talk ... Cassano G, Susca F, Lippe C, Guanti G (1999). "Two B1 and B2 bradykinin receptor antagonists fail to inhibit the Ca2+ response ... Alternate start codons result in two isoforms of the protein. Bradykinin receptor GRCh38: Ensembl release 89: ENSG00000168398 ...
subsequently angiotensin II was indicted - Ganong, Mulrow)). Denton and colleagues showed direct action of Angiotensin II on ... They had two sons. "". Archived from the original on 2010-02-21. Retrieved 2010-02-10. "Hon degree to Derek ... II. Renal physiology in electrolyte subtraction. Acta medica scandinavica, 140 suppl. 261, 1-202, 1951 Denton, D. A. (1957-01- ... For twelve years (1978-1991) he was with Professor Sune Bergstrom, Chairman of the Nobel Foundation, one of two foreign members ...
Katz AM (1990). "Angiotensin II: Hemodynamic regulator or growth factor?". J Mol Cell Cardiol. 22 (7): 739-747. doi:10.1016/ ... Peptide separation by two-dimensional chromatography and electrophoresis. Katz AM, Chernoff AI (1959). "Structural similarities ... KATZ, AM; DREYER, WJ; ANFINSEN, CB (Nov 1959). "Peptide separation by two-dimensional chromatography and electrophoresis". The ... 180 (2): 392-402. doi:10.1152/ajplegacy.1955.180.2.392. PMID 14361747. KATZ, A. M.; KATZ, L. N.; WILLIAMS, F. L. (1 November ...
In 2013 MERS-CoV was identified in three members of a dromedary camel herd held in a Qatar barn, which was linked to two ... angiotensin converting enzyme 2 (ACE2). However, it was later discovered that neutralization of ACE2 by recombinant antibodies ... MERS-CoV genomes are phylogenetically classified into two clades, clade A and B. The earliest cases were of clade A clusters, ... On 2 May 2014, the Corona Map was launched to track the MERS coronavirus in realtime on the world map. The data is officially ...
An octapeptide has eight amino acids (e.g., angiotensin II).. *A nonapeptide has nine amino acids (e.g., oxytocin). ... Two naturally occurring milk peptides are formed from the milk protein casein when digestive enzymes break this down; they can ... An oligopeptide consists of only a few amino acids (between two and twenty). ... A decapeptide has ten amino acids (e.g., gonadotropin-releasing hormone & angiotensin I). ...
An octapeptide has eight amino acids (e.g., angiotensin II).. *A nonapeptide has nine amino acids (e.g., oxytocin). ... A decapeptide has ten amino acids (e.g., gonadotropin-releasing hormone & angiotensin I). ... An oligopeptide consists of only a few amino acids (between two and twenty). ... 4 (2): 215-28. PMID 11378961.. *^ Hummel J, Niemann M, Wienkoop S; et al. (2007). "ProMEX: a mass spectral reference database ...
ACE (Angiotensin converting enzyme) then removes a further two residues, converting angiotensin I into angiotensin II. ACE is ... ACE inhibitors do not completely prevent the formation of angiotensin II, as blockage is dose-dependent, so angiotensin II ... Ng KK, Vane JR (1967). "Conversion of Angiotensin I to Angiotensin II". Nature. 216 (5117): 762-6. doi:10.1038/216762a0. PMID ... The conversion of the inactive angiotensin I to the potent angiotensin II was thought to take place in the plasma. However, in ...
The gene product interacts with the angiotensin II type I receptor and negatively regulates angiotensin II signaling. ... "The angiotensin II type I receptor-associated protein, ATRAP, is a transmembrane protein and a modulator of angiotensin II ... Type-1 angiotensin II receptor-associated protein is a protein that in humans is encoded by the AGTRAP gene. This gene encodes ... "Entrez Gene: AGTRAP angiotensin II receptor-associated protein". Human AGTRAP genome location and AGTRAP gene details page in ...
... is largely responsible for converting angiotensin I to the vasoactive peptide angiotensin II. Angiotensin II has been ... Jenne DE, Tschopp J (1991). "Angiotensin II-forming heart chymase is a mast-cell-specific enzyme". Biochem. J. 276 (2): 567-8. ... "Entrez Gene: CMA1 chymase 1, mast cell". Urata H, Nishimura H, Ganten D (1996). "Chymase-dependent angiotensin II forming ... Caughey GH, Raymond WW, Wolters PJ (2000). "Angiotensin II generation by mast cell alpha- and beta-chymases". Biochim. Biophys ...
"Stochastic sensing of Angiotensin II with lysenin channels". Scientific Reports. 7 (1): 2448. Bibcode:2017NatSR...7.2448S. doi: ... As with most PFTs, lysenin oligomerization occurs in a two-step process, as was recently imaged. The process begins with ... Breaking the sphingomyelin asymmetry between the two leaflets of the lipid bilayer by punching holes in the membrane and ...;2-w. PMID 10684578. Sukumwang, N.; Umezawa, K. (2013). "Earthworm-Derived Pore-Forming Toxin Lysenin and Screening of ...
It is an angiotensin II receptor antagonist and works by blocking the effects of angiotensin II. It was patented in 1991 and ... In studies of angiotensin II receptor antagonists such as olmesartan, patients with unilateral or bilateral renal artery ... "Angiotensin II receptor blocker induced fetopathy: 7 cases". Klin Padiatr. 223 (1): 10-4. doi:10.1055/s-0030-1269895. PMID ... part II of II)". Int. J. Surg. Pathol. 22 (3): 202-11. doi:10.1177/1066896913502230. PMID 24021900. S2CID 20614874. Rubio-Tapia ...
Tanahashi N (April 2009). "[Roles of angiotensin II receptor blockers in stroke prevention]". Nippon Rinsho (in Japanese). 67 ( ... Once blood pressure is found to be high in diabetics, there are ways to treat it: Medications like the Angiotensin-converting ... S2CID 34378084.[dead link] Wachtell K, Devereux RB, Lyle AP (August 2007). "The effect of angiotensin receptor blockers for ... 24 (2): 155-60. doi:10.1097/HCO.0b013e328320d82a. PMID 19532102. Biria M, Howard PA, Vacek J (2008). "Do statins have a role in ...
Kalaitzidis, R; Bakris, G. L. (2009). "Effects of angiotensin II receptor blockers on diabetic nephropathy". Journal of ... For example, not only do angiotensin receptor blockers, and angiotensin-converting enzyme (ACE) inhibitors work to lower blood ... In chemistry, antagonism is a phenomenon wherein two or more agents in combination have an overall effect that is less than the ... 2-amidinopropane) dihydrochloride (AAPH)-induced oxidation: Synergistic and antagonistic effects". Journal of the American Oil ...
Adjunctive therapies include angiotensin II, hydrocortisone, thiamine, catecolamines, ascorbic acid and combinations of thereof ... "Angiotensin II for the Treatment of Vasodilatory Shock" (PDF). The New England Journal of Medicine. 377 (5): 419-430. doi: ... "Vasodilatory shock in the ICU and the role of angiotensin II". Current Opinion in Critical Care. 24 (4): 277-285. doi:10.1097/ ... and the renin-angiotensin aldosterone system. The definition of refractory shock or vasodilatory shock varies. In 2018, the ...
"Effect of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers on all-cause mortality, cardiovascular ... 37 (2): 99-105. PMID 18939392.. *^ a b c d e f g "Causes of Diabetes". National Institute of Diabetes and Digestive and Kidney ... are superior to other inhibitors of the renin-angiotensin system such as angiotensin receptor blockers (ARBs),[115] or ... with a glucose tolerance test, two hours after the oral dose a plasma glucose ≥ 11.1 mmol/l (200 mg/dl) ...
... correlation with disease activity and reduced angiotensin converting enzyme levels. Lühikokkuvõte, J Rheumatol. 1996 Oct;23(10 ... Haiguse ägenemine algab harilikult kõrge palavikuga 38 kuni 40 kraadi juures ja võib püsida 1 kuni 2 nädalat. ...
Camargo, A. C. M.; Krieger, E. M.; Stewart, J. M.; Ferreira, S. H. (1972). "Inhibition of the conversion of angiotensin I to II ...
ACTH " AM " Angiotensin " CT " Gastrin " Glukagon " GnRH " GH " GHIH " GHRH " GHS " IAPP " OT " PRL " TRH " VP ... C5a " CCL2 " CCL5 " GSM-CSF " LPS " MCP-1 " IL-1 " IL-2 " IL-3 " IL-4 " IL-5 " IL-6 " IL-8 " IL-10 " IL-12 " IL-13 " IL-15 " IL ... Wondene 2-methyoxyestradiol duwé aktivitas antitumorigenik kanti ngalonake proliferasi lan angiogenesis ing sèl tumor. ... ing umumne senyawa estrogen-katekol duwé wektu paruh kang cendek amarga langsung termetilasi dadi 2-methoxyestradiol lan 4- ...
Hosie AM, Wilkins ME, da Silva HM, Smart TG (Nov 2006). "Endogenous neurosteroids regulate GABAA receptors through two discrete ... the two GABA active binding sites at the α1 and β2 interfaces, and the benzodiazepine (BZD) allosteric binding site at the α1 ... 19 (2): 578-88. PMID 9880578.. *^ a b Majewska MD, Harrison NL, Schwartz RD, Barker JL, Paul SM (May 1986). "Steroid hormone ... 300 (1): 2-8. doi:10.1124/jpet.300.1.2. PMID 11752090.. *^ Perrais D, Ropert N (Jan 1999). "Effect of zolpidem on miniature ...
Nurturant maternal care, in turn, may enhance HPA functioning in at least two ways. First, maternal care is crucial in ... In the brain, cortisol acts on two types of receptor - mineralocorticoid receptors and glucocorticoid receptors, and these are ... The hypothalamic-neurohypophyseal system secretes two peptide hormones directly into the blood, vasopressin and oxytocin. .... ... 2: 35-44. PMC 2990232. PMID 21157520. Retrieved 14 February 2016.. *^ a b c Tian, Rui; Hou, Gonglin; Li, Dan; Yuan, Ti-Fei ( ...
Angiotensin converting enzyme inhibitors, adrenergic agents such as alpha-1 blockers and beta-blockers and alpha-2 agonists, ... It is strongly associated with smoking, hypertension, and diabetes.[2] Diagnosis[edit]. Intermittent claudication is a symptom ... 3 (2): 229-34. doi:10.2147/vhrm.2007.3.2.229. PMC 1994028. PMID 17580733.. ...
Boulay G, Chrétien L, Richard DE, Guillemette G (November 1994). "Short-term desensitization of the angiotensin II receptor of ... The core region has two zinc fingers that are responsible for recognizing the DNA sequences specific to this receptor. The N ... Type 2: G protein-coupled receptors (metabotropic receptors) - This is the largest family of receptors and includes the ... There are three main ways the action of the receptor can be classified: relay of signal, amplification, or integration.[2] ...
positive regulation of transcription from RNA polymerase II promoter. • negative regulation of cell proliferation. • signal ... 2004). "Autosomal dominant familial exudative vitreoretinopathy in two Japanese families with FZD4 mutations (H69Y and C181R ... 25 (2): 81-90. doi:10.1080/13816810490514270. PMID 15370539.. *. Holmen SL, Robertson SA, Zylstra CR, Williams BO (2005). "Wnt- ... 2005). "Generation and annotation of the DNA sequences of human chromosomes 2 and 4". Nature. 434 (7034): 724-31. doi:10.1038/ ...
Ballew JR, Fink GD (September 2001). "Characterization of the antihypertensive effect of a thiazide diuretic in angiotensin II- ... 2. proximal tubule Loop diuretics bumetanide,[17] ethacrynic acid,[17] furosemide,[17] torsemide Inhibits the Na-K-2Cl ... the term almost always refers to two specific classes that have their effect at similar locations: *Aldosterone antagonists: ... 2. proximal tubule[17]. Carbonic anhydrase inhibitors acetazolamide,[17] dorzolamide Inhibits H+ secretion, resultant promotion ...
The renal effect of fenoldopam and dopamine may involve physiological antagonism of the renin-angiotensin system in the kidney. ... 26 (2): 119-27. PMID 2474340.. *^ Epstein, Murray MD, "Diagnosis and Management of Hypertensive Emergencies," clinical ... 3 (6 Pt 2): 116S-119S. PMID 1974439.. *^ Gildea JJ (January 2009). "Dopamine and angiotensin as renal counterregulatory systems ... 115 (2): 349-55. doi:10.1111/j.1476-5381.1995.tb15884.x. PMC 1908310. PMID 7670737.. ...
Class II: LDLR is not properly transported from the endoplasmic reticulum to the Golgi apparatus for expression on the cell ... The risk was also found to be higher in people with a specific genotype of the angiotensin-converting enzyme (ACE).[21] ... 2 (72): 171-76. doi:10.1016/0002-9149(93)90155-6.. *^ a b c d e f g h i Repas TB, Tanner JR (February 2014). "Preventing early ... Having two abnormal copies (being homozygous) may cause severe cardiovascular disease in childhood. Heterozygous FH is a common ...
... with particular reference to blood pressure regulation in the renin-angiotensin system. ... Two terms 2007-11. J.R. Hardie. Geology/Education. Second to sixth terms ... 1821-2. Sir Thomas Brisbane. Astronomy. Governor NSW, Hon. President 1850-5. Hon. E. Deas-Thomson. Public Administration. ... An Australian Living National Treasure, author of many books including The Chant of Jimmy Blacksmith and Schindler's Ark[2]. ...
The two proposed mechanisms of HN's pathophysiology[7] both centre around how the glomerulus, a network of dense capillaries ... ACE inhibitors, angiotensin receptor blockers, direct renin inhibitors and aldosterone antagonists, are pharmacological ... The tissue hardens and thickens which is known as nephrosclerosis.[2] The narrowing of the blood vessels means less blood is ... It manifests as hypertensive nephrosclerosis (slerosis referring to the stiffening of renal components).[2] It should be ...
... in which case angiotensin II receptor antagonists (ARBs) are the next line of treatment. ... Bradykinin is also thought to be the cause of the dry cough in some patients on widely prescribed angiotensin-converting enzyme ... In humans, bradykinin is broken down by three kininases: angiotensin-converting enzyme (ACE), aminopeptidase P (APP), and ... Kuoppala A, Lindstedt KA, Saarinen J, Kovanen PT, Kokkonen JO (April 2000). "Inactivation of bradykinin by angiotensin- ...
... and is offered in 15 centers across the two countries.[4] ... Renin-angiotensin system. Metabolism. *Blood sugar regulation. ...
... specifically cell type II, which contain other G-protein coupled taste receptors), and its absence leads to reduced preference ... to two types of fatty acid (linoleic acid and oleic acid), as well as decreased neuronal response to oral fatty acids.[10] ...
... is a reversible inhibitor of dipeptidyl-peptidase II (serine peptidase) and cytosol alanyl aminopeptidase ( ... Prolactin modulators: Prolactin inhibitors: D2 receptor agonists (e.g., bromocriptine, cabergoline); Prolactin releasers: D2 ... Puromycin acts quickly and can kill up to 99% of nonresistant cells within 2 days.[citation needed] ... Integrin ligands (collagens, fibrinogen, fibronectin, laminins, ICAM-1, ICAM-2, osteopontin, VCAM-1, vitronectin) ...
The drug requires very expensive Phase I, II and III clinical trials, and most of them fail. Small companies have a critical ... Affecting blood pressure/(antihypertensive drugs): ACE inhibitors, angiotensin receptor blockers, beta-blockers, α blockers, ... The popularity of meprobamate paved the way for Librium and Valium, two minor tranquilizers that belonged to a new chemical ... 2.. *^ S., Van Wormer, Katherine (18 March 2015). Social welfare policy for a sustainable future : the U.S. in global context. ...
O'Dell SD, Day IN (Jul 1998). "Insulin-like growth factor II (IGF-II)". The International Journal of Biochemistry & Cell ... "Insulin-Like Growth Factor II". MeSH. NCBI.. *^ Pham NV, Nguyen MT, Hu JF, Vu TH, Hoffman AR (Nov 1998). "Dissociation of IGF2 ... IGF2, C11orf43, GRDF, IGF-II, PP9974, insulin like growth factor 2. External IDs. OMIM: 147470 MGI: 96434 HomoloGene: 510 ... negative regulation of transcription from RNA polymerase II promoter. • osteoblast differentiation. • in utero embryonic ...
renin-angiotensin system *ACE inhibitors. *Angiotensin II receptor antagonists. *Renin inhibitors. *Antihyperlipidemics * ... Dronabinol (Marinol/Syndros) is a Schedule II drug in the U.S.[9] ... in Schedule II". Retrieved 2019-02- ... 39 (2): 397-399. doi:10.1248/cpb.39.397. PMID 2054863.. *^ Marx, WM; Teleni L; McCarthy AL; Vitetta L; McKavanagh D; Thomson D ... hoe 2#section1 Muscimol. Chemical Data Sheet[permanent dead link], Database of Hazardous Materials, CAMEO chemicals ...
Gray, D.A.; Naudé, R.J.; Erasmus, T. (1988). "Plasma arginine vasotocin and angiotensin II in the water deprived common ostrich ... 89 (2): 251-256. doi:10.1016/0300-9629(88)91088-2.. *^ a b c d e f g h i j k Polly K.; Phillips & Sanborn Allen F. (1994). "An ... Two antidiuretic hormones, Arginine vasotocin (AVT) and angiotensin (AII) are increased in blood plasma as a response to ... doi:10.1007/s11250-009-9428-2. PMID 19693684.. *^ a b c d e f g h i Skadhauge, E; Warüi CN; Kamau JM; Maloiy GM (1984). " ...
Agapitov AV, Haynes WG (March 2002). "Role of endothelin in cardiovascular disease". J Renin Angiotensin Aldosterone Syst 3 (1 ... Poznate su tri izoforme (ET-1, -2, -3) sa različitim regionima izražavanja, i dva ključna tipa receptora, ETA i ETB. ...
"Randomized Trial of Icatibant for Angiotensin-Converting Enzyme Inhibitor-Induced Upper Airway Angioedema". The Journal of ... C1CC[[email protected]]2[[email protected]@H](C1)CC(N2C(=O)C3CC4=CC=CC=C4CN3C(=O)[[email protected]](CO)NC(=O)[[email protected]](CC5=CC=CS5)NC(=O)CNC(=O)C6C[[email protected]](CN6C(=O)C7CCCN7C(=O)C ... Prolactin modulators: Prolactin inhibitors: D2 receptor agonists (e.g., bromocriptine, cabergoline); Prolactin releasers: D2 ... 2S)-2-[[(3aS,7aS)-1-[2-[(2S)-2-[[(2S)-. 2-[[2-[[(4R)-1-[1-[2-[[(2R)-2-amino-5-(diaminomethylideneamino). pentanoyl]amino]-5-( ...
12 (2): 117-26. doi:10.1093/dnares/12.2.117. PMID 16303743.. *. Engemaier E, Römpler H, Schöneberg T, Schulz A (February 2006 ... doi:10.1007/s00335-005-0075-2. PMID 16341674.. *. Liebscher I, Müller U, Teupser D, Engemaier E, Engel KM, Ritscher L, Thor D, ...
An octapeptide has eight amino acids (e.g., angiotensin II).. *A nonapeptide has nine amino acids (e.g., oxytocin). ... A decapeptide has ten amino acids (e.g., gonadotropin-releasing hormone & angiotensin I). ... An oligopeptide consists of only a few amino acids (between two and twenty). ... 4 (2): 215-28. PMID 11378961.. *^ Hummel J, Niemann M, Wienkoop S; et al. (2007). "ProMEX: a mass spectral reference database ...
However, Angiotensin converting enzyme inhibitors and Angiotensin II receptor antagonists are favoured due to their anti- ... IgA1 is one of the two immunoglobulin subclasses (the other is IgD) that is O-glycosylated on a number of serine and threonine ... Importantly, angiotensin-converting enzyme inhibitors were used in both groups equally. Cyclophosphamide ( traded as endoxan & ... These tests would rule out kidney stones and bladder cancer, two other common urological causes of hematuria. In children and ...
... such as an angiotensin II receptor blocker (ARB)[17] which has a similar mechanism but does not affect bradykinin. However, ... Types I and II are caused by mutations in the SERPING1 gene, which result in either diminished levels of the C1-inhibitor ... "Investigation of angioedema associated with the use of angiotensin-converting enzyme inhibitors and angiotensin receptor ... Type II - normal levels, but decreased function of C1INH (15%);. *Type III - no detectable abnormality in C1INH, occurs in an X ...
Part II of the report from the Joint Task Force of European Respiratory Society (ERS) and European Academy of Allergy and ... dan inhibitor enzim pengubah angiotensin.[60] ... Diakses tanggal 2 September 2010. *^ a b c d British Guideline ... 2-5. *^ Jindal, editor-in-chief SK. Textbook of pulmonary and critical care medicine. New Delhi: Jaypee Brothers Medical ... 2): 71s-73s. PMID 15301800. Cite uses deprecated parameter ,month=. (bantuan). *^ Schiffman, George (18 December 2009). " ...
Angiotensin II receptor antagonist. *ACE inhibitor. *Alpha-adrenergic agonist. *Beta blocker. *Dopamine agonist ...
The angiotensin II receptors, (AGTR1) and (AGTR2), are a class of G protein-coupled receptors with angiotensin II as their ... The angiotensin receptor is activated by the vasoconstricting peptide angiotensin II. The activated receptor in turn couples to ... The AT4 receptor is activated by the angiotensin II metabolite angiotensin IV, and may play a role in regulation of the CNS ... Angiotensin II receptor antagonist. References[edit]. *^ de Gasparo M, Catt KJ, Inagami T, Wright JW, Unger T (2000). " ...
... angiotensin I) and two varieties (angiotensin II and angiotensin III) that elevate blood pressure and stimulate the adrenal ... Angiotensin ii definition, any of three oligopeptides occurring in plasma, an inactive form ( ... angiotensin ii in Medicine Expand. angiotensin II n. An octapeptide that is a potent vasopressor and a powerful stimulus for ... Angiotensin II is formed from inactive angiotensin I by the action of angiotensin-converting enzyme (or ACE). See also ACE ...
Inasmuch as the renin-angiotensin system can act as a protective mechanism again … ... development of collateral circulation occurs in at least two time-related phases: (1) the fast enhancement of the function of ... preexisting channels and (2) the slow formation of new vessels. ... Neovascularization produced by angiotensin II J Lab Clin Med. ... it is of interest to establish whether angiotensin II also produces stimulation of new vessel formation. Angiotensin II or ...
See how Renin and ACE work to cut Angiotensinogen down to size! Rishi is a pediatric infectious disease physician and works at Khan Academy.
Renin-angiotensin system Renin-angiotensin systemThe renin-angiotensin system (RAS) is a peptidergic system with endocrine ... Expression of feline angiotensin converting enzyme 2 and its interaction with SARS-CoV S1 protein.. Guo H, Guo A, Wang C, Yan B ... Expression of feline angiotensin converting enzyme 2 and its interaction with SARS-CoV S1 protein. [Res Vet Sci. 2008] ... Felis catus angiotensin I converting enzyme 2 (ACE2), mRNA Felis catus angiotensin I converting enzyme 2 (ACE2), mRNA. gi, ...
... which cleaves angiotensin I and angiotensin II to angiotensin-(1-7), in 574 diabetic patients, showing a 30 vs. 18% prevalence ... Angiotensin II Receptor Blockers and Nephropathy Trials Message Subject (Your Name) has forwarded a page to you from Diabetes ... 1051-P) reported that angiotensin II decreases the vasodilatory response to IGF-1, blocking IGF-1 stimulated PI3K and NOS in ... Barry Brenner, Boston, MA, discussed the Reduction of Endpoints in NIDDM with the Angiotensin II Antagonist Losartan (RENAAL) ...
... of the important actions of angiotensin II, and avoid the nonspecificity of the angiotensin I converting enzyme inhibitors. ... Pharmacological properties of angiotensin II receptor antagonists.. Timmermans PB1.. Author information. 1. Tularik Inc, South ... The availability of selective, potent, orally active and long acting nonpeptide angiotensin II type 1 (AT1) receptor ... antagonists has provided the opportunity to obtain the benefits of selectively blocking the renin-angiotensin-aldosterone ...
1996). Effects of angiotensin II receptor blockade during exercise: comparison of losartan and saralasin. J Cardiovasc ... Saralasin, a partial agonist angiotensin II receptor, does not appear to affect mean arterial pressure (MAP) and systemic ... Lowers blood pressure by blocking the vasoconstrictor effects of the hormone angiotensin II ...
Angiotensin II and Coronary Sympathetic Vasodilation. Kenneth M. Kessler, Rhonda M. Kessler ... There is no question that angiotensin II can play its enhancing effects on the sympathetic nervous system at various levels and ... Saino A, Pomidossi G, Perondi R, Valentini R, Rimini A, Di Francesco L, Mancia G. Intracoronary angiotensin II potentiates ... The suggestion is that higher local concentrations of either angiotensin II or perindoprilat are achieved when a vessel is ...
The angiotensin II receptors, (ATR1) and (ATR2), are a class of G protein-coupled receptors with angiotensin II as their ... angiotensin II. The AT1 and AT2 receptors share a sequence identity of ~30%, but have a similar affinity for angiotensin II, ... The angiotensin receptor is activated by the vasoconstricting peptide angiotensin II. The activated receptor in turn couples to ... The AT4 receptor is activated by the angiotensin II metabolite angiotensin IV, and may play a role in regulation of the CNS ...
Angiotensin II receptor blockers, as their name implies, block the action of angiotensin II at its receptors and therefore may ... "Angiotensin II". Drug Information Portal. U.S. National Library of Medicine. "Angiotensin II acetate". Drug Information Portal ... Angiotensin II (Ang II) is a medication that is used to treat hypotension resulting from septic shock or other distributive ... Angiotensin II is a naturally occurring hormone secreted as part of the renin-angiotensin system that results in powerful ...
Angiotensin Receptor Blocker, Angiotensin Blocker, Losartan, Cozaar, Irbesartan, Avapro, Candesartan, Atacand, Eprosartan, ... Irbesartan selectively and competitively blocks the binding of angiotensin II to the angiotensin I receptor. Angiotensin II ... Angiotensin II, formed from angiotensin I by angiotensin-converting enzyme (ACE), stimulates the adrenal cortex to synthesize ... This prevents angiotensin II-induced vasoconstriction and interferes with angiotensin II-mediated aldosterone secretion, ...
Angiotensin II and ET-1, both at 10 nmol/L, induced myocyte hypertrophy, as demonstrated by increased protein content and ... DOPAMINE D2 RECEPTOR STIMULATION INHIBITS ANGIOTENSIN II-INDUCED HYPERTROPHY IN CULTURED NEONATAL RAT VENTRICULAR MYOCYTES ... Therefore, the effects of the D2 receptor agonist bromocriptine and the D2 receptor antagonist haloperidol on angiotensin (Ang ... II- or endothelin (ET)-1-induced hypertrophy of cultured neonatal rat ventricular myocytes were investigated in the present ...
... ; The octapeptide angiotensin II (Ang II) exerts a wide range of effects on the cardiovascular system. It ... Ang II is formed by cleavage of Ang I by the angiotensin-converting enzyme (ACE) or chymases. Human heart chymase, a ... hydrolyzes the Phe8-His9 bond to yield the octapeptide hormone angiotensin II and His-Leu.; DRVYIHPF; H-Asp-Arg-Val-Tyr-Ile-His ... 2010). Angiotensin II/angiotensin II type I receptor (AT1R) signaling promotes MCF-7 breast cancer cells survival via PI3- ...
Angiotensin II has been investigated for the treatment, basic science, and diagnostic of Hypertension, Renin Angiotensin System ... The novelty of the medication lies in the fact that it is the first and only use of synthetic human angiotensin II to help ... As of December 21, 2017 the FDA approved La Jolla Pharmaceuticals Giapreza (angiotensin II) Injection for Intravenouse ... Angiotensin II is under investigation for the treatment of Sepsis, Septic Shock, Diabetes Mellitus, and Acute Renal Failure. ...
See how Angiotensin 2 effects 4 target organs to increase blood pressure. Rishi is a pediatric infectious disease physician ...
Angiotensin II (Ang II), the major bioactive peptide of the renin-angiotensin system, was originally described as a potent ... Angiotensin II regulates vascular and endothelial dysfunction: recent topics of angiotensin II type 1 receptor signaling in the ... Iwai N, Inagami T. Identification of two subtypes in the rat type-1 angiotensin II receptor. FEBS Lett. 1992; 298: 257-260. ... Elton TS, Stephan CC, Taylor GR, Kimball MG, Martin MM, Durand JN, Oparil S. Isolation of two distinct type 1 angiotensin II ...
... regulates the renin-angiotensin system by counterbalancing ACE activity. Accumulating evidence in recent years has demonstrated ... Angiotensin-converting enzyme 2 (ACE2), a first homolog of ACE, ... Angiotensin-converting enzyme 2 (ACE2), a first homolog of ACE ... Angiotensin-converting enzyme 2 (ACE2) in disease pathogenesis Circ J. 2010 Mar;74(3):405-10. doi: 10.1253/circj.cj-10-0045. ... regulates the renin-angiotensin system by counterbalancing ACE activity. Accumulating evidence in recent years has demonstrated ...
WebMD provides information about interactions between Aldactazide Oral and k-sparing-diuretics-angiotensin-ii-receptor-blocker- ... Angiotensin II Receptor Blocker (ARB)/K+ Sparing Diuretics Interactions. This information is generalized and not intended as ... If your doctor prescribes these two medicines together, you may need to check your blood level of potassium. The dose of your ... Enalapril: a new angiotensin converting enzyme inhibitor. Drug Intell Clin Pharm 1986 Mar;20(3):177-86. ...
Angiotensin II (1-100 nM) alone caused an increase in the... ... The effect of taurine on angiotensin II-induced hypertrophy of ... Baker, K.M., Booz, G.W., and Dostal, D.E., 1992 Cardiac actions of angiotensin II: Role of an intracardiac renin-angiotensin ... in the absence of angiotensin II had no effect on either hyperplastic growth or hypertrophy of the two types of cultured ... Angiotensin II (1-100 nM) alone caused an increase in the rate of protein synthesis and the surface area of myocytes without ...
Angiotensin II sustains brain inflammation in mice via TGF-β. Tobias V. Lanz,1,2 Zhaoqing Ding,1 Peggy P. Ho,1 Jian Luo,1 Ankur ... Regulation of blood pressure by the type 1A angiotensin II receptor gene. Proc Natl Acad Sci U S A. 1995;92(8):3521-3525.. View ... Angiotensin II, transforming growth factor-beta1 and repair in the infarcted heart. J Mol Cell Cardiol. 1998;30(8):1559-1569. ... Angiotensin II type 1 receptor expression on human leukocyte subsets: a flow cytometric and RT-PCR study. Regul Pept. 2006;134( ...
... Ke Su,1 Ping Zeng,1 Wei Liang,1 ... X. Chen, Z. Ren, W. Liang et al., "c-Abl mediates angiotensin II-induced apoptosis in podocytes," Journal of Molecular ... M. Alique, E. Civantos, E. Sanchez-Lopez et al., "Integrin-linked kinase plays a key role in the regulation of angiotensin II- ... Z. Ren, W. Liang, C. Chen, H. Yang, P. C. Singhal, and G. Ding, "Angiotensin II induces nephrin dephosphorylation and podocyte ...
A II) induced hypertension in which the mean arterial blood pressure did not exceed 150 mmHg, blood flow in tumor tissue ... Under angiotensin 11 (A II) induced hypertension in which the mean arterial blood pressure did not exceed 150 mmHg, blood flow ... 1985) Manipulation of experimental rat and rabbit liver tumor blood flow with angiotensin II. Cancer Res 45: 5390-5393.PubMed ... Sato H, Hoshi M, Urushiyama M, Sugiyama K. and Wakui A. (1989) Angiotensin II induced hypertension chemotherapy(IHC) and dose ...
Mice Transgenic for Human Angiotensin-converting Enzyme 2 Provide a Model for SARS Coronavirus Infection ... infection by introducing the human gene for angiotensin-converting enzyme 2 (hACE2) (the cellular receptor of SARS-CoV), driven ...
Moreover, ACE2 deficiency worsened the disease pathogenesis markedly, mainly by targeting the angiotensin II type 1 receptor ( ... Angiotensin-converting enzyme (ACE) and ACE2 are involved in several pathologies such as cardiovascular functions, renal ... Angiotensin II levels and western blotting. Ang II levels were detected as described previously21. Rat polyclonal anti-ACE2 ... A novel angiotensin-converting enzyme-related carboxypeptidase (ACE2) converts angiotensin I to angiotensin 1-9. Circ. Res. 87 ...
1 One of these factors is angiotensin II (Ang II). Whereas the role of Ang II in cardiomyocyte hypertrophy is well established, ... Profibrotic Effects of Angiotensin II in the Heart. A Matter of Mediators. Javier Díez ... Kupfahl C, Pink D, Friedrich K, Zurbrügg HR, Neuss M, Warnecke C, Fielitz J, Graf K, Fleck E, Regitz-Zagrosek V. Angiotensin II ... Review of aldosterone- and angiotensin II-induced target organ damage and prevention. Cardiovasc Res. 2004; 61: 663-670. ...
Buy our Angiotensin II Type 1 Receptor peptide. Ab176148 is a blocking peptide for ab124505 and has been validated in BL. Abcam ... Angiotensin II Type 1 Receptor peptide. See all Angiotensin II Type 1 Receptor proteins and peptides. ... Receptor for angiotensin II. Mediates its action by association with G proteins that activate a phosphatidylinositol-calcium ... Blocking - Blocking peptide for Anti-Angiotensin II Type 1 Receptor antibody (ab124505) ...
Angiotensin II. Angiotensinogen. Antihypertensive Agents. Angiotensin II Type 1 Receptor Blockers. Angiotensin Receptor ... Angiotensin II Antagonism of TGF-Beta 1: A Candesartan Dose - TGF-Beta 1 Response Relationship Study. ... Angiotensin II Antagonism of TGF-Beta 1. This study has been completed. ... The purpose of this study is to determine whether a treatment for diabetic nephropathy, the angiotensin receptor blocker ...
Aldosterone potentiates angiotensin II-induced signaling in vascular smooth muscle cells. Circulation. 2004; 109: 2792-2800. ... Aldosterone Synthase Inhibitor Ameliorates Angiotensin II-Induced Organ Damage. Anette Fiebeler, Jürg Nussberger, Erdenechimeg ... Schiffrin EL, Thome FS, Genest J. Vascular angiotensin II receptors in renal and DOCA-salt hypertensive rats. Hypertension. ... Immunosuppressive treatment protects against angiotensin II-induced renal damage. Am J Pathol. 2002; 161: 1679-1693. ...
  • The angiotensin II receptors, (AGTR1) and (AGTR2), are a class of G protein-coupled receptors with angiotensin II as their ligands. (
  • The AT1 and AT2 receptors share a sequence identity of ~30%, but have a similar affinity for angiotensin II, which is their main ligand. (
  • AT 2 receptors are more plentiful in the fetus and neonate. (
  • Angiotensin II receptor blockers, as their name implies, block the action of angiotensin II at its receptors and therefore may reduce its effects. (
  • There is no question that angiotensin II can play its enhancing effects on the sympathetic nervous system at various levels and that not only a presynaptic potentiation of norepinephrine secretion but also an amplification of the responsiveness of adrenergic receptors to neural stimuli is involved as indicated by the data of Lyons et al. (
  • It is certainly possible, on the basis of the in vitro findings of Kessler et al, R5 that this activity is increased by sympathetic influences also because of an enhanced effect of angiotensin II on its receptors. (
  • Such species like angiotensin III can then bind and interact with specific G protein coupled receptors like angiotensin receptor 1, or AT-1 1 where strong vasoconstricson can occur. (
  • The biological responses of Ang II are mediated by its interaction with 2 distinct high-affinity G protein-coupled receptors now designated Ang II type 1 receptor (AT 1 R) and Ang II type 2 receptor. (
  • 5 On the other hand, more recent findings suggest that fibrosis may represent the reparative response to myocardial inflammation induced by Ang II through the interaction with AT 1 receptors present in cells from the cardiac microvasculature. (
  • The reported results should help with designing ligands for angiotensin receptors and possibly to other peptide GPCRs. (
  • Two systems of nomenclature are used in reference to angiotensin-II receptor antagonists: one system employs Roman numerals, and the other is based on the amino acids that make up the A-I and A-II receptors (AT 1 receptor and AT 2 receptor). (
  • 2 Angiotensin-II receptor antagonists act by binding to specific membrane-bound receptors that displace A-II from its type 1-receptor subtype (AT 1 ). (
  • 3 AT-II pressor effects are mediated by AT 1 receptors. (
  • AT 2 receptors are found in many tissues, including those of the adrenal medulla, uterus, ovary and other brain regions, but they are not known to be related to cardiovascular homeostasis. (
  • An elegant set of renal transplant experiments between wild-type and AngII type 1 (AT1) receptor-knockout mice has revealed that arterial hypertension induced by AngII requires the presence of AT1 receptors in the kidney but not in any other tissue ( 1 ) and that hypertension mostly is the consequence of an increase in renal salt reabsorption ( 2 ). (
  • Angiotensin II is mediated by its interaction with, Angiotensin II type 1 membrane receptors. (
  • Angiotensin II (AngII) is a peptide hormone that plays important roles in energy metabolism via its angiotensin type 1 or type 2 receptors (AT1R and AT2R). (
  • Stimulation of angiotensin AT2 receptors by the non-peptide agonist, compound 21, evokes vasodepressor effects in conscious spontaneously hypertensive rats. (
  • Cardiovascular phenotype of mice lacking all three subtypes of angiotensin II receptors. (
  • It acts through at least two types of receptors termed AT1 and AT2. (
  • 1997). "Subtype 2 and atypical angiotensin receptors in the human heart. (
  • 2002). "Angiotensin receptors: signaling, vascular pathophysiology, and interactions with ceramide. (
  • AngII is known to exert its biological effects via two functional receptors, type 1 and type 2 angiotensin II receptors (AT1R and AT2R, respectively). (
  • In order to cause vessel narrowing, angiotensin II binds to proteins, called AT1 receptors, on the surface of smooth muscles within the blood vessels. (
  • By attaching to AT1 receptors on smooth muscle cells lining the blood vessels, this drug blocks angiotensin II from binding. (
  • ACE2 an entry receptor of SARS coronaviruses as well as SARS-CoV-2,.The coronavirus spike (S) glycoprotein is a class I viral fusion antigen located on the external envelope of the virion that takes part in a critical part in viral infection by identifying host cell receptors and facilitating fusion of the viral and cellular membranes. (
  • Valsartan is a prodrug that produces direct antagonism of angiotensin II receptors. (
  • Angiotensin (Ang) II exerts its important physiological functions through 2 distinct receptor subtypes, type 1 (AT 1 ) and type 2 (AT 2 ) receptors. (
  • Recently, new evidence has accumulated showing the existence of several novel receptor interacting proteins and various angiotensin II receptor activation mechanisms beyond the classical actions of receptors for Ang II. (
  • These associated proteins could contribute not only to Ang II receptors' functions, but also to influencing pathophysiological states. (
  • Receptor dimerization of Ang II receptors such as homodimer, heterodimer, and complex formation with other G protein-coupled receptors has also been focused on as a new mechanism of their activation or inactivation. (
  • These emerging concepts of regulation of Ang II receptors and a new insight into future drug discovery are discussed in this review. (
  • 1 Ang II binds 2 major receptors: the Ang II type-1 (AT 1 ) receptor and type-2 (AT 2 ) receptor. (
  • On the other hand, recent experimental studies have also demonstrated the existence of proteins interacting with Ang II receptors by screening with a yeast-based 2-hybrid protein-protein interaction assay technique and revealed their functions ( Table ). (
  • 2-9 Therefore, recent advances in studies of Ang II receptors could prove the existence of a variety of new players and targets in addition to the traditional "Ang II world" and provide a new insight into cardiovascular biology. (
  • Ang II receptors are members of the 7 transmembrane G protein-coupled receptors (GPCR). (
  • Recently, several GIPs have been reported to have unique roles in the regulation of AT 1 and AT 2 receptors via interaction with the C terminus of their receptors. (
  • Here, we review these GIPs and other aspects of Ang II receptors, and discuss the possibility of new drug discovery. (
  • Functional Ang II type 2 receptors (AT2R) are present in these cells and inhibit growth induced by epidermal growth factor. (
  • Moreover, the proposed antigrowth effects of AT 2 receptor signaling in pathological cardiac hypertrophy could not be shown in two mice models both deficient in AT 2 receptors. (
  • In response to mechanical stretch of neonatal cardiomyocytes, both AT 1 and AT 2 receptors are upregulated. (
  • In addition, the pro-senescence endothelial response to thrombin was associated with an overexpression of both angiotensin converting enzyme and AT1 receptors and was inhibited by perindoprilat and losartan. (
  • These data indicate that angiotensin II stimulates IP-10 production from endothelial cells via angiotensin II type 1 receptors. (
  • Angiotensin II receptor blockers, also known as ARB blockers or angiotensin 2 receptor blockers, are drugs used to treat high blood pressure and heart failure. (
  • Angiotensin II receptor blockers are often used in patients who cannot tolerate a common type of drugs known as ACE inhibitors. (
  • It covers topics related to angiotensin II receptor blockers (ARBs) and nephropathy. (
  • Angiotensin-II receptor antagonists (or blockers) are a newer class of antihypertensive agents. (
  • The effect of A-II is likely to be more completely blocked by the AT 1 receptor antagonism of angiotensin-II receptor blockers than by ACE inhibitors. (
  • 1 , 4 Angiotensin-II receptor blockers antagonize A-II-induced biologic actions, including smooth muscle contraction, sympathetic pressor mechanisms and aldosterone secretion. (
  • Two FDA officials are quarreling in public about their different views about the safety of angiotensin-receptor blockers (ARBs), according to a story by Thomas Burton in Friday's Wall Street Journal. (
  • Recently, a number of large-scale prospective studies have proven that blockade of the system with ACE inhibitors and angiotensin II receptor blockers (ARBs) retards the progression of diabetic nephropathy ( 5 - 11 ). (
  • Recent large-scale clinical trials, including HOPE (Heart Outcomes Prevention Evaluation), LIFE (Losartan Intervention for Endpoint), CHARM (Candesartan in Heart Failure-Assessment of Mortality and Morbidity), and VALUE (Valsartan Antihypertensive Long-term Use Evaluation), have demonstrated that ACE inhibitors or angiotensin II receptor blockers (ARB) prevent new onset of type 2 diabetes via their ability to attenuate AngII signaling ( 11 ). (
  • How should Angiotensin II Receptor Blockers be used? (
  • The importance of Ang II in the pathogenesis of vascular disease is reflected in the efficacy of angiotensin-converting enzyme inhibitors and Ang II receptor blockers in the treatment of atherosclerosis and hypertension. (
  • The drugs of choice for hypertension related to ADPKD are angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs). (
  • The majority of well-known Ang II actions are mediated via AT 1 receptor stimulation, and angiotensin converting enzyme inhibitors (ACEI) and AT 1 receptor blockers (ARBs) have been widely used as antihypertensive drugs, with the expectation of cardiovascular protective effects. (
  • Blood pressure meds could raise your depression risk - CNN, 10/10/16 - 'people taking one of two classes of drugs, known beta blockers or calcium channel antagonists, had twice the risk of being admitted into the hospital with a mood disorder, such as severe depression. (
  • However, people taking a class of drugs known as angiotensin blockers -- ACE inhibitors -- had a lower risk of developing severe mood disorders, even compared with healthy control groups with no history of hypertension or depression' - Note: It doesn't mention ARB's. (
  • If you Google 'angiotensin blockers' it brings up ARB's. (
  • 2016 Apr 7:1-9 - 'Among various antihypertensive drugs, angiotensin receptor blockers (ARBs) have an established efficacy and safety, making them a favourable choice. (
  • Angiotensin II receptor blockers (ARBs) are widely used for the treatment of hypertension. (
  • Angiotensin II receptor blockers (ARB) may reduce response to GIAPREZA. (
  • The angiotensin receptor is activated by the vasoconstricting peptide angiotensin II. (
  • Angiotensin II or cholecystokinin, an unrelated peptide, was incorporated in a slow-release formulation polyacrylamide gel and implanted in a pocket made in the rabbit cornea. (
  • It is a synthetic vasoconstrictor peptide that is identical to human hormone angiotensin II and is marketed under the brand name Giapreza. (
  • Angiotensin II is a naturally occurring peptide hormone of the renin-angiotensin-aldosterone-system (RAAS) that has the capacity to cause vasoconstriction and an increase in blood pressure in the human body. (
  • Angiotensin II (Ang II), the major bioactive peptide of the renin-angiotensin system, was originally described as a potent vasoconstrictor. (
  • Whereas the role of Ang II in cardiomyocyte hypertrophy is well established, 3 emerging experimental and clinical evidence is providing support for the notion that this peptide induces myocardial fibrosis. (
  • Whatever the pathway is, available data indicate that the profibrotic effect of Ang II results from synergistic cooperation between this peptide and other profibrotic factors. (
  • This is a fluorescent (FAM)-labeled Angiotensin II peptide, Abs/Em=494/518 nm. (
  • Detects a band of approximately 90 kDa (predicted molecular weight: 97 kDa).Can be blocked with Human Angiotensin Converting Enzyme 2 peptide (ab15352) . (
  • Carboxypeptidase which converts angiotensin I to angiotensin 1-9, a peptide of unknown function, and angiotensin II to angiotensin 1-7, a vasodilator. (
  • The AT2R is activated after specific binding of the eight amino acid peptide angiotensin II (AngII), which is generated from angiotensin I by the angiotensin-converting enzyme. (
  • Development of selective non-peptide angiotensin II type 2 receptor agonists. (
  • Recently, angiotensin 1-converting enzyme (ACE)2, a captopril-insensitive ACE homologue, was identified ( 12 , 13 ) and shown to cleave Ang-II into the biologically active peptide Ang-(1-7) ( 13 ). (
  • Among the cytokines, growth factors, mitogens, neurotrophins, and neuroactive peptides analyzed, only angiotensin II (Ang II), calcitonin gene- related peptide (CGRP), and vasoactive intestinal peptide (VIP) were found to regulate the expression of PN-1 on Schwann cells. (
  • In the last 30 years, structure/activity studies using peptide analogs yielded information about the structural requisites for angiotensin II (AngII) receptor binding and activation, as well as for other functional phenomena such as receptor desensitization and internalization. (
  • GIAPREZA mimics the body's endogenous regulatory peptide that is central to the renin-angiotensin-aldosterone system to increase blood pressure. (
  • LSBio ACE2 / ACE-2 Elisa Kits [LifeSpan BioSciences, Inc. (
  • Angiotensin-converting enzyme 2 (ACE2), a first homolog of ACE, regulates the renin-angiotensin system by counterbalancing ACE activity. (
  • To establish a small animal model of severe acute respiratory syndrome (SARS), we developed a mouse model of human severe acute respiratory syndrome coronavirus (SARS-CoV) infection by introducing the human gene for angiotensin-converting enzyme 2 (hACE2) (the cellular receptor of SARS-CoV), driven by the mouse ACE2 promoter, into the mouse genome. (
  • Angiotensin-converting enzyme (ACE) and ACE2 are involved in several pathologies such as cardiovascular functions, renal disease and acute lung injury. (
  • Moreover, ACE2 deficiency worsened the disease pathogenesis markedly, mainly by targeting the angiotensin II type 1 receptor (AT1). (
  • As such recombinant soluble ACE2 is currently being tested in phase 2 clinical trials as a potential therapy for the treatment of acute lung injury in humans 18 , 19 . (
  • Total RNA from a small part of the renal cortical biopsy specimens was reverse-transcribed, and the resultant cDNA was amplified for new major components of RAS (i.e., renin, renin receptor, angiotensinogen, ACE, ACE2, angiotensin II type 1 receptor, and angiotensin II type 2 receptor) and measured. (
  • ACE2 Protein binds to SARS Coronavirus-2 [ CoV-2019 ] Spike receptor binding domain. (
  • Previous studies have shown that activation of endogenous angiotensin-converting enzyme 2 (ACE2) results in various beneficial effects in the cardiovascular system. (
  • Angiotensin-(1-7) receptor blockade by d -Ala 7 -Ang-(1-7) prevented the ACE2-mediated improvements in intraperitoneal glucose tolerance, glycemia, and islet function and also impaired insulin sensitivity in both Ad-hACE2-eGFP- and Ad-eGFP-treated db/db mice. (
  • CONCLUSIONS These findings identify ACE2 as a novel target for the prevention of β-cell dysfunction and apoptosis occurring in type 2 diabetes. (
  • It is known that ACE2, which was discovered as a novel ACE-related carboxypeptidase in 2000, hydrolyzes Ang I to Ang-(1-9) and also Ang II to Ang-(1-7). (
  • We hypothesized that over-expression of ACE2 may be related to a reduction in Ang II level and the cardioprotective effect of olmesartan. (
  • These findings suggest that olmesartan may exhibit an ACE inhibitory action in addition to an Ang II receptor blocking action, prevent an increase in Ang II level, and protect cardiovascular remodeling through an increase in cardiac nitric oxide production and endogenous Ang-(1-7) via over-expression of ACE2. (
  • Abstract -There are strong data favoring the pathogenic role of angiotensin II type 1 receptor (AT 1 ) activation with subsequent promotion of myocyte growth and cardiac fibrosis in the development of cardiac hypertrophy and heart failure. (
  • ARBs interfere with the binding of formed angiotensin II to its endogenous receptor. (
  • AT 2 receptor stimulation by unbound Ang II could also be expected during treatment with ARBs. (
  • The availability of selective, potent, orally active and long acting nonpeptide angiotensin II type 1 (AT1) receptor antagonists has provided the opportunity to obtain the benefits of selectively blocking the renin-angiotensin-aldosterone system at the level of the AT1 receptor that mediates most, if not all, of the important actions of angiotensin II, and avoid the nonspecificity of the angiotensin I converting enzyme inhibitors. (
  • unlike angiotensin-converting enzyme inhibitors, they do not inhibit bradykinin metabolism or enhance prostaglandin synthesis. (
  • Cough occurs much less often with these agents than with angiotensin-converting enzyme inhibitors, and they do not adversely affect lipid profiles or cause rebound hypertension after discontinuation. (
  • Components of the renin-angiotensin-aldosterone system and sites at which angiotensin-converting enzyme (ACE) inhibitors work and angiotensin-II receptor antagonists interrupt the type 1-receptor subtype (AT 1 ) of angiotensin II. (
  • Interestingly, some clinical studies have demonstrated that treatment with either angiotensin I-converter enzyme inhibitors (ACEI) or angiotensin II receptor antagonist (ARA) reduces the incidence of diabetes mellitus in high risk patients ( 5 , 6 ). (
  • The enormous success of ACE inhibitors in hypertension and heart failure spurred hope that adding a second drug to block the renin-angiotensin system would yield improved outcomes. (
  • Heart Failure** Valsartan is indicated for the treatment of heart failure (NYHA class II-IV) in patients who are intolerant to angiotensin-converting enzyme inhibitors (ACE inhibitors) for various reasons, including those who experience ACE inhibitor adverse effects. (
  • To reduce impact to your patients, please consider switching them from ARB medications to other clinically appropriate drug therapies, such as angiotensin-converting enzyme inhibitors (ACE-I) 1 . (
  • May induce a more complete inhibition of the renin-angiotensin system than ACE inhibitors, do not affect the response to bradykinin, and are less likely to be associated with cough and angioedema. (
  • ET-1 inhibits inhibitors of calcification, matrix Gla and osteoprotegerin, while enhancing pro-calcific factors such as BMP-2 and osteopontin. (
  • ACE inhibitors suppress the renin-angiotensin-aldosterone system. (
  • 125 l-angiotensin II by platelets could be demonstrated in the presence of various enzyme inhibitors. (
  • However, these cells could not be used for studies of specific binding, since enzymatic degradation of 125 l-angiotensin II could not be prevented despite addition of various enzyme inhibitors. (
  • Thrombin induced the up-regulation of p53, a key regulator in cellular senescence and of p21 and p16, two cyclin-dependent kinase inhibitors. (
  • Angiotensin converting enzyme (ACE) inhibitors may increase response to GIAPREZA. (
  • There is also no question that the enhancing effect of angiotensin II on sympathetic cardiovascular influences is reciprocated because sympathetic nerve activity is an important determinant of renal secretion of renin R3 R4 and thus of the activity of the renin-angiotensin system. (
  • Furthermore, our results suggest that variable activity of the renin-angiotensin system may contribute to inconsistencies in the association between insulin resistance and hypertension. (
  • Genetic variation and activity of the renin-angiotensin system and severe hypoglycemia in type 1 diabetes. (
  • Morganti A, Grassi G, Giannattasio C, Bolla G, Turolo L, Saino A, Sala C, Mancia G, Zanchetti A. Effect of angiotensin converting enzyme inhibition on cardiovascular regulation during reflex sympathetic activation in sodium replete patients with essential hypertension. (
  • The octapeptide angiotensin II (Ang II) exerts a wide range of effects on the cardiovascular system. (
  • 3-6 Thus, Ang II plays a key role in the pathogenesis of cardiovascular diseases. (
  • 7 Most of the known physiological and pathophysiological effects of Ang II are mediated via the AT 1 R. 1-7 This receptor subtype is expressed in cardiovascular-relevant cell types including vascular smooth muscle cells (VSMCs), endothelial cells, cardiac myocytes, cardiac fibroblasts, and renal mesangial cells. (
  • hence, overexpression of the AT 1 R is one potential mechanism by which Ang II can contribute to cardiovascular disease. (
  • Since the publication of 2 clinical trials, RALES (Randomized Aldactone Evaluation Study) and EPHESUS (Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study), the role of aldosterone in cardiovascular remodeling has generated considerable attention. (
  • It plays a role in the central nervous system and cardiovascular functions that are mediated by the renin-angiotensin system . (
  • 1995). "Behavioural and cardiovascular effects of disrupting the angiotensin II type-2 receptor in mice. (
  • Here, we have summarized these emerging concepts concerning Ang II receptor interacting proteins and discuss new potent therapeutic targets in cardiovascular disease. (
  • Two of the most powerful cardiovascular regulators are the β-adrenergic and the renin-angiotensin system (RAS). (
  • The strength of the two systems is such that, between them, they virtually control cardiovascular physiology. (
  • It is tantalizing that angiotensin II improved the cardiovascular component of the SOFA score despite making zero difference in the composite SOFA score - arithmetic requires that angiotensin II must have impaired the function of some other organ(s) not reported in the manuscript (1). (
  • 1996). Effects of angiotensin II receptor blockade during exercise: comparison of losartan and saralasin. (
  • 7-10 In previous studies, we demonstrated that MR blockade with spironolactone or eplerenone prevented mortality and Ang II-induced organ damage. (
  • Although definitive evidence supporting dual blockade of the renin-angiotensin system has never been found, more than 200,000 patients in the US currently receive this therapy. (
  • OBJECTIVE -Recent studies have proved that blockade of the renin-angiotensin system (RAS) retards the progression of diabetic nephropathy, whereas hyporeninemia is known as a typical state in diabetic subjects. (
  • Deficiency or blockade of angiotensin II type 2 receptor delays tumorigenesis by inhibiting malignant cell proliferation and angiogenesis. (
  • OBJECTIVE- Blockade of angiotensin (Ang) II has been shown to prevent new-onset type 2 diabetes. (
  • Vascular calcification is reduced by ET-1 A receptor antagonists and to a greater extent than angiotensin receptor blockade although both agents reduce blood pressure. (
  • Angiotensin II blockade with sarcosine 1 -alanine 8 -angiotensin II (saralasin, P-113) was done in 40 studies of 20 hypertensive patients. (
  • Eleven of 12 patients with a depressor response to angiotensin II blockade had significant renovascular or renal disease, and nine of 10 had renal vein renin measurements that lateralized to the abnormal kidney. (
  • In these studies a correlation between the fall in blood pressure and the rise in plasma renin activity during angiotensin II blockade was observed while renin was unchanged in the absence of depressor responses. (
  • OBJECTIVE Several clinical studies have shown the benefits of renin-angiotensin system (RAS) blockade in the development of diabetes, and a local RAS has been identified in pancreatic islets. (
  • Our findings suggest that TRPC6 promotes albuminuria, perhaps by promoting angiotensin II-dependent increases in Ca 2+ , suggesting that TRPC6 blockade may be therapeutically beneficial in proteinuric kidney disease. (
  • Caution #3: Blockade of the renin-angiotensin-aldosterone system improves survival in animal models. (
  • Animal models confirm that blockade of the renin-angiotensin-aldosterone system may improve survival ( Laesser 2004 , Hirano 2014 )(3). (
  • Effects mediated by the AT 2 receptor are suggested to include inhibition of cell growth , fetal tissue development, modulation of extracellular matrix, neuronal regeneration, apoptosis , cellular differentiation , and maybe vasodilation and left ventricular hypertrophy . (
  • Angiotensin type 2 receptor-mediated apoptosis of human prostate cancer cells. (
  • 12 In the AT 2 receptor, IC3 is also important for its function involving reduction of SHP-1 activity and inhibition of extracellular signal regulated kinase (ERK) activity, and AT 2 receptor-induced apoptosis. (
  • The results indicate that increased expression of AT2R alone induced apoptosis in the prostate cancer lines, an effect that did not require Ang II. (
  • In angiotensin II-evoked apoptosis in cardiomyocytes, the proposed proapoptotic role of AT 2 activity could not be confirmed. (
  • In this review, we examine the putative individual components of AT 2 receptor signaling in the heart, ie, in cardiac growth, apoptosis, and fibrosis. (
  • However, transfection of Rcan1-1L vector promoted cell viability and ameliorated the apoptosis caused by Ang II. (
  • IP-10 neutralization with antibody blocked angiotensin II-induced apoptosis and cell senescence in endothelial cells. (
  • Sar 1 , Ile 8 ]AngII interacts with both the 'core' binding domain, where the small-molecule ligands of AT 1 R and AT 2 R bind, and the 'extended' binding domain, which is equivalent to the allosteric modulator binding site of muscarinic acetylcholine receptor. (
  • Because the renal consequences of WNK4 carrying pseudoaldosteronism type II mutations resemble the response to intravascular volume depletion (promotion of salt reabsorption without K + secretion), a condition that is associated with high angiotensin II (AngII) levels, it has been proposed that AngII signaling might affect WNK4 modulation of the NCC. (
  • Recent studies suggest that hypertension induced by angiotensin II (AngII) results primarily from the renal effects of this hormone. (
  • 2. Chronic infusions of AngII systemically, at doses that are initially subpressor, result in slowly progressive increases in arterial pressure ('slow-pressor' hypertension). (
  • In a mouse model of gradual hypertension induced by chronic administration of subpressor doses of angiotensin II (AngII), suppression of free radicals in the SFO by overexpression of CuZn-superoxide dismutase (CuZnSOD) prevented the alteration in neurovascular coupling and endothelium-dependent responses in somatosensory cortex induced by hypertension. (
  • Here, based on the in vitro studies on primary cultures of mouse white adipocytes, we report that, AT2R activation, either by AngII or AT2R agonist (C21), induces white adipocyte browning, by increasing PPARγ expression, at least in part, via ERK1/2, PI3kinase/Akt and AMPK signaling pathways. (
  • We focused on the effects of AngII on muscle mitochondria, especially on their biogenesis, as an underlining mechanism of type 2 diabetes. (
  • RESEARCH DESIGN AND METHODS- C2C12 cells and C57bl/6 mice were used to examine roles for AngII in the regulation of muscle mitochondria and to explore whether the effect was mediated by type 1 AngII receptor (AT1R) or type 2 receptor (AT2R). (
  • In this study, we hypothesized that hemorphins may also target angiotensin II (AngII) type 1 receptor (AT1R) as a key GPCR in the renin-angiotensin system. (
  • Interestingly, while LVV-hemorphin-7 alone had no significant effect on BRET signals between AT1R and Gαq or β-arrestin 2, it nicely potentiated AngII-induced BRET signals and significantly increased AngII potency. (
  • The BRET data were also correlated with AT1R downstream signaling with LVV-hemorphin-7 potentiating the canonical AngII-mediated Gq-dependent inositol phosphate pathway as well as the activation of the extracellular signal-regulated kinases (ERK1/2). (
  • To understand the relationship between putative neurohormonal factors operative in hypertension and coronary artery calcification (CAC), the relevant cellular actions of angiotensin (Ang II) and endothelin-1 (ET-1) are reviewed. (
  • To explore contractile actions of angiotensin II (AT2) on the muscularis mucosae (MM) of the bladder. (
  • Angiotensin II is formed from inactive angiotensin I by the action of angiotensin-converting enzyme (or ACE ). (
  • Expression of feline angiotensin converting enzyme 2 and its interaction with SARS-CoV S1 protein. (
  • See the reference protein sequence for angiotensin-converting enzyme 2 precursor (NP_001034545.1). (
  • Ang II is formed by cleavage of Ang I by the angiotensin-converting enzyme (ACE) or chymases. (
  • Enalapril: a new angiotensin converting enzyme inhibitor. (
  • Hyperkalemia in azotemic patients during angiotensin-converting enzyme inhibition and aldosterone reduction with captopril. (
  • Mice Transgenic for Human Angiotensin-converting Enzyme 2 Provide. (
  • Renin, an enzyme produced primarily by the juxtaglomerular cells of the kidney, catalyzes the conversion of angiotensinogen into an inactive substance, angiotensin I (A-I). Angiotensin-converting enzyme (ACE) then converts A-I to the physiologically active angiotensin II (A-II), which causes potent vasoconstriction, aldosterone secretion and sympathetic activation. (
  • Currently, they are considered reasonable alternatives for patients who have a compelling need for an angiotensin-converting enzyme (ACE) inhibitor but develop a cough while taking this medication. (
  • 3. angiotensin-converting enzyme inhibitor (n. (
  • It is the principle mediator of the renin-angiotensin system (RAS), synthesised from angiotensin I by the angiotensin-converting enzyme ACE. (
  • The active metabolite of ENALAPRIL and a potent intravenously administered angiotensin-converting enzyme inhibitor. (
  • ACE-2 (Angiotensin converting enzyme 2) an enzyme bound to cell membranes in various organs such as intestines arteries , lungs, heart & kidney. (
  • Angiotensin Converting Enzyme 2 (18-740 a.a. (
  • Anti-hypertensive Effects of Diminazene Aceturate: An Angiotensin- Converting Enzyme 2 Activator in Rats. (
  • Angiotensin I-converting enzyme (ACE)2, a new component of the RAS, has been identified in the pancreas, but its role in β-cell function remains unknown. (
  • Studies have reported an antihypertensive action via the inhibition of the angiotensin-converting enzyme, a key enzyme in the renin-angiotensin system. (
  • It has been reported that angiotensin 1-7 (Ang-(1-7)) potentiates the effect of bradykinin and acts as an angiotensin-converting enzyme (ACE) inhibitor. (
  • In endothelial cells, IP-10 significantly increased mRNA expression of renin, angiotensin-converting enzyme, and angiotensinogen. (
  • Recombinant human angotensin-converting enzyme 2 (rhACE2) as a treatment for patients with COVID-19 to block viral entry and decrease viral replication. (
  • Does angiotensin-converting enzyme 2 convert angiotensin 1 to angiotensin ii? (
  • Interruption of the renin-angiotensin system in hypertensive patients by captopril induces sustained reduction in aldosterone secretion, potassium retention and natruiresis. (
  • 20 Interestingly, it has been shown that myocardial osteopontin expression is markedly attenuated in Ang II-infused rats treated either with adrenalectomy or with the selective aldosterone blocker eplerenone. (
  • Background- Aldosterone and angiotensin (Ang) II both may cause organ damage. (
  • Conclusions- Aldosterone plays a key role in the pathogenesis of Ang II-induced organ damage. (
  • 1,2 The key enzyme in aldosterone production is aldosterone synthase (CYP11B2). (
  • 3 Angiotensin (Ang) II is the main stimulus for CYP11B2-related aldosterone synthesis. (
  • however, aldosterone levels can be elevated even though Ang II production is inhibited or its action is blocked. (
  • 9,10 The aim of the present study was to define the effect of FAD286 and the role of circulating or locally produced aldosterone in the pathogenesis of Ang II-induced renal and cardiac damage. (
  • The renin-angiotensin-aldosterone system plays an integral role in the pathophysiology of hypertension because it affects the regulation of fluid volume, electrolyte balance and blood volume. (
  • The renin-angiotensin-aldosterone system (RAAS) is a key modulator of blood pressure. (
  • Angiotensin II (ANG II) is an important physiological effector of blood pressure and volume regulation through vasoconstriction, sodium uptake, the release of aldosterone, and the stimulation of thirst. (
  • Involvement of Bone Morphogenetic Protein-6 in Differential Regulation of Aldosterone Production by Angiotensin II and Potassium in Human Adrenocortical Cells. (
  • J Renin Angiotensin Aldosterone Syst. (
  • Angiotensin II is a potent pressor hormone and a primary regulator of aldosterone secretion. (
  • Nonpeptide angiotensin II receptor antagonist that blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II. (
  • It reduces angiotensin II levels, decreasing aldosterone secretion. (
  • This agent prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion. (
  • It displaces angiotensin II from the AT1 receptor and may lower blood pressure by antagonizing AT1-induced vasoconstriction, aldosterone release, catecholamine release, arginine vasopressin release, water intake, and hypertrophic responses. (
  • Losartan is an ARB that blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II. (
  • Wang, D. H., Qiu, J., and Hu, Z. (1998) Differential regulation of angiotensin II receptor subtypes in the adrenal gland: role of aldosterone. (
  • Angiotensin II (Ang II) is the principal vasoactive substance of the renin-angiotensin system (RAS), having a variety of physiological actions including vasoconstriction, aldosterone release, and cell growth. (
  • 1. Plasma metabolic clearance rate of mono-[ 125 I]iodoangiotensin II was measured in seventeen patients with various disorders of the renin-angiotensin-aldosterone system. (
  • 1. Gli autori hanno misurato la clearance metabolica della mono-[ 125 I]iodoangiotensina II in 17 pazienti con varie alterazioni del sistema renina-angiotensina-aldosterone. (
  • 2. It is suggested that the intrinsic agonist activity of the analogues may fulfil the requirements for a permissive role for angiotensin in the aldosterone response to sodium deficiency. (
  • What is the primary function for the release of aldosterone and angiotensin ii? (
  • Which one causes more na and h2o reabsotbtion angiotensin II or aldosterone? (
  • I am a specialist in the renin angiotensin aldosterone system and happy to consult with you. (
  • Angiotensin ii stimulates the adrenal cortex to produce aldosterone which regulates salt and water reabsorption in the kidney. (
  • If someone was to have low angiotensin II and low aldosterone would you expect to see a lower renin also? (
  • If one has a low aldosterone and angiotensin ii, one would expect a high renin level. (
  • With primary (1°) hypoaldosteronism, feedback on the renin-angiotensin (AT) II- aldosterone (ALD) axis would cause the kidneys to increase renin and thereby AT II to try ^ adrenal ALD. (
  • If there is a normal level of renin, there should be a normal level of angiotensin II and aldosterone right? (
  • So low angiotensin II = low aldosterone? (
  • 13.Fujii H, Nakahama H, Yoshihara F, Nakamura S, Inenaga T, Kawano Y. Life-threatening Hyperkalemia during a Combined Therapy with the Angiotensin Receptor Blocker Candesartan and Spironolactone. (
  • 14.Phakdeekitcharoen B, Leelasa-nguan P. Effects of an ACE inhibitor or angiotensin receptor blocker on potassium in CAPD patients. (
  • The purpose of this study is to determine whether a treatment for diabetic nephropathy, the angiotensin receptor blocker candesartan, modifies mediators of kidney injury independent of blood pressure and the relationships to drug dose. (
  • Adding a non-steroidal anti-inflammatory drug (NSAID) to dual antihypertensive therapy (a diuretic plus either an ACE inhibitor or an angiotensin receptor blocker) is associated with an increase in risk for kidney injury, according to a large new retrospective study published in BMJ. (
  • Angiotensin type 2 receptor actions contribute to angiotensin type 1 receptor blocker effects on kidney fibrosis. (
  • With the large scale of angiotensin II receptor blocker (ARB) drug recalls, Humana anticipates the recalls to continue. (
  • Losartan, the first angiotensin receptor blocker, was shown to exert signific. (
  • Hans-Henrik Parving, Gentofte, Denmark, pointed out that kidney disease develops in 40% of patients with type 2 diabetes, with 25% of patients in Europe and 46% in the U.S. with end-stage renal disease (ESRD) having diabetes. (
  • What was not available in 1993 was "hard end point data" in type 2 diabetic subjects with nephropathy that showed losartan could slow the progression of advancing renal disease to nephropathy. (
  • Angiotensin II is under investigation for the treatment of Sepsis, Septic Shock, Diabetes Mellitus, and Acute Renal Failure. (
  • C. Guijarro and J. Egido, "Transcription factor- κ B (NF- κ B) and renal disease," Kidney International , vol. 59, no. 2, pp. 415-424, 2001. (
  • This study evaluates prospectively the effects of an anti-angiotensin II regimen on renal outcome in patients with mesangioproliferative glomerulonephritis followed-up for 10 years. (
  • Never treated patients with non-nephrotic proteinuria (1-3 g/day), microhematuria, no-evidence of renal failure or other relevant diseases and with diagnosis of I-II stage IgA- or pauciimmune-MsPGN were considered eligible. (
  • In ANG II hypertension, EET-B treatment markedly lowered renal inflammation. (
  • Overall, our results demonstrate that EET-B has anti-hypertensive properties, improves vascular function, and decreases renal inflammation and injury in ANG II hypertension. (
  • CONCLUSIONS -The results suggest that renal tissue RAS might be activated in the respect that ACE gene expression is upregulated in spite of a tendency to low renin expression in type 2 diabetic nephropathy. (
  • Approximately 62% of patients with renal insufficiency require at least 2 antihypertensive agents for optimal blood pressure control. (
  • To determine whether the absence of TRPC6 would alter susceptibility to hypertension and renal injury, we infused mice with angiotensin II continuously for 28 days. (
  • LJPC ) today announced the release of data from analyses of the impact of GIAPREZA™ (angiotensin II) on outcomes of a subset of patients with acute kidney injury requiring renal replacement therapy (AKI-RRT) enrolled in the ATHOS-3 (Angiotensin II for the Treatment of High Output Shock) study. (
  • The manuscript, entitled " Outcomes in patients with vasodilatory shock and renal replacement therapy treated with intravenous angiotensin II " was published online in Critical Care Medicine . (
  • What is missing from the ATHOS-II trial is improvement in any meaningful patient-centered outcome (e.g. survival, renal function, ICU length of stay). (
  • 22-24 However, recent studies suggest that the AT 1B R predominantly mediates Ang II-induced contraction in mouse abdominal aorta, femoral artery, and mesenteric resistance vessels. (
  • Analysis of these data suggests that Ang II mediates the loading signal in stretched HPLFs to induce expressions of TGF-β1 and ALP. (
  • The SFO mediates the dysfunction via two signaling pathways. (
  • 3 A large body of data has suggested that the renin-angiotensin system mediates part of its physiological and pathophysiological actions via generation of reactive oxygen species (ROS) and stimulation of inflammation. (
  • Barry Brenner, Boston, MA, discussed the Reduction of Endpoints in NIDDM with the Angiotensin II Antagonist Losartan (RENAAL) trial of 1,513 patients with type 2 diabetes and nephropathy from 250 centers in 29 countries. (
  • The angiotensin-II receptor antagonists that have been labeled for use in hypertension by the U.S. Food and Drug Administration (FDA) are losartan (Cozaar), valsartan (Diovan), irbesartan (Avapro), candesartan (Atacand) and telmisartan (Micardis). (
  • To evaluate the role for AT1-R and AT2-R in Ang-II sensitivity, full concentration response curves were obtained for Ang-II in the presence of losartan or PD123319. (
  • 2. The pharmacokinetic profiles of losartan and EXP3174 of orally administ. (
  • Included are ANGIOTENSIN II analogs such as SARALASIN and biphenylimidazoles such as LOSARTAN. (
  • To determine the effect of chronic pretreatment with apelin, losartan and their combination on ischemia-reperfusion (IR) injury in the isolated perfused rat heart and on the expression of apelin-13 receptor (APJ) and angiotensin type 1 receptor (AT1R) in the myocardium. (
  • Gonzalez EA, Leitão SAT, Dos Santos Soares D, Tavares AMV, Giugliani R, Baldo G, & Matte U. Cardiac pathology in Mucopolysaccharidosis I mice: Losartan modifies ERK1/2 activation during cardiac remodeling. (
  • Displacement of Ang II binding using the selective ligands losartan and CGP 42112 led to a severalfold increase of PN-1 protein and mRNA over basal levels, indicating that the observed effect was mediated by specific binding sites. (
  • Saino et al 1 and Lyons et al 2 published provocative findings regarding the vascular level interaction of the sympathetic and renin-angiotensin systems. (
  • It would be important, however, to device a way to see whether this is the case also in vivo and what is the relative importance of this mechanism in the overall positive feed-back interaction between the sympathetic and the renin-angiotensin systems. (
  • Recently, the focus of interest on the role of the renin angiotensin system in the pathophysiology of hypertension has shifted towards greater emphasis on new developments in local renin angiotensin systems in specific tissues. (
  • Objective: To investigate the hypothesis that high fructose intake induces activation of the renin-angiotensin systems (RAS), resulting in hypertension and metabolic syndrome. (
  • The angiotensin II type 2 receptor (AT2R) shares a high degree of homology with its well-known sister gene, the angiotensin II type 1 receptor (AT1R), and is similarly a part of the renin-angiotensin II system (RAS). (
  • Hyperactivity of the ACE/Ang-II/AT1 receptor (AT1R) axis of the RAS leads to a cascade of events implicated in the development of β-cell dysfunction, including the following: increased islet fibrosis ( 6 ), oxidative stress ( 7 , 8 ), and inhibition of proinsulin biosynthesis and first-phase and glucose-responsive insulin secretion ( 3 , 5 , 9 ). (
  • To investigate this, we examined the effects of LVV-hemorphin-7 on AT1R transiently expressed in human embryonic kidney (HEK293) cells using bioluminescence resonance energy transfer (BRET) technology for the assessment of AT1R/Gαq coupling and β-arrestin 2 recruitment. (
  • Angiotensin II (Ang II) is well-considered to be the principal effector of the renin-angiotensin system (RAS), which binds with strong affinity to the angiotensin II type 1 (AT1R) and type 2 (AT2R) receptor subtype. (
  • The haemodynamic and non-haemodynamic effects of Ang II, including its ability to regulate blood pressure, maintain water-electrolyte balance and promote vasoconstriction and cellular growth are well-documented to be mediated primarily by the AT1R. (
  • The AT 2 receptor remains enigmatic and controversial - is probably involved in vascular growth. (
  • Following vascular occlusion, development of collateral circulation occurs in at least two time-related phases: (1) the fast enhancement of the function of preexisting channels and (2) the slow formation of new vessels. (
  • It is concluded that angiotensin II not only facilitates the activation of preexisting collateral vascular pathways but also has angiogenic properties and therefore could play an active role not only in the fast but also in the slow phase of the development of collateral circulation. (
  • Saralasin, a partial agonist angiotensin II receptor, does not appear to affect mean arterial pressure (MAP) and systemic vascular resistance (SVR) during exercise. (
  • 1. Angiotensin (Ang) II causes growth-related effects on vascular smooth muscle cells in vitro and in vivo. (
  • The studies by Lassègue et al 1 and Wang et al 2 in this issue of Circulation Research go a long way in elucidating the molecular basis for the effects of Ang II on vascular smooth muscle cell growth. (
  • Using knockout mice, Wang et al 2 prove that it is gp91 phox , present primarily in endothelial cells and adventitial fibroblasts but also expressed to a much lesser degree in smooth muscle cells, that is chiefly responsible for Ang II-stimulated vascular oxidative stress and smooth muscle growth in vivo. (
  • Olmesartan blocks the vasoconstrictor effects of angiotensin II by selectively blocking binding of angiotensin II to the AT-1 receptor in vascular smooth muscle. (
  • 1,2 ⇓ At the same time, emerging data have implicated inflammation as a process involved in the initiation and progression of atherosclerosis, but it is also present in hypertension, diabetes mellitus, and other conditions associated with vascular damage. (
  • 3,4 ⇓ In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology , Liu et al 5 show that angiotensin II (Ang II)-enhanced NADPH oxidase activity contributes to adhesion molecule (ICAM) expression, leukocyte infiltration, and vascular growth in rats, independently of its effects on blood pressure. (
  • Enhanced expression levels of vascular cell adhesion molecule (VCAM)-1, tissue factor, transforming growth factor (TGF)-β and MMP-2 and 9 characterized the senescence-associated secretory phenotype of atrial ECs. (
  • Angiotensin II promotes vascular inflammation, which plays important roles in vascular injury. (
  • Angiorensin ii is a potent vasoconstrictor and proinflammatory chemical that has effects on vascular endothelium that contribute to atherosclerosis and hypertension. (
  • The most important is known as angiotensin II, a powerful vasoconstrictor that stimulates steroid production by the adrenal glands, reduces fluid loss from the kidneys, and also functions as a neurotransmitter. (
  • Cell culture studies have shown that Ang II stimulates osteopontin mRNA expression in cardiac cells, including fibroblasts 9,18 and microvascular endothelial cells. (
  • Ang II also stimulates bone resorption. (
  • This supports a previous report that Ang II stimulates ROS production in adventitial fibroblasts by inducing other components of the NADPH oxidase. (
  • Attenuation of cuff-induced neointimal formation by overexpression of angiotensin II type 2 receptor-interacting protein 1. (
  • Aoyagi Y, Furuyama T, Inoue K, Matsuda D, Matsubara Y, Okahara A, Ago T, Nakashima Y, Mori M, & Matsumoto T. Attenuation of Angiotensin II-Induced Hypertension in BubR1 Low‐Expression Mice Via Repression of Angiotensin II Receptor 1 Overexpression. (
  • Ste20-related kinase SLK phosphorylates ser188 of rhoA to induce vasodilation in response to angiotensin II type 2 receptor activation. (
  • IP-10 levels in conditioned media detected by ELISA increased in response to angiotensin II compared to control, which was blocked by the pretreatment with valsartan. (
  • Angiotensin II (Ang II) is a potent smooth muscle mitogen and hypertrophic agent. (
  • When you have documented [that] the patient has microalbuminuria, you start lifelong treatment with agents interfering with the renin-angiotensin system. (
  • At a symposium at the 61st Scientific Sessions of the ADA in June 2001, the results of three recent diabetic nephropathy trials with angiotensin II subtype 1 receptor antagonists were presented. (
  • Before describing the phenotypic response to the modulation of the AT 2 receptor system in the myocardium, we will briefly review AT 1 and AT 2 receptor subtype signaling. (
  • Therefore, the effects of the D2 receptor agonist bromocriptine and the D2 receptor antagonist haloperidol on angiotensin (Ang) II- or endothelin (ET)-1-induced hypertrophy of cultured neonatal rat ventricular myocytes were investigated in the present study. (
  • Angiotensin II and ET-1, both at 10 nmol/L, induced myocyte hypertrophy, as demonstrated by increased protein content and synthesis, [Ca 2+ ] i levels, protein kinase C (PKC) activity and phosphorylation of extracellular signal-regulated kinase, c-Jun N-terminal kinase and mitogen-activated protein kinase (MAPK) p38 (p38). (
  • The effect of taurine on angiotensin II-induced hypertrophy of cultured neonatal rat heart cells (myocytes and nonmyocytes) was examined. (
  • Exposure of the cells to taurine (20 mM) in the absence of angiotensin II had no effect on either hyperplastic growth or hypertrophy of the two types of cultured cardiac cells. (
  • Angiotensin II (Ang II) plays an important role in cardiomyocyte hypertrophy. (
  • The present study was designed to determine the effect of HGF on cardiomyocyte hypertrophy and to explore the combined effect of HGF and Ang II on cardiomyocyte hypertrophy. (
  • Ang II (1 µM) increased cardiomyocyte hypertrophy. (
  • Similar to Ang II, treatment with 1 µM HGF promoted cardiomyocyte hypertrophy. (
  • Moreover, the combination of 1 µM Ang II and 10 ng/mL HGF clearly induced a combined pro-hypertrophy effect on cardiomyocytes. (
  • The present study demonstrates for the first time a novel, combined effect of HGF and Ang II in promoting cardiomyocyte hypertrophy. (
  • In fact, in addition to Ang II, large numbers of intracellular or extracellular factors affect cardiomyocyte hypertrophy in vivo (14). (
  • The most straightforward one is that nox1 is not expressed in smooth muscle cells in vivo or that expressed nox1 plays a small role, if any, in smooth muscle hypertrophy and hyperplasia in response to Ang II in vivo. (
  • An emerging hypothesis suggests that the activity of the angiotensin II type 2 receptor (AT 2 ) may counterregulate AT 1 receptor effects during cardiac development and during the evolution of cardiac hypertrophy and heart failure. (
  • 21 These conclusions were based on the observation that AT 1A R knockout (AT 1 R −/− ) mice were found to exhibit low blood pressure and attenuated Ang II pressor response. (
  • 13 Fourth, Matsui et al 14 report in this issue of Hypertension that mice lacking osteopontin do not develop myocardial fibrosis in response to Ang II-induced hypertension. (
  • Ohinata K, Fujiwara Y, Fukumoto S, Iwai M, Horiuchi M, Yoshikawa M. Angiotensin II and III suppress food intake via angiotensin AT(2) receptor and prostaglandin EP(4) receptor in mice. (
  • 1995). "Effects on blood pressure and exploratory behaviour of mice lacking angiotensin II type-2 receptor. (
  • Defects in insulin sensitivity, glucose tolerance, and glucose uptake exhibited by Mas receptor knockout mice ( 20 ) further implicate the loss of Ang-(1-7) signaling in the development of type 2 diabetes and metabolic syndrome. (
  • In contrast to the counterregulatory hypothesis, studies in mice with an overabundance of, or a deficiency in, the AT 2 receptor do not suggest that AT 2 signaling is essential for cardiac development. (
  • These results suggest that angiotensin II type 2 receptor as well as type 1 receptor may be involved in the development of diabetic nephropathy in the STZ-induced diabetic mice, and these mice are beneficial models of early diabetic nephropathy. (
  • IP-10 expression was higher in the endothelium of coronary blood vessels in mice infused with angiotensin II than in control. (
  • Diabetic nephropathy is a frequent microvascular complication that occurs in approximately 40% of patients with either type 1 or type 2 diabetes. (
  • Recently proposed mechanisms for the development of diabetic nephropathy include glomerular hyperfiltration ( 1 ), disorientation of intracellular signal transduction ( 2 ), and involvement of advanced glycation end products ( 3 ). (
  • Activation of the renin-angiotensin system (RAS) by high glucose, mechanical stress, and proteinuria has been implicated in the major changes associated with diabetic nephropathy ( 4 ). (
  • We investigated whether angiotensin II was involved with diabetic nephropathy in the mouse model. (
  • They are important in the renin-angiotensin system: they are responsible for the signal transduction of the vasoconstricting stimulus of the main effector hormone, angiotensin II. (
  • Quantitative real-time PCR analysis revealed that angiotensin II significantly increased IP-10 mRNA expression compared to control. (
  • Since the first angiotensin-II receptor antagonists were introduced a few years ago, numerous clinical trials have been conducted on their use in patients with hypertension and their potential use in patients with congestive heart failure. (
  • Finally, taurine partially prevented the rise in [Ca 2+ ] i mediated by angiotensin II in cardiac cells. (
  • On the one hand, a number of findings indicate that the interaction of Ang II with the Ang II type-1 (AT 1 ) receptor located in cardiac fibroblasts results in induction of fibroblast hyperplasia, activation of collagen biosynthetic pathways, and inhibition of collagen degradative pathways. (
  • 8 In addition, several lines of evidence point to osteopontin as a critical mediator of the proinflammatory and profibrotic cardiac effects of Ang II. (
  • First, monoclonal antibodies directed against osteopontin have been found completely to block the stimulatory effects of Ang II on cultured rat cardiac fibroblasts. (
  • Angiotensin II (Ang II), the central product of the renin-angiotensin system, is believed to be one of the most important regulators of the initiation of a positive feedback regulation of the cardiac hypertrophic response (4). (
  • The role of AT 2 receptor signaling in cardiac fibrosis is, however, still debatable because of conflicting data in the same two studies. (
  • Above all, Human adult cardiac myocytes (HACMs) were exposed to 200 nmol/L Ang II for 4 days. (
  • Like its family members, the AT2R traverses the cell membrane seven times creating an NH 2 -terminal and three loops on the extracellular side and a COOH-terminal plus three loops on the intracellular side. (
  • Such renin release allows for the production of the alpha-2-globulin angiotensinogen predominantly in the liver and to some extent, the kidneys and other organs. (
  • Angiotensin I, itself a decapeptide with weak biological activity, is produced from angiotensinogen and then quickly converted to angiotensin II by angiotensin converting enzymes (ACE). (
  • Immunolocalization of angiotensin I/II (Ang I/II), which was converted from angiotensinogen, was detected in rat PDL tissues. (
  • This brief review is focused on recent evidence that inappropriate activation of renin in distal nephron segments, by acting on angiotensinogen generated in the proximal tubule cells and delivered to the distal nephron may contribute to increased distal intrarenal angiotensin II formation, sodium retention and development and progression of hypertension. (
  • Moreover, the detection of angiotensinogen- and renin-mRNA in these cultures suggested an endogenous production of Ang II. (
  • The Food and Drug Administration approved the use of angiotensin II in December 2017 to treat low blood pressure resulting from septic shock. (
  • As of December 21, 2017 the FDA approved La Jolla Pharmaceutical's Giapreza (angiotensin II) Injection for Intravenouse Infusion for the indication of acting as a vasoconstrictor to increase blood pressure in adults with septic or other distributive shock. (
  • 2017 Feb. 28 (2):691-701. (
  • In December 2017, GIAPREZA™ (angiotensin II) was approved by the U.S. Food and Drug Administration (FDA) to increase blood pressure in adults with septic or other distributive shock. (
  • Inasmuch as the renin-angiotensin system can act as a protective mechanism against local ischemia by activating preexisting collateral vessels, it is of interest to establish whether angiotensin II also produces stimulation of new vessel formation. (
  • 1,2,4,6,7 In addition, AT 1 Rs mediate many of their pathophysiological effects by stimulating reactive oxygen species generation via an reduced nicotinamide-adenine dinucleotide/reduced nicotinamide-adenine dinucleotide phosphate oxidase-dependent mechanism. (
  • Angiotensin II increases glucose utilization during acute hyperinsulinemia via a hemodynamic mechanism. (
  • To evaluate a possible hemodynamic mechanism for the effects of AII on glucose utilization, we measured blood flow to two areas that differ in their sensitivity to insulin: the kidneys and the leg. (
  • 3. A possible additional control mechanism of angiotensin II degradation is suggested. (
  • 24: 641-646) reported that long-term treatment of hypertensive patients with olmesartan resulted in a reduction in plasma Ang II level, though the mechanism was not determined. (
  • The mechanism by which angiotensin II (AII) exerts its pressor effect was examined in a saltwater teleost and elasmobranch. (
  • In addition to the possibilities they presented we would like to suggest that there is the potential that the enhanced vasoconstriction is being mediated by angiotensin per se, which in the presence of catecholamines is being transformed from a subpressor to pressor effect. (
  • However, the dose of perindoprilat used in our study was not, as suggested by Drs Kessler and Kessler, converted from a subpressor to pressor dose by noradrenergic preconstriction as perindoprilat (5 nmol/mL) virtually abolishes the vasoconstricting action of angiotensin I (200 pmol/min) when coinfused at the brachial artery (unpublished data), though it has no effect on basal forearm blood flow. (
  • Slow pressor' hypertension from low-dose chronic angiotensin II infusion. (
  • An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II. (
  • In this study, we found that angiotensin II-stimulated human endothelial cells increased the release of a CXC chemokine, IP-10, according to an antibody array. (
  • For instance, the ability of Ang II to stimulate fibroblasts and alter the metabolism of fibrillar collagen may be mediated by transforming growth factor-β 1 , endothelin-1, and plasminogen activator inhibitor-1. (
  • At this time, the place for the newest class of antihypertensive drugs, the angiotensin II receptor antagonists, remains uncertain. (
  • The AT1 receptor is the best elucidated angiotensin receptor. (
  • Ang I-mediated effects are much more effectively inhibited by Ang II antagonism than by ACE inhibition. (
  • Transforming growth factor-β1 (TGF-β1) induces cerebrovascular dysfunction and astrogliosis through angiotensin II type 1 receptor-mediated signaling pathways. (
  • Uniquely, the rodent genome harbors 2 distinct AT 1 R genes: AT 1A R and AT 1B R. 9-15 The AT 1A R gene has been localized to chromosomes 17 and 13 of the rat and mouse, respectively, whereas the AT 1B R gene has been localized to chromosomes 2 and 3 of the rat and mouse, respectively. (
  • 29 The rAT 1B R gene is also composed of 3 exons, with exons 1 and 2 encoding the 5′-UTR and the third exon harboring the ORF. (
  • HPLFs that were stimulated by Ang II also increased their gene expressions of TGF-β1 and ALP. (
  • Furthermore, the antagonist for Ang II type 2 receptor, rather than for type 1, significantly inhibited gene expressions induced by the stretch loading. (
  • Angiotensin II receptor type 2 , also known as the AT 2 receptor or AGTR2 , is a human gene . (
  • 1995). "Molecular characterization and chromosome localization of a human angiotensin II AT2 receptor gene highly expressed in fetal tissues. (
  • Assignment of the human angiotensin II type 2 receptor gene (AGTR2) to chromosome Xq22-q23 by fluorescence in situ hybridization. (
  • 1994). "Human type 2 angiotensin II receptor gene: cloned, mapped to the X chromosome, and its mRNA is expressed in the human lung. (
  • 1994). "Molecular cloning and expression of the gene encoding human angiotensin II type 2 receptor. (
  • The AT4 receptor is activated by the angiotensin II metabolite angiotensin IV, and may play a role in regulation of the CNS extracellular matrix, as well as modulation of oxytocin release. (
  • The renin-angiotensin system (RAS) is a peptidergic system with endocrine characteristics regarding to the regulation of the blood pressure and hydro-electrolytic balance. (
  • These cells might serve as an in vivo model of angiotensin II receptor regulation in clinical studies. (
  • Conclusions: Thrombin promotes premature ageing and senescence of atrial ECs and may pave the way to deleterious remodeling of atrial tissue by a local up-regulation of the angiotensin system and by promoting pro-inflammatory, pro-thrombotic, pro-fibrotic and pro-remodeling responses. (
  • The angiotensin II -induced rats showed increases in the media/lumen ratios which were attenuated by 43.6% and 47.2% in the small arteries of heart and kidneys, respectively. (
  • It is believed that treatment with an ARB increases the level of plasma angiotensin II (Ang II) because of a lack of negative feedback on renin activity. (
  • Angiotensin II increases expression of IP-10 and the renin-angiotensin system in endothelial cells. (
  • Angiotensin II increases thrombin formation and impairs thrombolysis ( Celi 2010 , Dielis 2007 ). (
  • Indeed, the presence of AT1 and AT2 angiotensin receptor subtypes was demonstrated in cultured Schwann cells as well as in the rat sciatic nerve. (
  • 1992). "Molecular cloning, sequence analysis and expression of a cDNA encoding human type-1 angiotensin II receptor. (
  • Kessler K, Harakal C. Potentiation of the vasoconstrictor effect of angiotensin by catecholamines in vitro. (
  • Drs Kessler and Kessler suggest that the vasoconstricting effect of angiotensin II may be enhanced by sympathetically mediated vasoconstriction. (
  • These analyses of the effect of angiotensin II on AKI patients requiring dialysis in the ATHOS-3 study demonstrated angiotensin II is a promising therapy to address this unmet need. (
  • Objective: We investigated endothelial dysfunction and the role of angiotensin (Ang)-II type I (AT1-R) and type II (AT2-R) receptor in the changes in the Ang-II sensitivity in experimental preeclampsia in the rat. (
  • Indeed, it has been demonstrated that, upon acting on the AT1 receptor, angiotensin II activates matrix metalloproteases that release the epidermal growth factor (EGF), binding to its receptor promotes the activation of mammalian target of rapamycin (mTOR) and ribosomal S6 kinase-1, both of which inhibit phosphatidylinositol 3-kinase insulin signaling, thus favoring insulin resistance ( 2 - 4 ). (
  • This brings us to the present study by Lassègue et al, 1 demonstrating for the first time the importance of the newly discovered nox1 in Ang II-stimulated and platelet-derived growth factor-stimulated short-term ROS generation and activation of the growth-promoting signaling proteins Akt and p38 mitogen-activated protein kinase in cultured rat smooth muscle cells. (
  • Kim M, Do GY, Kim I. Activation of the renin-angiotensin system in high fructose-induced metabolic syndrome. (
  • 9 Activation requires the participation of two low-molecular weight guanine nucleotide-binding proteins, Rac 2 (or Rac 1) and Rap1A. (
  • Recent reviews suggest that activity of the angiotensin II type 2 receptor (AT 2 ) may counterbalance the putative detrimental effects of angiotensin II type 1 receptor (AT 1 ) activation in heart failure via mediating opposite cellular functions. (
  • These data indicate that IP-10 is involved not only in leukocyte-endothelial interaction but also in the circuit of endothelial renin-angiotensin system activation that potentially promotes atherosclerosis. (
  • It is formed through a chemical conversion of angiotensin i to angiotensin ii mediated by sympathetic activation of ace. (
  • Despite the widespread use of these agents in clinical practice, our understanding of the mechanisms through which Ang II exerts its effects on the vasculature is not complete. (
  • Design and Synthesis of Angiotensin IV Peptidomimetics Targeting the Insulin-Regulated Aminopeptidase (IRAP) (Ph.D. thesis). (
  • Angiotensin II (1-100 nM) alone caused an increase in the rate of protein synthesis and the surface area of myocytes without altering the rate of DNA synthesis or cell number. (
  • Following a 24 hr pretreatment with 20 mM taurine, the stimulation in protein synthesis by angiotensin II (1 nM) was significantly suppressed. (
  • Similarly, taurine treatment of nonmyocytes reduced the degree of angiotensin II-induced promotion of hyperplastic growth (DNA synthesis and cell number). (
  • Renin leads to angiotensin i and ii synthesis. (
  • Human heart chymase, a chymotrypsin-like serine proteinase, hydrolyzes the Phe8-His9 bond to yield the octapeptide hormone angiotensin II and His-Leu. (
  • The novelty of the medication lies in the fact that it is the first and only use of synthetic human angiotensin II to help maintain body blood pressure. (
  • The immunomodulator FTY720 interferes with effector functions of human monocyte-derived dendritic cells," European Journal of Immunology , vol. 35, no. 2, pp. 533-545, 2005. (
  • Hoshi M. (1988) Increase of blood flow in human tumors under angiotensin II induced hypertension. (
  • Hoshi M, Abe I, Sugiyama K, Ishizuka K, Sato H, Urushiyama M. and Wakui A. (1991) Selective enhancement of the image intensity of contrast media on dynamic CT under angiotensin II human(TY-10721) induced hypertension state. (
  • 18,19 In addition, Ang II has been shown to increase osteopontin mRNA expression in fresh samples of human myocardium. (
  • The sequence and genomic organization of the human type 2 angiotensin II receptor. (
  • Molecular cloning of the human angiotensin II type 2 receptor cDNA. (
  • ACE-2 Human Recombinant Protein is shipped on ice packs. (
  • The binding of 125 I-angiotensin II to human blood cells was investigated. (
  • Thus our study shows specific binding of 125 l-angiotensin II to human platelets. (
  • In the present study, we aimed to investigate the role of Rcan1-1L in angiotensin II (Ang II)-exposed human cardiomyocytes. (
  • The media/lumen ratio of the small arteries in the heart and kidneys were increased by 117% and 168% by angiotensin II infusion. (
  • These findings demonstrated that lentil extract attenuated angiotensin II -induced hypertension and associated pathological changes, including remodelling and perivascular fibrosis in the small resistant arteries of heart and kidneys. (
  • and renin, angiotensin II type 1a receptor (AT1aR), and angiotensin II type 1b receptor (AT1bR) in the kidneys. (
  • 7 The multiple actions of Ang II, mediated through the AT 1 R, are a result of complex intracellular signaling pathways including stimulation of the phospholipase C/inositol 1,4,5-trisphosphate/diacylglycerol cascade, mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinases, tyrosine kinases, and RhoA/Rho kinase. (
  • Angiotensin II type 2 receptor stimulation: a novel option of therapeutic interference with the renin-angiotensin system in myocardial infarction? (
  • Ang-(1-7) properties are mediated by the G-protein-coupled receptor Mas ( 14 ), causing vasodilation, inhibition of fibrosis ( 15 ), stimulation of prostaglandin E (PGE)2 ( 16 ), and nitric oxide releases ( 17 ). (
  • In this review, we conclude that the collective evidence does not strongly support a net beneficial effect of AT 2 stimulation in the diseased myocardium. (
  • Thus, to confer counterregulatory effects, AT 2 receptor stimulation should oppose one or more of the phenotypic effects of AT 1 receptor stimulation. (
  • The vasopressor effects of angiotensin have been studied since it was first isolated in the late 1930s. (
  • Instead, they block the effects of angiotensin, preventing the hormone from narrowing the blood vessels. (
  • The possibility that the beneficial effects of taurine in the treatment of heart failure might be related to its suppression of angiotensin II-mediated cellular responses is discussed. (
  • Two randomized controlled trials, using a combination regimen of ADM,5-FU and MMC for advanced gastric carcinoma, showed significant augmentation of anti-tumor effects without increase of side effects. (
  • 4 Several potential pathways may mediate the profibrotic effects of Ang II on the heart. (
  • 5 - 9 The antihypertensive effects of these drugs should become apparent within two to four weeks after the initiation of therapy. (
  • We demonstrate anti-hypertensive and kidney protective effects of this EET analog in ANG II induced hypertension. (
  • The objective of the study was to investigate whether chronic administration of the Morton lentil polyphenol extract (MLPE), which possesses rich phenolic compounds and a high antioxidant activity, had any protective effects on angiotensin II -induced hypertension. (
  • Recent accumulating evidence has suggested that the AT 2 receptor not only opposes the AT 1 receptor but also has unique effects beyond an interaction with AT 1 receptor signaling. (
  • The participation of the Angiotensin-(1-7) receptor Mas and nitric oxide (NO) in the effects of DIZE was evaluated using A-779 and L-NAME, respectively. (
  • The incomplete effects of captopril on the inhibition of Ang II formation might be caused by alternative Ang II forming enzyme(s), as was demonstrated by the additive effects of soybean trypsin inhibitor added to captopril. (
  • Angiotensin II is a naturally occurring hormone secreted as part of the renin-angiotensin system that results in powerful systemic vasoconstriction. (
  • Angiotensin II is a polypeptide hormone that functions in the body to control arterial blood pressure. (