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 ...
  • ACE2, a close homologue of ACE, functions as a negative regulator of the angiotensin system and was identified as a key receptor for SARS (severe acute respiratory syndrome) coronavirus infections. (
  • The mechanism of entry of SARS-COV-2 into the human host cell is through the ACE2 receptor. (
  • In coronavirus infection disease (Covid-19), SARS-CoV-2 binds ACE2 which is highly expressed by the epithelial cells of blood vessel, intestine and lung. (
  • The expression of ACE2 is augmented by angiotensin converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), ibuprofen, statins, thiazolidinedione and by cigarette smoking. (
  • Polymorphism of ACE2 has been associated with different cardio-metabolic disorders, thus implication of ACE2 and angiotensin receptor type 2 (ATR2) receptors in Covid-19-induced pneumonia should be considerably regarded with ACE2 polymorphisms. (
  • Covid-19 leads to significant lung injury through down-regulation of ACE2, which is attenuated by administration of angiotensin-receptor blockers (ARBs). (
  • Therefore, ACE2 receptors are protective against SARS-CoV-2 pathogenesis. (
  • Therefore, ACE2 is regarded as an important entry-point for SARS-CoV-2 and up-regulation of ACE2 by ACEIs, ARBs and during development of cytokine storm is regarded as a protective compensatory mechanism to overcome hyperinflammatory-induced ALI and ARDS. (
  • Pathological activation of ADAM17 (A disintegrin and metalloproteinase -17) may potentiate inflammation and diminish ACE2-mediated tissue protection through proteolytic shedding, contributing to SARS-CoV-2 pathogenesis . (
  • We aim to examine plasma soluble ACE2 and angiotensin profiles in relation to outcomes by enrolling consecutive patients admitted for COVID-19 with baseline blood collection at admission and repeated sampling at 7 days. (
  • Moreover, patients having an upward trajectory of soluble ACE2 were characterized by an imbalance in the Ang 1-7/Ang II ratio. (
  • The observed dysregulation of ACE2 and angiotensin peptides with disease progression suggest a potential role of ADAM17 inhibition and enhancing the beneficial Ang 1-7/Mas axis to improve outcomes against SARS-CoV-2 infection. (
  • Aligned ACE2 protein sequences from human, rhesus macaque, African green monkey, cat, dog, American mink, mouse, and chicken cells in study of susceptibility to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) of cell lines and substrates used to diagnose and isolate influenza and other viruses. (
  • The now familiar spiked virus enters human cells via the also pervasive angiotensin-converting enzyme 2, or ACE2, receptor. (
  • The virus' binding to the receptor for ACE2 has been shown to decrease ACE2 levels and increase levels of the powerful blood vessel constrictor angiotensin II, because less angiotensin II gets degraded and fewer vasodilators get produced, which worsens the patient's prognosis. (
  • Histopathology and localization of SARS-CoV-2 and its host cell entry receptor ACE2 in tissues from naturally infected US- farm ed mink (Neovison vison). (
  • We characterized the pathological findings in 72 mink from US farm s with SARS-CoV-2 outbreaks, localized SARS-CoV-2 and its host cellular receptor angiotensin-converting enzyme 2 (ACE2) in mink respiratory tissues, and evaluated the utility of various test methods and specimens for SARS-CoV-2 detection in necropsy tissues. (
  • The SARS-CoV-2 receptor ACE2 was extensively detected by IHC within turbinate epithelium, with decreased detection in lower respiratory tract epithelium and alveolar macrophages. (
  • They identified a new association with a rare genetic variant at the Xp22.2 locus (rs190509934) that downregulates the expression of angiotensin-converting enzyme 2 (ACE2). (
  • If the vaccinated subject is subsequently exposed to the SARS-CoV-2 coronavirus, its T-cell protection and neutralising antibodies are expected to inhibit the viral spike protein from binding to the usual human cell surface of the ACE2 (angiotensin converting enzyme 2), thus possibly attenuating or stopping the SARS-CoV-2 infection that triggers COVID-19. (
  • The virus uses a special protein (angiotensin-converting enzyme 2, or ACE2) to sneak into cells and reproduce. (
  • Interestingly, Study 2 found in one of their datasets that the Caucasian samples actually had higher ACE2 expression compared to the Asian samples, but this trend disappeared after other independent variables were accounted for. (
  • Interestingly, while two of the studies found no relationship and Study 2 found a positive correlation between smoking and ACE2 expression, there are rat-model studies published in 2015 (5) and 2017 (6) that actually found the opposite. (
  • In the case of SARS-CoV-2, angiotensin-converting enzyme 2 (ACE2) has been identified as a necessary receptor, but not all ACE2-expressing cells are equally infected, suggesting that other extracellular factors are involved in host cell invasion by SARS-CoV-2. (
  • Here, we present evidence that extracellular vimentin might act as a critical component of the SARS-CoV-2 spike protein-ACE2 complex in mediating SARS-CoV-2 cell entry. (
  • We demonstrate direct binding between vimentin and SARS-CoV-2 pseudovirus coated with the SARS-CoV-2 spike protein and show that antibodies against vimentin block in vitro SARS-CoV-2 pseudovirus infection of ACE2-expressing cells. (
  • Angiotensin II Receptor Blockers (ARBs) are drugs that are used to treat high blood pressure and heart failure. (
  • BACKGROUND: Randomised controlled trials have shown a reduced risk of heart failure (HF) hospitalisation among users of ACE inhibitors (ACEIs) or angiotensin II type 1 receptor antagonists (angiotensin receptor blockers [ARBs]), but these results have limited generalisability. (
  • During the pandemic, a hypothesis has been proposed that angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs) could be risk factors for the development of severe SARS-COV-2 infection. (
  • OBJECTIVE: To evaluate the effects of treatments based on angiotensin II receptor blockers (ARBs) on the risk of myocardial infarction (MI), cardiovascular and all-cause death, as compared with conventional treatment or placebo. (
  • Angiotensin II receptor blockers ( ARBs ), also known as angiotensin receptor blockers , are a class of medication primarily used to treat high blood pressure , heart failure , coronary heart disease , and kidney disease . (
  • Those people taking angiotensin receptor blockers (ARBs) were 35-40% less likely to develop AD than those using other antihypertensives. (
  • Indeed, as a consequence of AT 1 blockade, ARBs increase angiotensin II levels several-fold above baseline by uncoupling a negative-feedback loop. (
  • The general approach to therapy of ischemic nephropathy involves control of hypertension, preferably with angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs). (
  • It has been suggested that angiotensin converting enzyme inhibitors (ACE-1 inhibitors), such as enalapril and ramipril, and angiotensin receptor antagonists (colloquially called angiotensin receptor blockers or ARBs), such as candesartan and valsartan, may be of value in preventing and treating the effects of the coronavirus SARS-CoV-2 (also known as 2019-nCoV), the cause of the infection called COVID-19. (
  • The two others are not recruiting: "Recombinant human angiotensin-converting enzyme 2 (rhACE2) as a treatment for patients with COVID-19" (registered on 21 February but listed on as withdrawn) and "Clinical study for the effects of ACEIs/ARBs on the infection of novel coronavirus pneumonia (CoVID-19)" (registered on 2 March). (
  • Also known as ARBs, these are heart medications that block the angiotensin II hormone and widen or dilate blood vessels to improve blood flow. (
  • 3 These disparities exist despite similar proportions of blacks, whites, and Hispanics meeting recommendations for glycolated hemoglobin and blood pressure control and similar proportions with rennin-angiotensin system blockade via use of angiotensin-converting enzyme (ACE) inhibitors or angiotensin II type 1 receptor blockers (ARBs). (
  • Rather than lowering levels of angiotensin II (as ACE inhibitors do), angiotensin II receptor blockers prevent this chemical from having any effects on the heart and blood vessels. (
  • ACE Inhibitors/Angiotensin II type 1 receptor antagonists do not reduce hospitalisations in older patients with heart failure. (
  • Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers can reduce proteinuria. (
  • This shift of pressure natriuresis provides the basis for the chronic blood pressure-lowering effects in hypertensive patients of the angiotensin-converting enzyme inhibitors and angiotensin II receptor antagonists. (
  • May induce a more complete inhibition of the renin-angiotensin system than ACE inhibitors, does not affect the response to bradykinin, and is less likely to be associated with cough and angioedema. (
  • Overexpression of the alpha-2,6-sialyltransferase in MDCK cells increases influenza virus sensitivity to neuraminidase inhibitors. (
  • ACE-1 inhibitors inhibit the conversion of angiotensin I to angiotensin II and of angiotensin(1-9) to angiotensin(1-7). (
  • Inhibitors of ACE-2 have been developed, but none has been marketed. (
  • Some ACE inhibitors have been found to slow the process that leads to kidney damage in many people with type 2 diabetes. (
  • For hypertension not controlled by diuretics, calcium channel blockers or angiotensin-converting enzyme inhibitors are generally useful. (
  • To block VASOCONSTRICTION and HYPERTENSION effect of angiotensin II, patients are often treated with ACE INHIBITORS or with ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS. (
  • Two of the drugs being trialed, lopinavir and ritonavir, being trialed are protease inhibitors. (
  • Reeder, Guy S. Angiotensin converting enzyme inhibitors and receptor blockers in acute myocardial infarction: Clinical trials. (
  • Acesso em: 8 dez 2014. (
  • Strippoli Giovanni FM, Bonifati Carmen, Craig Maria E, Navaneethan Sankar D, Craig Jonathan C. Angiotensin converting enzyme inhibitors and angiotensin II receptor antagonists for preventing the progression of diabetic kidney disease. (
  • Some blood pressure medications are considered safe to use during pregnancy , but angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers and renin inhibitors are generally avoided during pregnancy . (
  • 2. Patients treated with angiotensin converting enzyme inhibitors (ACE-I) or angiotensin receptor blockers (ARB) on the day of surgery. (
  • Angiotensin-converting enzyme (ACE) plays a central role in generating angiotensin II from angiotensin I, and capillary blood vessels in the lung are one of the major sites of ACE expression and angiotensin II production in the human body. (
  • These study results suggest that both systemic angiotensin II and myeloid leukocyte-bound angiotensin converting enzyme (ACE)-1 promote protection against pathogens via distinct mechanisms. (
  • For instance, the local availability and functional consequence of angiotensin II (Ang II), the bioactive substance of the system, may depend on the Angiotensin converting enzyme (ACE) concentration or on the Ang II receptor density [ 4 ]. (
  • 72 Chinese primary IgAN patients who had undergone renal biopsy in Zhongshan Hospital between January 2009 and June 2009, had not received glucocorticoid, immunosuppressants, angiotensin converting enzyme inhibitor or angiotensin IIreceptor blocker, and gave informed consent were included in the study. (
  • We conclude that acute hypoxia is associated with a reversible decrease in pulmonary angiotensin converting enzyme availability. (
  • 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). (
  • Dysregulation of ACE (Angiotensin-Converting Enzyme)-2 and Renin-Angiotensin Peptides in SARS-CoV-2 Mediated Mortality and End-Organ Injuries. (
  • ACE ( angiotensin -converting enzyme )-2 as the target for SARS-CoV-2 also negatively regulates the renin-angiotensin system . (
  • SARS-CoV-1 and SARS-CoV-2, which share about 80% structural identity, do this by harnessing the action of the angiotensin converting enzyme, ACE-2, which is expressed in the membranes of many cells in the body, including lung alveolar epithelial cells. (
  • Captopril is a specific competitive inhibitor of angiotensin I-converting enzyme (ACE), the enzyme responsible for the conversion of angiotensin I to angiotensin II. (
  • Angiotensin I is then converted by angiotensin converting enzyme (ACE) to angiotensin II, a potent endogenous vasoconstrictor substance. (
  • Moreover, this increase in left ventricular mass index occurs in children who have ADPKD with borderline hypertension (75th to 95th percentile) and is prevented with angiotensin-converting enzyme inhibitor (ACEI) monotherapy. (
  • Competitive inhibitor of angiotensin-converting enzyme. (
  • It is produced from angiotensin I after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME . (
  • Angiotensin-converting enzyme DD genotype in patients with primary pulmonary hypertension: increased frequency and association with preserved haemodynamics. (
  • Impact of angiotensin-converting enzyme, angiotensinogen, endothelial NO synthase, and bradykinin receptor B2 gene polymorphisms on myocardium in patients with hypertension and in athletes]. (
  • Neutral endopeptidase and angiotensin I converting enzyme insertion/deletion gene polymorphism in humans. (
  • The influence of I/D polymorphism of the angiotensin I converting enzyme (ACE) gene and 4G/5G polymorphism of plasminogen activator inhibitor (PAI-1) gene promoter on the haemostatic system in patients with essential hypertension and dyslipidemia]. (
  • Effects of angiotensin-converting enzyme gene polymorphism and serum vitamin D levels on ambulatory blood pressure measurement and left ventricular mass in Turkish hypertensive population. (
  • Angiotensin-converting enzyme 2 is a protein on the surface of various cells that interacts with peptide hormones angiotensin I and II. (
  • Tumor necrosis factor-α produced in the kidney contributes to angiotensin II-dependent hypertension. (
  • Because Th1 cells generate interferon-γ and tumor necrosis factor-α (TNF-α), we hypothesized that interferon-γ and TNF-α propagate renal damage during hypertension induced by activation of the renin-angiotensin system. (
  • As angiotensin II-infused TNF knockout mice had exaggerated endothelial nitric oxide synthase expression in the kidney and enhanced nitric oxide bioavailability, we examined the actions of TNF-α generated from renal parenchymal cells in hypertension by transplanting wild-type or TNF knockout kidneys into wild-type recipients before the induction of hypertension. (
  • The angiotensin II subtype 1 receptor (AT1R) has been linked to the development and progression of renovascular hypertension. (
  • Hypertension , 51 (2 PART 2), 466-473. (
  • and releases arachidonic acid from tissue phospholipids which mediate or modulate one or more cardiovascular effects of angiotensin Bay 65-1942 HCl II and has been implicated in hypertension. (
  • These data suggest that angiotensin II-induced hypertension and associated cardiovascular pathophysiological changes are mediated by cPLA2? (
  • is crucial for the development of Ang II-induced hypertension and associated cardiovascular dysfunction and hypertrophy cardiac fibrosis inflammation oxidative stress and activation of ERK1/2 and cSrc in mice. (
  • Therefore it appears that metabolites of AA with Bay 65-1942 HCl pro-hypertensive effects contribute to the development of hypertension caused by Ang II in these mice. (
  • Hypertension , 64 (2), 227-228. (
  • Savoia, C & Volpe, M 2014, ' Impact of the direct angiotensin II type 2 receptor stimulation on renal function: Toward a sex-specific therapeutic approach for hypertension ', Hypertension , vol. 64, no. 2, pp. 227-228. (
  • Seidelin, PH & Struthers, AD 1991, ' Angiotensin II augments the stroke volume response to isoprenaline in man ', Journal of Hypertension , vol. 9, no. 11, pp. 1041-1047. (
  • Angiotensin II receptor blockers are used primarily for the treatment of hypertension where the person is intolerant of ACE inhibitor therapy primarily because of persistent cough . (
  • Hypertension;79(2): 365-378, 2022 02. (
  • Its beneficial effects in hypertension and heart failure appear to result primarily from suppression of the renin-angiotensin-aldosterone system. (
  • by the risk of hypertension, you may be prescribed to avoid herbs that can lower your blood pressure any medication if you're type 2 diabetes and undiabetes. (
  • Renal injury from angiotensin II-mediated hypertension. (
  • In addition to hypertension, the resultant angiotensin in ADPKD is a pivotal factor in cyst proliferation and expansion, increased sympathetic and endothelin activity, oxidant injury, and fibrosis. (
  • hypertension treatment antidepressant is diagnosed with angiotensin II receptor blockers. (
  • Renin-angiotensin gene polymorphism in children with uremia and essential hypertension. (
  • Journal of human hypertension 2004 Feb 18 (2): 119-25. (
  • Polymorphism in angiotensin II receptor genes and hypertension. (
  • Angiotensin II type 1 receptor A1166C gene polymorphism and essential hypertension in San Luis. (
  • Heran Balraj S, Wong Michelle MY, Heran Inderjit K, Wright James M. Blood pressure lowering efficacy of angiotensin receptor blockers for primary hypertension. (
  • Angiotensin II acts on a number of different angiotensin receptors. (
  • Peripheral action of angiotensin was cardioaccelerator via direct stimulation of beta-receptors of the atria in isolated atrial preparations. (
  • Increased levels of circulating angiotensin II result in unopposed stimulation of the AT 2 receptors, which are, in addition, upregulated. (
  • they have differential affinity for angiotensin receptors , although their exact role is still unclear. (
  • Role of angiotensin II AT1 receptors. (
  • Angiotensin II is an agonist at both angiotensin AT 1 and angiotensin AT 2 receptors. (
  • Angiotensin(1-7) is an antagonist at angiotensin AT 1 receptors and an agonist at MAS-1 receptors. (
  • Angiotensin receptor antagonists block the actions of angiotensin II and angiotensin(1-7) at angiotensin AT 1 receptors. (
  • It selectively and competitively blocks the vasoconstricting and aldosterone-secreting effects of angiotensin II by selectively antagonising its binding to AT1 receptors. (
  • Transplant recipients lacking TNF solely in the kidney had blunted hypertensive responses to angiotensin II and augmented renal endothelial nitric oxide synthase expression, confirming a role for kidney-derived TNF-α to promote angiotensin II-induced blood pressure elevation by limiting renal nitric oxide generation. (
  • Intrarenal angiotensin II plays an important role in renal fibrosis in primary IgA nephropathy. (
  • Intrarenal Ang II plays an important role in renal fibrosis in IgAN, particularly at the tubulointerstitial level. (
  • Intervention in the renin-angiotensin-aldosterone system (RAAS) has convincingly shown to delay progression of renal disease in patients with diabetes mellitus with elevated urinary albumin excretion (UAE) in several large trials. (
  • Our objective was to assess circulating, renal, cardiac, and vascular Ang II in a canine model of rapid ventricular pacing-induced heart failure that evolves from early left ventricular dysfunction to overt congestive heart failure. (
  • Overt congestive heart failure was characterized by further impaired cardiac function and cardiac enlargement, reduced renal perfusion pressure, urinary sodium retention, and increased plasma renin activity and plasma Ang II. (
  • In early left ventricular dysfunction dogs, renal cortical, renal medullary, ventricular, and aortic Ang II were unchanged, and atrial Ang II was decreased. (
  • The greatest increase in tissue Ang II occurred in the renal medulla. (
  • We conclude that early increases in local renal, myocardial, and vascular Ang II do not occur in this model of early left ventricular dysfunction and may even be suppressed. (
  • In contrast, increased myocardial and particularly renal Ang II in association with increased circulating Ang II are hallmarks of overt experimental congestive heart failure. (
  • Dual blockade of renin-angiotensin system increases risks of hypotension, hyperkalemia, and renal impairment. (
  • Analysis of renal structural and functional features in two rat strains with a different susceptibility to glomerular sclerosis. (
  • Renal Volume, Renin-Angiotensin-Aldosterone System, Hyperten. (
  • Renal cyst enlargement in ADPKD in adults is associated with stimulation of both the circulating and intrarenal renin-angiotensin-aldosterone system. (
  • The effect of renin-angiotensin-aldosterone system inhibition with dual blockade, ACEI and angiotensin receptor antagonists, on renal volume and kidney function is under study in the Halt Progression of Polycystic Kidney Disease (HALT PKD) trial. (
  • 2 Similarly, the incidence of reported end-stage renal disease in people with diabetes is more than 4 times as high in African Americans and 4 to 6 times as high in Mexican Americans than in the general population of diabetes patients. (
  • Angiotensin II, a key effector peptide of the system, causes vasoconstriction and exerts multiple biological functions. (
  • AngII not only activates the angiotensin type 1 receptor (AT 1 R) to mediate vasoconstriction but also angiotensin type 2 receptor (AT 2 R) to cause vasodilation. (
  • Angiotensin II, the production of which has been reported to increase after burn, is thought to be one of the primary mediators of postburn mesenteric vasoconstriction. (
  • Angiotensin is a peptide hormone that causes vasoconstriction and an increase in blood pressure . (
  • Angiotensin II acts on the CNS to increase vasopressin production, and also acts on venous and arterial smooth muscle to cause vasoconstriction. (
  • Conversely, when sodium intake is reduced below normal, increased levels of angiotensin II cause sodium and water retention and oppose reductions in arterial blood pressure that would otherwise occur. (
  • Aliskiren/valsartan formulated 150 mg-160 mg (a partial dose of each of 2 RAAS inhibitor drugs) was considered a partial dose (submaximum). (
  • Moreover administration of inhibitor of AA metabolism ETYA blocked Ang II-induced increase in SBP in cPLA2? (
  • Objective: To investigate the role of angiotensin II as a mediator of burn- and sepsis-induced gut ischemia and reperfusion injury and to determine whether treatment with the angiotensin II inhibitor DuP753 can attenuate mucosal injury and bacterial translocation in a burn/endotoxemia porcine model. (
  • ACE is a target of ACE inhibitor drugs, which decrease the rate of angiotensin II production. (
  • Colucci, Wilson S. Angiotensin II receptor blocker and neprilysin inhibitor therapy in heart failure due to systolic dysfunction. (
  • Acesso em: 8 dez 2014. (
  • abstract = "Many studies in experimental animal models suggest that there is an interaction between angiotensin II and the sympathetic nervous system. (
  • ABSTRACT The aim of this study in 2006-08 was to determine the prevalence and risk factors of CVD in an Iranian population of patients with type 2 diabetes mellitus. (
  • Angiotensinogen is made by the liver and forms angiotensin I in the blood. (
  • The expression of intrarenal renin, angiotensinogen (AGT), Ang II, Ang IIreceptor was examined by immunohistochemistry staining (IHCS). (
  • Angiotensinogen is an α-2-globulin produced constitutively and released into the circulation mainly by the liver. (
  • Plasma angiotensinogen levels are increased by plasma corticosteroid , estrogen , thyroid hormone , and angiotensin II levels. (
  • Angiotensin I ( CAS # 11128-99-7), also called proangiotensin , is formed by the action of renin on angiotensinogen . (
  • Angiotensinogen is converted to angiotensin I by renin. (
  • Angiotensin II also increases aldosterone secretion, therefore, it acts as an endocrine , autocrine / paracrine , and intracrine hormone. (
  • Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion. (
  • Angiotensin II also stimulates aldosterone secretion from the adrenal cortex, thereby contributing to sodium and fluid retention. (
  • Inhibition of ACE results in decreased plasma angiotensin II and increased plasma renin activity (PRA), the latter resulting from loss of negative feedback on rennin release caused by reduction in angiotensin II.The reduction of angiotensin II leads to decreased aldosterone secretion, and, as a result, small increases in serum potassium may occur along with sodium and fluid loss. (
  • Reduces angiotensin II levels, decreasing aldosterone secretion. (
  • Spironolactone and chlorthalidone in uncontrolled elderly hypertensive patients treated with calcium antagonists and angiotensin II receptor-blocker: effects on endothelial function, inflammation, and oxidative stress. (
  • The purpose of the present study was to evaluate the differences between spironolactone and chlorthalidone in hypertensive elderly patients treated with calcium antagonists and angiotensin II receptor blockers. (
  • activation most likely through the release of arachidonic acid and generation of eicosanoids with predominant pro-hypertensive effects and activation of one or more signaling molecules including ERK1/2 and cSrc. (
  • selectively catalyzes release of AA from tissue lipids12 and Ang II is known to Bay 65-1942 HCl activate cPLA2 to release AA cPLA2 appears to mediate the hypertensive effect of Ang II via AA release. (
  • Irbesartan and losartan have trial data showing benefit in hypertensive patients with type 2 diabetes , [ citation needed ] and may delay the progression of diabetic nephropathy . (
  • Association of aldosterone synthase gene -344T/C polymorphism with plasma aldosterone and angiotensin II concentration in hypertensive patients]. (
  • Although angiotensin II is one of the most powerful sodium- and water-retaining hormones in the body, neither a decrease nor an increase in circulating angiotensin II has a large effect on extracellular fluid volume or blood volume. (
  • Although angiotensin II (Ang II) has been implicated in the pathophysiology of congestive heart failure, its temporal and regional changes during the development and progression of the disease are poorly defined. (
  • van Ginkel, S.L.. / The effect of exercise and ACE inhibition on angiotensin II . (
  • Captopril prevents the conversion of angiotensin I to angiotensin II by inhibition of ACE, a peptidyldipeptide carboxy hydrolase. (
  • This inhibition has been demonstrated in both healthy human subjects and in animals by showing that the elevation of blood pressure caused by exogenously administered angiotensin I was attenuated or abolished by captopril. (
  • can blood pressure medication change your personality of the two number in the pressure is the normal blood pressure, the pressure readings are too low. (
  • Results showed that treatment with angiotensin II was associated with increased bacterial clearance from the blood and the peritoneal cavity, as well as a modified host immune response, following CLP. (
  • Oxytocinase (EC, a pregnancy-related oxytocin-inactivating α-aminoacyl hydrolase, also has the ability to degrade vasopressin, angiotensin II and some synthetic peptides. (
  • Two such peptides, S-benzyl-L-cysteine-p-nitroanilide (BCN) and L-leucine-p-nitroanilide (LN) with proven substrate specificity, have been widely used to study oxytocinase activity in vitro. (
  • The trial provided substantial evidence of the effectiveness of angiotensin II in raising blood pressure over placebo in patients with distributive shock, while keeping catecholamine levels constant. (
  • 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. (
  • Secondly, Ang II could be administered to specific patients. (
  • In this perspective, could we hypothesize that an early infusion of Ang II has a positive effect on these patients? (
  • Thirdly, the safety profile of Ang II has never been tested in patients with vasodilatory shock and concurrent myocardial dysfunction. (
  • If put into practice in human patients, are there any patient-specific risk factors or considerations clinicians should be aware of if angiotensin II treatment were to be administered to a patient undergoing septic shock? (
  • It is too soon to say which patients might benefit from the immune effects of angiotensin II in sepsis. (
  • Further studies that can identify patients who may benefit from angiotensin II are still needed. (
  • To investigate the relationship of intrarenal angiotensin II (Ang II) expression with clinicpathological injury index and intrarenal expression and regulation of RAS (renin-angiotensin system) components in IgAN (immunoglobulin A nephropathy) patients. (
  • In this month's EM Quick Hits podcast: Anand Swaminathan on the approach to cardiogenic shock, Hania Bielawska on the myths of radiation dose in pregnant patients, Hans Rosenberg & Michael Gottlieb on PoCUS in airway management, Menaka Pai on VIPIT following AstraZeneca COVID-19 vaccination, Brit Long & Michael Gottlieb on Angiotensin II for emergency clinicians, Michael Schull on tips on the safety of short-term steroid use. (
  • Individual patients show a large variability in albuminuria response to angiotensin receptor blockers (ARB). (
  • Data from patients with type 2 diabetes and microalbuminuria (n = 49) treated with irbesartan 300 mg/day were used for discovery. (
  • Therefore, the aims of this study were to first discover and validate a serum metabolite classifier that predicts response in albuminuria to angiotensin II receptor blocker (ARB) therapy in patients with diabetes mellitus and micro- or macroalbuminuria, and secondly, to integrate the identified metabolites in a molecular process model capturing disease pathophysiology at the interface of drug mechanism of action to decipher the underlying molecular processes driving albuminuria response to ARB. (
  • In contrast, when angiotensin levels cannot be decreased in response to increased sodium intake (high angiotensin II curve), as occurs in some hyper-tensive patients who have impaired ability to decrease renin secretion, the pressure natriuresis curve is not nearly as steep. (
  • METHODS: In this multicentre, placebo-controlled, double-blind, randomised, phase 2 clinical trial, we enrolled patients (aged 22-89 years) with postherpetic neuralgia of at least 6 months' duration from 29 centres across six countries. (
  • Coinfection with SARS-CoV-2 and other respiratory pathogens in patients with COVID-19 in Guangzhou, China. (
  • The epidemiology and clinical characteristics of co-infection of SARS-CoV-2 and influenza viruses in patients during COVID-19 outbreak. (
  • The high prevalence of CVD in Iranian patients with type 2 diabetes underscores the importance of better detection and treatment of metabolic risk factors of CVD in these patients. (
  • RÉSUMÉ La présente étude visait à déterminer la prévalence et les facteurs de risque des maladies cardio-vasculaires dans une population iranienne de patients atteints de diabète de type 2 entre 2006 et 2008. (
  • Les antécédents et les examens cliniques de 752 patients consultant dans un centre de recherche sur l'endocrinologie et le métabolisme ont été consignés et des analyses en laboratoire ont été réalisées. (
  • The protein expression of PLA2 but not PLC?2 PLD1 or PLD2 was also absent in cPLA2? (
  • 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). (
  • Hoffmann M , Kleine-Weber H , Pöhlmann S . A multibasic cleavage site in the spike protein of SARS-CoV-2 is essential for infection of human lung cells. (
  • A BLAST search restricted to mammalian protein sequence, a transmembrane domain, and 2-heptad repeats. (
  • The spike protein is a large type I transmembrane protein containing two subunits, S1 and S2. (
  • The California based biotech plans to use a well-known replicating cell line (human erythroleukemia, K562) to integrate the spike protein of SARS-CoV-2 or its S1 domain onto the cell membrane simulating that the viral protein is introduced on a decoy cell surface to evoke T cell and B cell immunity to COVID-19. (
  • Angiotensin II also increases the ability of white blood cells to kill bacteria through phagocytosis. (
  • Excessive Angiotensin II Does Not Cause Large Increases in Extracellular Fluid Volume Because Increased Arterial Pressure Counterbalances Angiotensin-Mediated Sodium Retention. (
  • The reason for this is that with large increases in angiotensin II levels, as occurs with a renin-secreting tumor of the kidney, the high angiotensin II levels initially cause sodium and water retention by the kidneys and a small increase in extracellular fluid volume. (
  • This also initi-ates a rise in arterial pressure that quickly increases kidney output of sodium and water, thereby overcom-ing the sodium- and water-retaining effects of the angiotensin II and re-establishing a balance between intake and output of sodium at a higher blood pres-sure. (
  • Conclusions: Angiotensin II appears to play a pivotal role in the bum- and endotoxin-induced intestinal ischemia and reperfusion injury, with subsequent increases in permeability and bacterial translocation. (
  • benazepril increases effects of synthetic human angiotensin II by unspecified interaction mechanism. (
  • quinapril increases effects of synthetic human angiotensin II by unspecified interaction mechanism. (
  • [6] They work by blocking the angiotensin II receptor type 1 (AT 1 ) thereby preventing the effects of angiotensin II . (
  • Virgin, pregnant (at different days of gestation) and post-partum Sprague-Dawley rats were used to determine uterine artery hemodynamics using micro ultrasound and plasma angiotensin II levels by ELISA. (
  • azilsartan decreases effects of synthetic human angiotensin II by pharmacodynamic antagonism. (
  • synthetic human angiotensin II and finerenone both increase serum potassium. (
  • olmesartan decreases effects of synthetic human angiotensin II by pharmacodynamic antagonism. (
  • Further analysis showed that the effects of angiotensin II treatment on bacteremia burden following CLP were negated by selective angiotensin type 1 receptor (AT1R) deletion in myeloid-lineage leukocytes. (
  • EMA401, an orally administered highly selective angiotensin II type 2 receptor antagonist, as a novel treatment for postherpetic neuralgia: a randomised, double-blind, placebo-controlled phase 2 clinical trial. (
  • These treatments included intraperitoneal angiotensin II alone, intraperitoneal angiotensin II plus losartan, subcutaneous angiotensin II, or vehicle. (
  • Similar results were observed when angiotensin II was co-administered with losartan, suggesting that the effects of angiotensin II on bacteremia burden are mediated via AT1R. (
  • Losartan is an angiotensin II receptor antagonist. (
  • The renin-angiotensin system (RAS) plays a key role in maintaining blood pressure homeostasis, as well as fluid and salt balance. (
  • Multiple short-term effects of lead on the renin-angiotensin system. (
  • Biological Function Essential counter-regulatory carboxypeptidase of the renin-angiotensin hormone system that is a critical regulator of blood volume, systemic vascular resistance, and thus cardiovascular homeostasis (PubMed:27217402). (
  • A number of studies have shown that activation of intrarenal renin-angiotensin system (RAS) plays an important role in development and progression of chronic kidney disease (CKD). (
  • Thus, changes in activity of the renin-angiotensin system act as a powerful amplifier of the pressure natriuresis mechanism for maintaining stable blood pressures and body fluid volumes. (
  • Angiotensin II (Ang II) is the key peptide hormone in the renin-angiotensin-aldosterone system (RAAS). (
  • Mit der Einführung des ACE-Hemmers Captopril begann 1981 die Erfolgsgeschichte der therapeutischen Intervention in das Renin-Angiotensin-System (RAS) bei kardiovaskulären und renalen Erkrankungen. (
  • Journal of the Renin-Angiotensin-Aldosterone System , 2 (4), 205-210. (
  • Renin-angiotensin system (RAS) is a signaling pathway for regulation of blood pressure, blood volume, natriuresis, and other vascular functions. (
  • It is part of the renin-angiotensin system , which regulates blood pressure. (
  • A simplified version of the pharmacology of the renin-angiotensin system is shown in the diagram below. (
  • Therapeutisch werden standardmäßig Medikamente zur Senkung des Blutzuckerspiegels (Inhibitoren des Renin-Angiotensin-Aldosteron-Systems (RAAS), Metformin, Inhibitoren des Natrium-Glucose-Transporters-2 (SGLT2) und des Blutdrucks (Erstlinien Therapie mit Inhibitoren des RAAS, sekundäre Therapie mit Statinen sowie Nikotinentwöhnung und salzarme Ernährung) eingesetzt. (
  • Journal of the renin-angiotensin-aldosterone system : JRAAS 2002 Jun 3 (2): 109-15. (
  • Journal of the renin-angiotensin-aldosterone system : JRAAS 2003 Mar 4 (1): 27-30. (
  • Impact of genetic polymorphisms of the renin-angiotensin system and of non-genetic factors on kidney transplant function--a single-center experience. (
  • Importantly, angiotensin II is Food and Drug Administration (FDA)-approved to treat hypotension of the type that often accompanies sepsis. (
  • The angiotensin II type 2 receptor (AT2R) is a new target for neuropathic pain. (
  • E 2 decreases expression of the angiotensin II type 1 receptor (AT 1 R), a receptor with known relevance to water and salt intakes, in multiple areas of the brain where ERα and ERβ are differentially expressed. (
  • As a result of more about 106% of those with latest medicine for diabetes type 2 a high risk of developing it needs to achieve the health condition. (
  • type 2 it drugs in diabetes medicines Patanjali pipeline and are completely superior to detect it management. (
  • We report a patient with type 2 diabetes mellitus and chronic lymphocytic leukemia who had been infected for 42 weeks with SARS-CoV-2. (
  • In this context, teeth proved to be important elements in this type of identification, due to the high probability that there are not two people having the same exact dental features, as well as the relatively high degree of physical and chemical resistance of dental structures 15 . (
  • Converts angiotensin I to angiotensin 1-9, a nine-amino acid peptide with anti-hypertrophic effects in cardiomyocytes, and angiotensin II to angiotensin 1-7, which then acts as a beneficial vasodilator and anti-proliferation agent, counterbalancing the actions of the vasoconstrictor angiotensin II (PubMed:10969042, PubMed:10924499, PubMed:11815627, PubMed:19021774, PubMed:14504186). (
  • Para inhibir el efecto vasoconstrictor e hipertensivo de la angiotensina II, a menudo se trata a los pacientes con INHIBIDORES DE LA ECA o con BLOQUEANTES DEL RECEPTOR DE TIPO 1 DE LA ANGIOTENSINA II. (
  • Based on the agreements emanating from the special protocol assessment to assess blood pressure effects, the data from this single study supported approval of angiotensin II by the Food and Drug Administration for marketing in the USA. (
  • The effects of lead (7439921) on the relationship between plasma renin and angiotensin II were studied. (
  • The effects of lead, 0.5 milligrams per minute, administered by continuous infusion for 3 hours, on these parameters and on arterial angiotensin II were measured. (
  • Interestingly, no difference in adverse effects was remarkable between the two groups. (
  • Matthew D. Taylor, MD, provides insight into the potential effects of angiotensin II on bacterial clearance and the systemic inflammatory response in clinical sepsis. (
  • To assess the effects of angiotensin II on the immune response to CLP, the researchers randomly assigned 4 cohorts of mice to 4 different treatments. (
  • There are theoretical reasons as to why angiotensin II might be preferable to norepinephrine - the current first-line drug - that include but are not limited to its associated immune effects. (
  • Because angiotensin II has several important effects in increas-ing tubular reabsorption of sodium, a reduced level of angiotensin II decreases tubular reabsorption of sodium and water, thus increasing the kidneys' excretion of sodium and water. (
  • The use of drugs to block the effects of angiotensin II has proved to be important clinically for improv-ing the kidneys' ability to excrete salt and water. (
  • Many of the Ang II effects on glomerulosa cells involve a precisely coordinated regulation of signaling cascades and gene expression. (
  • The development of genome-wide gene arrays has allowed the definition of transcriptome-wide effects of Ang II in adrenocortical cells. (
  • Analysis of the Ang II gene targets reveals broad effects on cellular gene expression, particularly the rapid induction of numerous transcription factors that may regulate long-term steroid metabolism and cell growth/proliferation. (
  • The effects of angiotensin II were studied on isolated atrial preparations of nonreserpinised and reserpinised rabbits, before and after treating the preparations by propranolol. (
  • The angiotensin II receptor blockers have differing potencies in relation to blood pressure control, with statistically differing effects at the maximal doses. (
  • However, recent data suggest AT 2 receptor stimulation may be less beneficial than previously proposed, and may even be harmful under certain circumstances through mediation of growth promotion, fibrosis , and hypertrophy , as well as eliciting proatherogenic and proinflammatory effects. (
  • Nonpeptide angiotensin II receptor antagonist that blocks the vasoconstricting and aldosterone-secreting effects of angiotensin II. (
  • The mechanistic basis for the disparate effects of angiotensin II on coronary collateral growth. (
  • Together, the results reveal selective effects of ER subtypes on ingestive behaviors, advancing our understanding of E 2 's inhibitory role in the controls of fluid intake by female rats. (
  • During septic shock, fluid therapy is aimed at increasing cardiac output and improving tissue oxygenation, but it poses two problems: it has inconsistent and transient efficacy, and it has many well-documented deleterious effects. (
  • Estradiol (E 2 ) decreases both water and saline intakes by female rats. (
  • Surprisingly, little information is available about the RAS expression and regulation in the human kidney and particularly in kidney diseases and data on the intrarenal RAS expression and regulation were mostly obtained in animals [ 1 , 2 ]. (
  • Hypercalcemia stimulates expression of intrarenal phospholipase A2 and prostaglandin H synthase-2 in rats. (
  • Angiotensin also stimulates the release of aldosterone from the adrenal cortex to promote sodium retention by the kidneys. (
  • In overt congestive heart failure dogs, Ang II was increased in the kidney and heart compared with normal dogs and in all tissues compared with early left ventricular dysfunction dogs. (
  • In addition, angiotensin II acts at the Na + /H + exchanger in the proximal tubules of the kidney to stimulate Na reabsorption and H + excretion which is coupled to bicarbonate reabsorption. (
  • Genetic identification of two major modifier loci of polycystic kidney disease progression in pcy mice. (
  • 2015. The two kidney to one kidney transition and transplant glomerulopathy: a podocyte perspective. . (
  • 2012. Angiotensin II-dependent persistent podocyte loss from destabilized glomeruli causes progression of end stage kidney disease. . (
  • 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. (
  • 3. The pressor responses to intraventricular perfusions of angiotensin II were normal in Long-Evans rats, virtually absent in rats homozygous for hereditary hypothalamic diabetes insipidus, irrespective of whether they were injected with vasopressin tannate or not, and intermediate in rats heterozygous for hypothalamic diabetes insipidus. (
  • 4. The results suggest that the pressor response to intraventricular angiotensin II is related to the release of vasopressin. (
  • Judged by the Ki values of the octapeptides which negatively reflect their inactivation or hydrolysis by oxytocinases, it is concluded that the enzyme component which inactivates angiotensin II is predominant in all the samples tested followed by the oxytocin and vasopressin-inactivating components. (
  • This study aimed to investigate the inhibitory effect of blueberry anthocyanin (BBA) on Angiotensin II (Ang II)-induced apoptosis of human umbilical vein endothelial cells (HUVECs), and its regulation mechanisms involving Bax and Caspase 3. (
  • Angiotensin I (a decapeptide) is converted by ACE-1 to angiotensin II (an octapeptide). (
  • Renin, an enzyme synthesized by the kidneys, is released into the circulation where it acts on a plasma globulin substrate to produce angiotensin I, a relatively inactive decapeptide. (
  • The use of angiotensin II to raise the mean arterial pressure (MAP) could provide additional therapy and the opportunity to evaluate a catecholaminesparing effect by decreasing the dose of concomitant catecholamines while maintaining a target MAP. (
  • Thus, the inabil-ity to suppress angiotensin II formation when there is excess sodium reduces the slope of pressure natriure-sis and makes arterial pressure very salt sensitive. (
  • Microbial infection) Acts as a receptor for human coronaviruses SARS-CoV and SARS-CoV-2, as well as human coronavirus NL63/HCoV-NL63. (
  • Isoform 2]: (Microbial infection) Non-functional as a receptor for human coronavirus SARS-CoV-2. (
  • severe acute respiratory syndrome coronavirus 2 from patient with coronavirus disease, United States. (
  • US CDC Real-time reverse transcription PCR panel for detection of severe acute respiratory syndrome coronavirus 2. (
  • Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes respiratory disease in mink similar to human COVID-19. (
  • Compared to adults, children with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) have predominantly mild or asymptomatic infections, but the underlying immunological differences remain unclear. (
  • In most cases, SARS-CoV-2, the novel coronavirus that causes COVID-19, enters the body via the airway. (
  • Loss of furin cleavage site attenuates SARS-CoV-2 pathogenesis. (
  • This study expands on the knowledge of the pathology and pathogenesis of natural SARS-CoV-2 infection in mink and supports their further investigation as a potential animal model of SARS-CoV-2 infection in humans. (
  • Plasma Ang I, Ang 1-7 ( angiotensin 1-7) levels, and the Ang 1-7/Ang II ( angiotensin II ) ratio were elevated during SARS-CoV-2 infection related to downregulation of ACE activity at baseline. (
  • The objective of the study was to conduct a meta-analysis of the association between ACEI or ARB use and SARS-COV-2 infection severity or mortality. (
  • We searched PubMed, EMBASE, Google scholar and the Cochrane Database of Systematic Reviews for observational studies published between December 2019 and August 4, 2020 Studies were included if they contained data on ACEI or ARB use and SARS-COV-2 infection severity or mortality. (
  • At present, the evidence available does not support the hypothesis of increased SARS-COV-2 risk with ACEI or ARB drugs. (
  • Angiotensin II was found to be associated with an increase in the myeloid innate immune response during severe systemic infection, suggesting angiotensin II may improve immune responses in the setting of clinical sepsis. (
  • We have now sought evidence for such an interaction using angiotensin II and beta-adrenoceptor stimulation with isoprenaline. (
  • NICE is unable to make a recommendation on angiotensin II for treating vasosuppressor-resistant hypotension caused by septic or distributive shock. (
  • A basal secretion rate of 16 ± 3 × 10 -15 mol of immunoreactive angiotensin 11/min was calculated for intact rats. (
  • Lever-pressing behavior caused by intraseptal Angiotensin II in water-satiated rats. (
  • 2. Rats were treated with bosentan or vehicle (5% gum arabic) for 7 days by gavage. (
  • Unfortunately, these two classes of drugs may lead to increased serum creatinine levels and hyperkalemia, limiting their utility. (
  • Telmisartan belongs to the class of drugs called Angiotensin II receptor antagonists that works by blocking the angiotensin II receptor, relaxing the blood vessels and lowering the blood pressure. (
  • Telmisartan belongs to the class of drugs called Angiotensin II receptor antagonists. (
  • When blood pressure changes, Angiotensin II is produced and released into the bloodstream. (
  • Interferon deficiency had no impact on blood pressure elevation or urinary albumin excretion during chronic angiotensin II infusion. (
  • Note that when the angiotensin control of natriuresis is fully functional, the pressure natriuresis curve is steep (normal curve), indicating that only minor changes in blood pressure are needed to increase sodium excretion when sodium intake is raised. (
  • II formation appropriately in response to excess sodium, the same rise in sodium intake causes blood pressure to rise as much as 50 mm Hg. (
  • 90mmHg systolic blood pressure [2] ) at the juxtaglomerular cells , or decreased delivery of Na+ and Cl- to the macula densa . (
  • selection was based on blood pressure and reported sodium intake levels as described below to ensure a wide range of values for these two related measures. (
  • Olkem Beta 50 Tablet 10's is a combination of two high blood pressure-lowering medicines: Telmisartan and Metoprolol. (
  • It works by blocking the angiotensin II receptor, thereby relaxing the blood vessels and lowering the blood pressure. (
  • 2015. NMDA Receptor Plasticity in the Hypothalamic Paraventricular Nucleus Contributes to the Elevated Blood Pressure Produced by Angiotensin II. . (
  • supplements to take for high blood pressure taurine to reduce blood pressure, including various foods, vitamins, potassium, which can lead to angiotensin II. (
  • Angiotensin II also increased cardiac infiltration of F4/80+ macrophages and CD3+ T lymphocytes cardiovascular oxidative stress expression of endoplasmic reticulum stress markers p58and CHOP in cPLA2? (
  • The effect of comparable levels of hypoxemia on the conversion of continuous intravenous infusions of pharmacological doses (1000 times physiological) of angiotensin I was greater: from 55 ± 14 to 33 ± 13% (P (
  • This study provides evidence that a physiological dose of angiotensin II can synergistically augment the stroke volume effect of beta-agonism in man. (
  • Normal pregnancy is associated with decreased uterine vascular contraction and increased blood flow even though angiotensin II (AngII) levels are increased. (
  • This conclusion is based on our finding that infusion of Ang II increased SBP measured by tail cuff as well as radio telemetry in cPLA2? (
  • mice.16 31 32 In the present study Ang II infusion increased the urinary output of PGEM TXB2 20 in cPLA2? (
  • Isoprenaline significantly reduced total peripheral resistance and this reduction was not affected by concomitant infusion of angiotensin II. (
  • Two techniques that are currently being investigated are neurostimulation and the spinal infusion pump. (
  • Angiotensin II activates cPLA2? (
  • After the S1 subunit of the spike binds to the ACE-2 enzyme on the cell membrane surface, TMPRSS2 activates the spike and cleaves ACE-2. (
  • The issue of whether angiotensin II receptor antagonists slightly increase the risk of myocardial infarction (MI or heart attack) is currently being investigated. (
  • Kim D , Quinn J , Pinsky B , Shah NH , Brown I . Rates of co-infection between SARS-CoV-2 and other respiratory pathogens. (
  • Host and viral determinants for efficient SARS-CoV-2 infection of the human lung. (
  • Here, we describe clinical features, virology, longitudinal cellular, and cytokine immune profile, SARS-CoV-2-specific serology and salivary antibody responses in a family of two parents with PCR-confirmed symptomatic SARS-CoV-2 infection and their three children, who tested repeatedly SARS-CoV-2 PCR negative. (
  • These data indicate that children can mount an immune response to SARS-CoV-2 without virological confirmation of infection, raising the possibility that immunity in children can prevent the establishment of SARS-CoV-2 infection. (
  • This finding pointed to the importance of interferons (IFNs), during the initial infection, for clearing SARS-CoV-2 and concerns about using glucocorticoids, which could inhibit IFN signaling in COVID-19 treatment. (
  • The proactive approach to international collaboration and sharing of resources have enabled the discovery of previously unknown pathophysiological mechanisms of SARS-CoV-2 infection and revealed the complex genetic architecture of COVID-19. (
  • While we have made an impressive sprint to uncover the genetic anchors for response to COVID-19 infection just two years into the pandemic, the next major challenge is to use these biologic findings to inform treatment and prevention. (
  • Most important of these in terms of SARS-2 is the lungs, as they are the primary site of infection, and along with the oral cavity, that is where infection will begin. (
  • Our results suggest new therapeutic strategies for preventing and slowing SARS-CoV-2 infection, focusing on targeting cell host surface vimentin. (

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