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 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.
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 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 3.4.15.1.
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.
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 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 3.4.99.19.
Agents that antagonize ANGIOTENSIN RECEPTORS. Many drugs in this class specifically target the ANGIOTENSIN TYPE 1 RECEPTOR.
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.
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.
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.
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.
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.
An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.
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 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.
PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.
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.
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.
Agents that antagonize the ANGIOTENSIN II TYPE 2 RECEPTOR.
An ANGIOTENSIN II analog which acts as a highly specific inhibitor of ANGIOTENSIN TYPE 1 RECEPTOR.
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.
An angiotensin-converting enzyme inhibitor that is used to treat HYPERTENSION and HEART FAILURE.
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.
One of the ANGIOTENSIN-CONVERTING ENZYME INHIBITORS (ACE inhibitors), orally active, that has been used in the treatment of hypertension and congestive heart failure.
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 hormone secreted by the ADRENAL CORTEX that regulates electrolyte and water balance by increasing the renal retention of sodium and the excretion of potassium.
Drugs used to cause constriction of the blood vessels.
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.
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
Drugs used in the treatment of acute or chronic vascular HYPERTENSION regardless of pharmacological mechanism. Among the antihypertensive agents are DIURETICS; (especially DIURETICS, THIAZIDE); ADRENERGIC BETA-ANTAGONISTS; ADRENERGIC ALPHA-ANTAGONISTS; ANGIOTENSIN-CONVERTING ENZYME INHIBITORS; CALCIUM CHANNEL BLOCKERS; GANGLIONIC BLOCKERS; and VASODILATOR AGENTS.
Peptides composed of between two and twelve amino acids.
Compounds with a BENZENE fused to IMIDAZOLES.
An inhibitor of glutamate decarboxylase. It decreases the GAMMA-AMINOBUTYRIC ACID concentration in the brain, thereby causing convulsions.
Enzyme that is a major constituent of kidney brush-border membranes and is also present to a lesser degree in the brain and other tissues. It preferentially catalyzes cleavage at the amino group of hydrophobic residues of the B-chain of insulin as well as opioid peptides and other biologically active peptides. The enzyme is inhibited primarily by EDTA, phosphoramidon, and thiorphan and is reactivated by zinc. Neprilysin is identical to common acute lymphoblastic leukemia antigen (CALLA Antigen), an important marker in the diagnosis of human acute lymphocytic leukemia. There is no relationship with CALLA PLANT.
A potent inhibitor of membrane metalloendopeptidase (ENKEPHALINASE). Thiorphan potentiates morphine-induced ANALGESIA and attenuates naloxone-precipitated withdrawal symptoms.
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.
The physiological narrowing of BLOOD VESSELS by contraction of the VASCULAR SMOOTH MUSCLE.
The relationship between the dose of an administered drug and the response of the organism to the drug.
A strain of Rattus norvegicus with elevated blood pressure used as a model for studying hypertension and stroke.
Persistent high BLOOD PRESSURE due to KIDNEY DISEASES, such as those involving the renal parenchyma, the renal vasculature, or tumors that secrete RENIN.
A strain of Rattus norvegicus used as a normotensive control for the spontaneous hypertensive rats (SHR).
Compounds with a six membered aromatic ring containing NITROGEN. The saturated version is PIPERIDINES.
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.
A diet which contains very little sodium chloride. It is prescribed by some for hypertension and for edematous states. (Dorland, 27th ed)
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.
The nonstriated involuntary muscle tissue of blood vessels.
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.
Excision of kidney.
The circulation of the BLOOD through the vessels of the KIDNEY.
The consumption of liquids.
Methods used for the assessment of placental function.
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.
A guanidinium antihypertensive agent that acts by blocking adrenergic transmission. The precise mode of action is not clear.
Peptides composed of two amino acid units.
Hypertension due to RENAL ARTERY OBSTRUCTION or compression.
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 long-acting angiotensin-converting enzyme inhibitor. It is a prodrug that is transformed in the liver to its active metabolite ramiprilat.
The main trunk of the systemic arteries.
Any member of the group of ENDOPEPTIDASES containing at the active site a serine residue involved in catalysis.
Elements of limited time intervals, contributing to particular results or situations.
The movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM.
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.
The octapeptide amide of bovine angiotensin II used to increase blood pressure by vasoconstriction.
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 albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
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)
Compounds which inhibit or antagonize biosynthesis or actions of proteases (ENDOPEPTIDASES).
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.
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.
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.
Liquid chromatographic techniques which feature high inlet pressures, high sensitivity, and high speed.
Any of the tubular vessels conveying the blood (arteries, arterioles, capillaries, venules, and veins).
The number of times the HEART VENTRICLES contract per unit of time, usually per minute.
A benzoic-sulfonamide-furan. It is a diuretic with fast onset and short duration that is used for EDEMA and chronic RENAL INSUFFICIENCY.
An angiotensin-converting enzyme inhibitor. It is used in patients with hypertension and heart failure.
Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.
Inflammation of the connective and adipose tissues surrounding the KIDNEY.
A ubiquitous sodium salt that is commonly used to season food.
A member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23.
The vessels carrying blood away from the heart.
A non-essential amino acid that is synthesized from GLUTAMIC ACID. It is an essential component of COLLAGEN and is important for proper functioning of joints and tendons.
A branch of the abdominal aorta which supplies the kidneys, adrenal glands and ureters.
Treatment process involving the injection of fluid into an organ or tissue.
The portion of the descending aorta proceeding from the arch of the aorta and extending to the DIAPHRAGM, eventually connecting to the ABDOMINAL AORTA.
The outer zone of the KIDNEY, beneath the capsule, consisting of KIDNEY GLOMERULUS; KIDNEY TUBULES, DISTAL; and KIDNEY TUBULES, PROXIMAL.
A layer of epithelium that lines the heart, blood vessels (ENDOTHELIUM, VASCULAR), lymph vessels (ENDOTHELIUM, LYMPHATIC), and the serous cavities of the body.
A condition of markedly elevated BLOOD PRESSURE with DIASTOLIC PRESSURE usually greater than 120 mm Hg. Malignant hypertension is characterized by widespread vascular damage, PAPILLEDEMA, retinopathy, HYPERTENSIVE ENCEPHALOPATHY, and renal dysfunction.
A subclass of PEPTIDE HYDROLASES that catalyze the internal cleavage of PEPTIDES or PROTEINS.
The rate dynamics in chemical or physical systems.
Arteries which arise from the abdominal aorta and distribute to most of the intestines.
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.
Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.
Sodium excretion by URINATION.
Inorganic or organic derivatives of phosphinic acid, H2PO(OH). They include phosphinates and phosphinic acid esters.
Enzymes that act at a free C-terminus of a polypeptide to liberate a single amino acid residue.
A serine protease found in the azurophil granules of NEUTROPHILS. It has an enzyme specificity similar to that of chymotrypsin C.
The process of cleaving a chemical compound by the addition of a molecule of water.
The physiological widening of BLOOD VESSELS by relaxing the underlying VASCULAR SMOOTH MUSCLE.
A cluster of convoluted capillaries beginning at each nephric tubule in the kidney and held together by connective tissue.
A characteristic feature of enzyme activity in relation to the kind of substrate on which the enzyme or catalytic molecule reacts.
Narrowing or occlusion of the RENAL ARTERY or arteries. It is due usually to ATHEROSCLEROSIS; FIBROMUSCULAR DYSPLASIA; THROMBOSIS; EMBOLISM, or external pressure. The reduced renal perfusion can lead to renovascular hypertension (HYPERTENSION, RENOVASCULAR).
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
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.
Derivatives of BENZOIC ACID. Included under this heading are a broad variety of acid forms, salts, esters, and amides that contain the carboxybenzene structure.
Either of the pair of organs occupying the cavity of the thorax that effect the aeration of the blood.
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.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Exogenous or endogenous compounds which inhibit SERINE ENDOPEPTIDASES.
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.
The hollow, muscular organ that maintains the circulation of the blood.
Benzopyrroles with the nitrogen at the number one carbon adjacent to the benzyl portion, in contrast to ISOINDOLES which have the nitrogen away from the six-membered ring.
Members of the class of compounds composed of AMINO ACIDS joined together by peptide bonds between adjacent amino acids into linear, branched or cyclical structures. OLIGOPEPTIDES are composed of approximately 2-12 amino acids. Polypeptides are composed of approximately 13 or more amino acids. PROTEINS are linear polypeptides that are normally synthesized on RIBOSOMES.
The flow of BLOOD through or around an organ or region of the body.
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.
Proteolytic enzymes from the serine endopeptidase family found in normal blood and urine. Specifically, Kallikreins are potent vasodilators and hypotensives and increase vascular permeability and affect smooth muscle. They act as infertility agents in men. Three forms are recognized, PLASMA KALLIKREIN (EC 3.4.21.34), TISSUE KALLIKREIN (EC 3.4.21.35), and PROSTATE-SPECIFIC ANTIGEN (EC 3.4.21.77).
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.
A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.
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).
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.
A direct-acting vasodilator that is used as an antihypertensive agent.
Drugs used to cause dilation of the blood vessels.
A structure, situated close to the intraventricular foramen, which induces DRINKING BEHAVIOR after stimulation with ANGIOTENSIN II.
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.
The vessels carrying blood away from the capillary beds.
A chelating agent that sequesters a variety of polyvalent cations such as CALCIUM. It is used in pharmaceutical manufacturing and as a food additive.
Injections made into a vein for therapeutic or experimental purposes.
Either of two extremities of four-footed non-primate land animals. It usually consists of a FEMUR; TIBIA; and FIBULA; tarsals; METATARSALS; and TOES. (From Storer et al., General Zoology, 6th ed, p73)
Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury.
Accumulation of a drug or chemical substance in various organs (including those not relevant to its pharmacologic or therapeutic action). This distribution depends on the blood flow or perfusion rate of the organ, the ability of the drug to penetrate organ membranes, tissue specificity, protein binding. The distribution is usually expressed as tissue to plasma ratios.
The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.
A widely used non-cardioselective beta-adrenergic antagonist. Propranolol has been used for MYOCARDIAL INFARCTION; ARRHYTHMIA; ANGINA PECTORIS; HYPERTENSION; HYPERTHYROIDISM; MIGRAINE; PHEOCHROMOCYTOMA; and ANXIETY but adverse effects instigate replacement by newer drugs.
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 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.
Isopropyl analog of EPINEPHRINE; beta-sympathomimetic that acts on the heart, bronchi, skeletal muscle, alimentary tract, etc. It is used mainly as bronchodilator and heart stimulant.
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.
The regular and simultaneous occurrence in a single interbreeding population of two or more discontinuous genotypes. The concept includes differences in genotypes ranging in size from a single nucleotide site (POLYMORPHISM, SINGLE NUCLEOTIDE) to large nucleotide sequences visible at a chromosomal level.
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.
A process leading to shortening and/or development of tension in muscle tissue. Muscle contraction occurs by a sliding filament mechanism whereby actin filaments slide inward among the myosin filaments.
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 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.
Any of various animals that constitute the family Suidae and comprise stout-bodied, short-legged omnivorous mammals with thick skin, usually covered with coarse bristles, a rather long mobile snout, and small tail. Included are the genera Babyrousa, Phacochoerus (wart hogs), and Sus, the latter containing the domestic pig (see SUS SCROFA).
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.
A group of lysosomal proteinases or endopeptidases found in aqueous extracts of a variety of animal tissues. They function optimally within an acidic pH range. The cathepsins occur as a variety of enzyme subtypes including SERINE PROTEASES; ASPARTIC PROTEINASES; and CYSTEINE PROTEASES.
Sodium chloride used in foods.
A method of measuring the effects of a biologically active substance using an intermediate in vivo or in vitro tissue or cell model under controlled conditions. It includes virulence studies in animal fetuses in utero, mouse convulsion bioassay of insulin, quantitation of tumor-initiator systems in mouse skin, calculation of potentiating effects of a hormonal factor in an isolated strip of contracting stomach muscle, etc.
Any of the ruminant mammals with curved horns in the genus Ovis, family Bovidae. They possess lachrymal grooves and interdigital glands, which are absent in GOATS.
A common name used for the genus Cavia. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research.
A method of studying a drug or procedure in which both the subjects and investigators are kept unaware of who is actually getting which specific treatment.
A subfamily in the family MURIDAE, comprising the hamsters. Four of the more common genera are Cricetus, CRICETULUS; MESOCRICETUS; and PHODOPUS.
The presence of proteins in the urine, an indicator of KIDNEY DISEASES.
The concentration of osmotically active particles in solution expressed in terms of osmoles of solute per liter of solution. Osmolality is expressed in terms of osmoles of solute per kilogram of solvent.
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.
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.
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.
An alpha-1 adrenergic agonist used as a mydriatic, nasal decongestant, and cardiotonic agent.
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.
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.
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 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)

Role of aromaticity of agonist switches of angiotensin II in the activation of the AT1 receptor. (1/927)

We have shown previously that the octapeptide angiotensin II (Ang II) activates the AT1 receptor through an induced-fit mechanism (Noda, K., Feng, Y. H., Liu, X. P., Saad, Y., Husain, A., and Karnik, S. S. (1996) Biochemistry 35, 16435-16442). In this activation process, interactions between Tyr4 and Phe8 of Ang II with Asn111 and His256 of the AT1 receptor, respectively, are essential for agonism. Here we show that aromaticity, primarily, and size, secondarily, of the Tyr4 side chain are important in activating the receptor. Activation analysis of AT1 receptor position 111 mutants by various Ang II position 4 analogues suggests that an amino-aromatic bonding interaction operates between the residue Asn111 of the AT1 receptor and Tyr4 of Ang II. Degree and potency of AT1 receptor activation by Ang II can be recreated by a reciprocal exchange of aromatic and amide groups between positions 4 and 111 of Ang II and the AT1 receptor, respectively. In several other bonding combinations, set up between Ang II position 4 analogues and receptor mutants, the gain of affinity is not accompanied by gain of function. Activation analysis of position 256 receptor mutants by Ang II position 8 analogues suggests that aromaticity of Phe8 and His256 side chains is crucial for receptor activation; however, a stacked rather than an amino-aromatic interaction appears to operate at this switch locus. Interaction between these residues, unlike the Tyr4:Asn111 interaction, plays an insignificant role in ligand docking.  (+info)

The subtype 2 of angiotensin II receptors and pressure-natriuresis in adult rat kidneys. (2/927)

The present work examined the effects of the subtype 2 of angiotensin II (AT2) receptors on the pressure-natriuresis using a new peptide agonist, and the possible involvement of cyclic guanosine 3', 5' monophosphate (cyclic GMP) in these effects. In adult anaesthetized rats (Inactin, 100 mg kg(-1), i.p.) deprived of endogenous angiotensin II by angiotensin converting enzyme inhibition (quinapril, 10 mg kg(-1), i.v.), T2-(Ang II 4-8)2 (TA), a highly specific AT2 receptor agonist (5, 10 and 30 microg kg(-1) min(-1), i.v.) or its solvent was infused in four groups. Renal functions were studied at renal perfusion pressures (RPP) of 90, 110 and 130 mmHg and urinary cyclic GMP excretion when RPP was at 130 mmHg. The effects of TA (10 microg kg(-1) min(-1)) were reassessed in animals pretreated with PD 123319 (PD, 50 microg kg(-1) min(-1), i.v.), an AT2 receptor antagonist and the action of the same dose of PD alone was also determined. Increases in RPP from 90 to 130 mmHg did not change renal blood flow (RBF) but induced 8 and 15 fold increases in urinary flow and sodium excretion respectively. The 5 microg kg(-1) min(-1) dose of TA was devoid of action. The 10 and 30 microg kg(-1) min(-1) doses did not alter total RBF and glomerular filtration rate, but blunted pressure-diuresis and natriuresis relationships. These effects were abolished by PD. TA decreased urinary cyclic GMP excretion. After pretreatment with PD, this decrease was reversed to an increase which was also observed in animals receiving PD alone. In conclusion, renal AT2 receptors oppose the sodium and water excretion induced by acute increases in blood pressure and this action cannot be directly explained by changes in cyclic GMP.  (+info)

Contractile effects by intracellular angiotensin II via receptors with a distinct pharmacological profile in rat aorta. (3/927)

1. We studied the effect of intracellular angiotensin II (Ang II) and related peptides on rat aortic contraction, whether this effect is pharmacologically distinguishable from that induced by extracellular stimulation, and determined the Ca2+ source involved. 2. Compounds were delivered into the cytoplasm of de-endothelized aorta rings using multilamellar liposomes. Contractions were normalized to the maximum obtained with phenylephrine (10(-5) M). 3. Intracellular administration of Ang II (incorporation range: 0.01-300 nmol mg(-1)) resulted in a dose-dependent contraction, insensitive to extracellular administration (10(-6) M) of the AT1 receptor antagonist CV11947, the AT2 receptor antagonist PD 123319, or the non-selective AT receptor antagonist and partial agonist saralasin ([Sar1,Val5,Ala8]-Ang II (P<0.05). 4. Intracellular administration of CV11947 or PD 123319 right shifted the dose-response curve about 1000 fold or 20 fold, respectively. PD 123319 was only effective if less than 30 nmol mg(-1) Ang II was incorporated. 5. Contraction was partially desensitized to a second intracellular Ang II addition after 45 min (P<0.05). 6. Intracellular administration of Ang I and saralasin also induced contraction (P<0.05). Both responses were sensitive to intracellular CV11947 (P<0.05), but insensitive to PD 123319. The response to Ang I was independent of intracellular captopril. 7. Contraction induced by extracellular application of Ang II and of Ang I was abolished by extracellular pre-treatment with saralasin or CV11947 (P<0.05), but not with PD 123319. Extracellular saralasin induced no contraction. 8. Intracellular Ang II induced contraction was not affected by pre-treatment with heparin filled liposomes, but completely abolished in Ca2+-free external medium. 9. These results support the existence of an intracellular binding site for Ang II in rat aorta. Intracellular stimulation induces contraction dependent on Ca2+-influx but not on Ins(1,4,5)P3 mediated release from intracellular Ca2+-stores. Intracellular Ang I and saralasin induce contraction, possibly via the same binding site. Pharmacological properties of this putative intracellular receptor are clearly different from extracellular stimulated AT1 receptors or intracellular angiotensin receptors postulated in other tissue.  (+info)

In vivo enzymatic assay reveals catalytic activity of the human renin precursor in tissues. (4/927)

The aspartyl protease renin is secreted into the circulation of mammals in 2 forms: the proteolytically processed active form of the enzyme and the precursor form, prorenin. Prorenin has no detectable enzymatic activity in the circulation, but it is the exclusive form of the enzyme produced by several tissues that also produce the other components of the renin enzymatic cascade (renin-angiotensin system). To test whether prorenin might be enzymatically active in these tissues, transgenic mice expressing the human renin substrate (angiotensinogen) exclusively in the pituitary gland were mated to mice expressing either active human renin or prorenin in the same tissue. Measurement of in vivo product formation in pituitary glands of double-transgenic mice revealed that human prorenin was enzymatically active, and Western blot analysis demonstrated that this prorenin was in the precursor form with its prosegment attached. This in vivo enzymatic assay demonstrates for the first time that human prorenin can be activated within tissues by nonproteolytic means, where it could contribute to the activity of a localized renin-angiotensin system.  (+info)

Effects of aminopeptidase P inhibition on kinin-mediated vasodepressor responses. (5/927)

We studied in anesthetized rats whether aminopeptidase P (AMP) may be involved in bradykinin (BK) metabolism and responses. For this we inhibited AMP with the specific inhibitor apstatin (Aps). Studies were done with Aps alone or together with the angiotensin-converting enzyme inhibitor lisinopril (Lis). Aps increased the vasodepressor response to an intravenous bolus of BK (400 ng/kg): vehicle, -3.0 +/- 0.7 mmHg; Aps, -7.8 +/- 0.7 mmHg (P < 0.01 vs. vehicle); Lis, -23.8 +/- 1.8 mmHg; Aps + Lis, -37.5 +/- 1.9 mmHg (P < 0.01 vs. Lis). Aps did not affect the vasodepressor response to BK given into the descending aorta. Plasma BK increased only in Aps + Lis-treated rats (in pg/ml): control, 48.0 +/- 1.4; Lis, 57.5 +/- 7.6; Aps + Lis, 121. 8 +/- 30.6 (P < 0.05 vs. control or Lis), whereas in rats infused with BK (400 ng. kg-1. min-1 for 5 min), Aps increased plasma BK (in pg/ml): control, 51.9 +/- 2.5; Aps, 83.5 +/- 20.5; Lis, 725 +/- 225; Aps + Lis, 1,668 +/- 318 (P < 0.05, Aps vs. control and Lis vs. Aps + Lis). In rats with aortic coarctation hypertension, the acute antihypertensive effects of Aps plus Lis were greater than Lis alone (P < 0.01). Hoe-140, a BK B2-receptor antagonist, abolished the difference. We concluded that in the rat AMP contributes to regulation of BK metabolism and responses.  (+info)

In vivo assessment of captopril selectivity of angiotensin I-converting enzyme inhibition: differential inhibition of acetyl-ser-asp-lys-pro and angiotensin I hydrolysis. (6/927)

Angiotensin I-converting enzyme (ACE) is a zinc metallopeptidase that plays a major role in blood pressure regulation. The demonstration that the hemoregulatory peptide acetyl-Ser-Asp-Lys-Pro (AcSDKP) is a natural and specific substrate of the N-active site of ACE suggests that this enzyme may have a new physiological role such as the modulation of hematopoietic stem cells. In vitro studies have shown that ACE inhibitors displayed various potencies in inhibiting the degradation of different natural or synthetic substrates of ACE, among which captopril inhibits AcSDKP hydrolysis more potently than angiotensin I hydrolysis. To look for this selectivity in vivo, we investigated the pharmacodynamic effect of increasing doses of captopril (0.01-10 mg/kg) during the 90 min after i.v. administration to spontaneously hypertensive rats. Plasma and urinary AcSDKP levels were measured. The renin-angiotensin system was evaluated by measurements of ACE activity in plasma samples, using the synthetic substrate Hip-His-Leu, by determinations of plasma renin concentrations and measurements of arterial blood pressure. The results showed that captopril (0.01-0.3 mg/kg) selectively inhibited AcSDKP hydrolysis, with limited effects on the renin-angiotensin system. AcSDKP levels in plasma and urine rose to a plateau 4 times the basal level for doses more than 0.3 mg/kg. All of the parameters reflecting the renin-angiotensin system were significantly affected at doses of 1 and 10 mg/kg. The present study therefore confirms that captopril can be used to protect hematopoietic stem cells during antitumor chemotherapy while having only a limited effect on cardiovascular homeostasis.  (+info)

Angiotensin-converting enzyme-independent contraction to angiotensin I in human resistance arteries. (7/927)

BACKGROUND: In vitro studies of myocardial tissue suggest that angiotensin II (Ang II) may be generated by both ACE and chymase. A similar dual pathway may exist in the vasculature. We studied the effects of ACE and chymase inhibitors on the contractile response to angiotensin I (Ang I) in human resistance arteries to investigate ACE-independent generation of Ang II. METHODS AND RESULTS: Subcutaneous resistance arteries (250 to 350 microm) were obtained from gluteal biopsies from volunteers and New Zealand White rabbits and mounted on a wire myograph. Contractile ability was tested with high-potassium depolarization and norepinephrine 10 micromol/L and endothelial integrity by relaxation to acetylcholine 3 micromol/L. Cumulative concentration-response curves were constructed for Ang I in the presence of enalaprilat 1 micromol/L, chymostatin 10 micromol/L, or both inhibitors together. In the rabbit, enalaprilat completely inhibited the Ang I response. In human vessels, enalaprilat or chymostatin alone had no effect, but the combination of enalaprilat and chymostatin almost completely inhibited the response to Ang I. CONCLUSIONS: A dual pathway for Ang II generation exists in human resistance arteries, mediated by ACE and a chymostatin-sensitive enzyme, probably chymase. We confirm that a marked species difference exists in the mechanism of Ang II generation between the human and the rabbit. More efficacious suppression of the renin-angiotensin system may require development of novel enzyme inhibitors or combinations of currently available drugs.  (+info)

Functional evidence for subfornical organ-intrinsic conversion of angiotensin I to angiotensin II. (8/927)

Using extracellular electrophysiological recording in an in vitro slice preparation, we investigated whether ANG I can be locally converted to the functionally active ANG II within the rat subfornical organ (SFO). ANG I and ANG II (10(-8)-10(-7) M) excited approximately 75% of all neurons tested with both peptides (n = 25); the remainder were insensitive. The increase in firing rate and the duration and the latency of the responses of identical neurons, superfused with equimolar concentrations of ANG I and ANG II, were not different. The threshold concentrations of the ANG I- and ANG II-induced excitations were both 10(-9) M. Inhibition of the angiotensin-converting enzyme by captopril (10(-4) M; n = 8) completely blocked the ANG I-induced excitation, a 10-fold lower dose was only effective in two of four neurons. The AT1-receptor antagonist losartan (10(-5) M; n = 6) abolished the excitation caused by ANG I and ANG II. Subcutaneous injections of equimolar doses of ANG I and ANG II (200 microliters; 2 x 10(-4) M) in water-sated rats similarly increased water intake by 2.4 +/- 0.5 (n = 16) and 2. 7 +/- 0.4 ml (n = 20) after 1 h, respectively. Control rats receiving saline drank 0.07 +/- 0.06 ml under these conditions. Pretreatment with a low dose of captopril (2.3 x 10(-3) M) 10 min before the injection of ANG I caused a water intake of 2.8 +/- 0.5 ml (n = 10), whereas a high dose of captopril (4.6 x 10(-1) M) suppressed the dipsogenic response of ANG I entirely (n = 11). These data provide direct functional evidence for an SFO-intrinsic renin-angiotensin system (RAS) and underline the importance of the SFO as a central nervous interface connecting the peripheral with the central RAS.  (+info)

P18 Angiotensin-(1-7)[Ang-(1-7)] is a bioactive component of the renin-angiotensin system (RAS), which has depressor, vasodilatory, and antihypertensive actions. In normal pregnancy we questioned whether the known rise in plasma Ang II is counterbalanced by an increase in plasma Ang-(1-7) and whether plasma Ang-(1-7)levels are decreased in preeclampsia and may thus be a factor involved in the development of hypertension. Nulliparous preeclamptic patients (PREE) and third trimester normotensive pregnant contols (NPC)(matched for parity, race, and gestational age) were enrolled (n=15/group). A nonpregnant group (CON)(n=15) was also included for comparison. PREE had no previous history of hypertension. Mean gestational age of preeclamptic subjects was 33.9±1.2 vs 33.7±1.2 weeks for normotensive pregnant subjects (n.s.,p=0.9). PREE subjects had significant hypertension (159±3/98±2 mmHg) and all had ≥3† proteinuria. Plasma Ang I, Ang II, and renin activity (PRA) were significantly elevated in ...
Angiotensin I 3 x 10 ug $55.00 - Angiotensin I is a purified peptide used for calibration of mass spectometers in MALDI-MS or ESI-MS. -
Angiotensin-(1-12) [Ang-(1-12)], C-terminally extended form of Ang I, is an alternative precursor of Ang II. Although angiotensinogen, a precursor of both Ang I and Ang-(1-12), is reportedly one of markers of kidney disease, little is known about role of Ang-(1-12) in pathological status especially in human. To address this issue, we measured plasma and urinary Ang-(1-12) by enzyme immunoassay in 4 healthy volunteers and 15 patients with biopsy-proven chronic kidney diseases (CKD). CKD group included minor glomerular abnormality (n=3), IgA nephropathy (n=8), minimal change nephritic syndrome (n=4). Ang-(1-12) level was 55-fold higher in urine than in plasma (Figure; 4.12±1.55 vs 0.075±0.006 ng/mL, P,0.05). Neither plasma Ang-(1-12) nor urinary Ang-(1-12) was correlated with blood pressure. Plasma Ang-(1-12) was positively correlated with urinary protein and tended to be negatively correlated with estimated glomerular filtration ratio (eGFR; Figure). Plasma Ang-(1-12) was higher in the CKD ...
The angiotensin type 2 receptor (AT2R) and the receptor Mas are components of the protective arms of the renin-angiotensin system (RAS), i.e. they both mediate tissue protective and regenerative actions. The spectrum of actions of these two receptors and their signalling mechanisms display striking similarities. Moreover, in some instances, antagonists for one receptor are able to inhibit the action of agonists for the respective other receptor. These observations suggest that there may be a functional or even physical interaction of both receptors. This article discusses potential mechanisms underlying the phenomenon of blockade of angiotensin-(1-7) [Ang-(1-7)] actions by AT2R antagonists and vice versa. Such mechanisms may comprise dimerization of the receptors or dimerization-independent mechanisms such as lack of specificity of the receptor ligands used in the experiments or involvement of the Ang-(1-7) metabolite alamandine and its receptor MrgD in the observed effects. We conclude that ...
Peptides , Angiotensins and Related Peptides , ClearPoint Angiotensin I, human, 13C and 15N labeled; This peptide is angiontensin I (Ang I) with valine and isoleucine universally labeled with 13C and N. Ang I is a precursor to Ang II, which has been implicated in cardiovascular functions, cell proliferation, fibrosis, and apoptosis. The 10-mer Ang I peptide is converted to Ang II through the cleavage of the Phe8-His9 bond of Ang I by angiotensin-converting enzyme (ACE) or human chymase.; DR-V*-Y-I*-HPFHL [Val* = Val(U-13C5,15N); Ile* = Ile(U-13C6,15N)]; H-Asp-Arg-Val*-Tyr-Ile*-His-Pro-Phe-His-Leu-OH [Val* = Val(U-13C5,15N); Ile* = Ile(U-13C6,15N)]
Recent progress in cardiovascular therapy suggests that stimulation of Angiotensin Converting Enzyme 2 (ACE2), production of Angiotensin-(1-7) Ang-(1-7), and activation of the Ang-(1-7) receptor, Mas, are viable targets for disease prevention and treatment. The ACE2/Ang-(1-7)/Mas axis has been shown to counteract many of the physiological effects of the Angiotensin II (Ang II) Type 1 Receptor (AT1R), including vasoconstrictor and proliferative actions. In addition, activation of the ACE2/Ang-(1-7)/Mas axis also attenuates many of the pathophysiological states that involve increased production of Ang II by Angiotensin Converting Enzyme (ACE), and subsequent activation of the AT1R (ACE/Ang II/AT1R axis). For example, many studies targeting the ACE2/Ang-(1-7)/Mas axis have revealed its broad therapeutic potential for the treatment of hypertension, hypertension-related pathology, myocardial infarction, and heart failure. Furthermore, ACE2 can form endogenous Ang-(1-7) from Ang II and has recently ...
BioAssay record AID 37650 submitted by ChEMBL: Tested for inhibitory concentration that causes inhibition of Angiotensin I converting enzyme obtained from rabbit lung acetone powder extract).
|p|AVE 0991 is an agonist of angiotensin-(1-7) receptor [1].|/p||p|As an ang-(1-7) mimic, AVE0991 acts as a nonpeptide agonist of angiotensin-(1-7) receptor. In water-loaded mice (C57BL/6), AVE0991(0.58 nmol/g)produces a significant decrease of water dier
G protein-coupled receptor Mas1 is a receptor for angiotensin (Ang)-(1-7), and ACE2/ Ang-(1-7)/MAS1 receptor axis have been shown to antagonize ACE1/Ang-II/AT1 receptor axis. However, this idea recently looks to become skeptical, and the physiological role of MAS1 in the hearts remains to be determined. C57BL-Tg(alpha-MHC-MAS)A and B overexpress mouse MAS1 gene in cardiomyocytes and die earlier due to heart failure. C57BL-Tg(alpha-MHC-MAS) B mice express MAS1 gene much more highly than A mice, and careful breeding is necessary ...
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Monoklonale und polyklonale Angiotensin I Converting Enzyme 1 Antikörper für viele Methoden. Ausgesuchte Qualitäts-Hersteller für Angiotensin I Converting Enzyme 1 Antikörper. Hier bestellen.
Wang X, Sirianni A, Pei Z, Cormier K, Smith K, Jiang J, Zhou S, Wang H, Zhao R, Yano H, Kim JE, Li W, Kristal BS, Ferrante RJ, Friedlander RM (2011). J Neurosci, 31(41):14496-507
How is Ang I)-converting enzyme abbreviated? ACE stands for Ang I)-converting enzyme. ACE is defined as Ang I)-converting enzyme rarely.
ACE-hæmmere hæmmer enzymet Angiotensin Converting Enzyme og dermed omdannelsen af angiotensin I til II, hvorved universel vasodilatation uden sympatikusaktivering indtræder.
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TY - JOUR. T1 - A peptide from corn gluten hydrolysate that is inhibitory toward angiotensin I converting enzyme. AU - Suh, Hyung Joo. AU - Whang, J. H.. AU - Lee, H.. PY - 1999/12/1. Y1 - 1999/12/1. N2 - A peptide (F4) that inhibits angiotensin I converting enzyme (ACE) was isolated from corn gluten hydrolysate prepared with Pescalase, a serine protease from Bacillus licheniformis. The N-terminal amino acid sequence of F4 was Pro-Ser-Gly-Gln-Tyr-Tyr, having the IC50 value of 0.1 mM. The peptide (F4), at 30 mg kg-1 body weight of rat, antagonized the rats pressor response to angiotensin I.. AB - A peptide (F4) that inhibits angiotensin I converting enzyme (ACE) was isolated from corn gluten hydrolysate prepared with Pescalase, a serine protease from Bacillus licheniformis. The N-terminal amino acid sequence of F4 was Pro-Ser-Gly-Gln-Tyr-Tyr, having the IC50 value of 0.1 mM. The peptide (F4), at 30 mg kg-1 body weight of rat, antagonized the rats pressor response to angiotensin I.. KW - ...
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 ...
TY - JOUR. T1 - Val-tyr, an Angiotensin I Converting Enzyme Inhibitor from Sardines that have Resistance to Gastrointestinal Proteases. AU - Seki, Eiji. AU - Osajima, Katsuhiro. AU - Matsufuji, Hiroshi. AU - Matsui, Toshiro. AU - Osajima, Yutaka. PY - 1995/1/1. Y1 - 1995/1/1. N2 - The NH2-terminal residue of a dipeptide is an important determinant of the resistance to peptidases of porcine small mucosa. NH2-terminal Val or Ile, and COOH-terminal Trp or Tyr dipeptides had higher angiotensin I converting enzyme(ACE)inhibitory activity and digestive resistance than other dipeptides. We defined Val-Tyr as a main inhibitor in alkaline protease hydrolyzates from sardines. Attempts to isolate and measurement of Val-Tyr were done from the short chain peptides that reduced blood pressure. The content of Val-Tyr was 51 mg per 100 g of the short chain peptides, represented 1.3% of the total ACE inhibitory activity of the short chain peptides. Isolated Val-Tyr was resistant to gastrointestinal proteases. ...
OBJECTIVE Obesity promotes hypertension, but it is unclear if sex differences exist in obesity-related hypertension. Angiotensin converting enzyme 2 (ACE2) converts angiotensin II (AngII) to angiotensin-(1-7) (Ang-[1-7]), controlling peptide balance. We hypothesized that tissue-specific regulation of ACE2 by high-fat (HF) feeding and sex hormones contributes to sex differences in obesity-hypertension. METHODS AND RESULTS HF-fed females gained more body weight and fat mass than males. HF-fed males exhibiting reduced kidney ACE2 activity had increased plasma angiotensin II levels and decreased plasma Ang-(1-7) levels. In contrast, HF-fed females exhibiting elevated adipose ACE2 activity had increased plasma Ang-(1-7) levels. HF-fed males had elevated systolic and diastolic blood pressure that were abolished by losartan. In contrast, HF-fed females did not exhibit increased systolic blood pressure until females were administered the Ang-(1-7) receptor antagonist, D-Ala-Ang-(1-7). Deficiency of ACE2
Ang-(1-7) [angiotensin-(1-7)] constitutes an important functional end-product of the RAS (renin-angiotensin system) endogenously formed from AngI (angiotensin I) or AngII (angiotensin II) through the catalytic activity of ACE2 (angiotensin-converting enzyme 2), prolyl carboxypeptidase, neutral endopeptidase or other endopeptidases. Ang-(1-7) lacks the pressor, dipsogenic or stimulatory effect on aldosterone release characteristic of AngII. In contrast, it produces vasodilation, natriuresis and diuresis, and inhibits angiogenesis and cell growth. At the central level, Ang-(1-7) acts at sites involved in the control of cardiovascular function, thus contributing to blood pressure regulation. This action may result from its inhibitory neuromodulatory action on NE [noradrenaline (norepinephrine)] levels at the synaptic cleft, i.e. Ang-(1-7) reduces NE release and synthesis, whereas it causes an increase in NE transporter expression, contributing in this way to central NE neuromodulation. Thus, by ...
Anti-Human Angiotensin I Antibody, clone Ang E9 (BGN/KA/4H) , Mouse Anti-Human Monoclonal Antibody validated in E (ABD10296), Abgent
Malena Pérez, Larissa Martins, Murilo Dias, Camila Pereira, Jefferson Leite, et al.. Interleukin‐17/interleukin‐17 receptor axis elicits intestinal neutrophil migration, restrains gut dysbiosis and lipopolysaccharide translocation in high‐fat diet‐induced metabolic syndrome model. Immunology, Wiley, 2019, 156 (4), pp.339-355. ⟨10.1111/imm.13028⟩. ⟨hal-02126376⟩ ...
1. A synthetic 3-([14C]valine)-labelled tetradecapeptide renin substrate was used to measure renin concentration. Renin liberated 14C-labelled angiotensin I, which was separated from the labelled substrate by paper chromatography. The conversion of substrate into angiotensin I was quantitated by liquid-scintillation counting of radioactivity. 2. The rate of conversion of the substrate into angiotensin I was shown to be linearly related to renin concentration and time under suitable conditions. Angiotensin generation measured in this system agrees well with that measured by bioassay. 3. It is suggested that the use of a pure substrate offers advantages that include the standardization of current units of renin measurement.. ...
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PRIMARY OBJECTIVES:. I. To evaluate the response rate of chemotherapy-refractory sarcomas to 20 mg per day of single-agent Ang(Angiotensin)-(1-7) or 10 mg per day of single-agent Ang-(1-7) if excessive toxicity is observed at the 20 mg dose.. II. To evaluate toxicities associated with single-agent Ang-(1-7) when given to patients with chemotherapy-refractory sarcomas.. SECONDARY OBJECTIVES:. I. To assess time to progression (TTP) and overall survival (OS) in patients treated with Ang-(1-7).. II. To evaluate accumulation of Ang-(1-7) after 21 days of continuous treatment and quantify changes in plasma levels of angiogenic peptides including placental growth factor (PlGF).. OUTLINE:. Patients receive therapeutic angiotensin-(1-7) subcutaneously (SC) once daily in the absence of disease progression or unacceptable toxicity.. After completion of study treatment, patients are followed every 3 months for 2 years, every 6 months for 3 years, and then annually thereafter. ...
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ACE inhibitors prevent the conversion of angiotensin I to angiotensin II by angiotensin converting enzyme (ACE) in the lungs, in turn reducing effects of angiotensin II. These effects include:. ...
Common Name metronidazole In this put ~s into factsheet: How does Metronidazole by AA Pharma be in action? What will it do for me? How should I conversion to an act Metronidazole by AA Pharma ...
ACE - ACE (untagged)-Human angiotensin I converting enzyme (peptidyl-dipeptidase A) 1 (ACE), transcript variant 1 available for purchase from OriGene - Your Gene Company.
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Complete information for ACE gene (Protein Coding), Angiotensin I Converting Enzyme, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
Complete information for ACE gene (Protein Coding), Angiotensin I Converting Enzyme, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
sp:ACE_MOUSE] Ace, AW208573, CD143; angiotensin I converting enzyme (peptidyl-dipeptidase A) 1; K01283 peptidyl-dipeptidase A [EC:3.4.15.1] ...
sp:ACE_MOUSE] Ace, AW208573, CD143; angiotensin I converting enzyme (peptidyl-dipeptidase A) 1; K01283 peptidyl-dipeptidase A [EC:3.4.15.1] ...
As we celebrate Fathers Day today, bringing Good Dadhood to a close for another year, here are three splendid poems by Angi Holden, with a great photo ... to finish GD2021 with a flourish! Is He Your Real Dad? She understood the question,its roots in biology and DNA,though its significance hadalways seemed misplaced. Her friend…
Immune regulation plays a critical role in controlling potentially dangerous inflammation and maintaining health. The Fas ligand/Fas receptor axis has been studied extensively as a mechanism of killin
Effect of ANG I co-infused with A. gangetica on the SBP (a), DBP (b), MAP (c), and HR (d). Values are presented as mean ± SEM. * indicates statistical signific
AngII (angiotensin II), ACE (angiotensin I-converting enzyme) and the AT(1) receptor (AngII type I receptor) are associated with the inflammatory process and microvascular dysfunction of AKI (acute kidney injury) induced by renal I/R (ischaemia/reperfusion). However, Ang-(1-7) [angiotensin-(1-7)], ACE2 (angiotensin I-converting enzyme 2) and the Mas receptor also play a role in renal disease models. Therefore, in the present study, we have examined the renal profile of Ang-(1-7), ACE2 and the Mas receptor in renal I/R and compared them with that of AngII, ACE and the AT(1) receptor. Male Wistar rats were submitted to left nephrectomy and ischaemia (45 min) followed by reperfusion (2 or 4 h) in the right kidney. At 4 h of reperfusion, renal AngII was increased (P , 0.01) and renal Ang-(1-7) was decreased substantially (P , 0.05), although plasma levels of both angiotensins were unchanged. in addition, renal I/R decreased the renal mRNA expression of renin (P , 0.05), AT(1) receptors (P , 0.001) ...
Looking for online definition of angi(o)- in the Medical Dictionary? angi(o)- explanation free. What is angi(o)-? Meaning of angi(o)- medical term. What does angi(o)- mean?
Background: The renin angiotensin system has become the focus of recent interest in stroke research as accumulating evidence indicates that activation of the angiotensin converting enzyme 2/angiotensin-(1-7)/mas (ACE2-Ang-(1-7)-Mas) axis exerts neuroprotective benefit in animal stroke models. Pre- and post-stroke activation of this axis by intracerebroventricular infusion of Ang-(1-7) reduces infarct size and improves neurological function in rats. The recent development of an orally active formulation of Ang-(1-7) in hydroxypropylβ-cyclodextrin [HPβCD/Ang-(1-7)] provides a non-invasive avenue for testing the efficacy of systemic post-stroke administration of Ang-(1-7). We tested the hypothesis that post-stroke oral gavage of HPβCD/Ang-(1-7) exerts neuroprotection in a rat model of ischemic stroke.. Methods: Male SD rats underwent ischemic stroke by endothelin-1-induced middle cerebral artery occlusion and were randomly divided into 2 groups of 12 each that received oral gavages of dH2O or ...
Preeclampsia, a multisystemic syndrome, is an important cause of maternal and fetal morbidity and mortality. A mismatch between the vasoconstrictor peptide, Ang II and the vasodilator Ang-(1-7)/Mas axis may lead to vasoconstriction and endothelial dysfunction. Moreover, Ang-(1-7) is decreased in preeclamptic patients. However it is not clear whether the reduction in the activity of the Ang-(1-7)/Mas axis is a contributing factor for development of preeclampsia. The aim of this study was to evaluate whether Mas-deficiency is involved in pregnancy-induced hypertension. Thirteen weeks old Mas−/− and WT female mice were used. Values of blood pressure versus pregnancy time were measured. After anesthesia by inhalation of 2% isoflurane, pups were collected and weighted. Pregnant Mas−/− mice presented increased blood pressure (96 ± 3 before fertilization to 129 ± 5 on 18th day in KO and 95 ± 3 before fertilization to 111 ± 7 mmHg at day 18 in WT), associated with 36% intrauterine growth ...
BACKGROUND: The relationship between circulating levels of angiotensinogen and hypertension in the epidemiologic setting has not been studied much. Recent findings related to the association between hypertension and polymorphisms of the angiotensinogen gene have generated new interest in this potential pathway to hypertension. OBJECTIVES: To examine environmental factors associated with levels of circulating angiotensinogen as determinants of hypertension in populations of African origin. METHODS: We recruited 1557 participants from communities in Nigeria (n = 611), Zimbabwe (n = 161), Jamaica (n = 476), and Maywood, Illinois, USA (n = 309). RESULTS: Mean angiotensinogen levels varied widely across groups (Nigeria 1381 ng/ml angiotensin I generated, Zimbabwe 1638 ng/ml angiotensin and I generated Jamaica 1801 ng/ml angiotensin I generated, and Maywood 2039 ng/ml angiotensin I generated). Average body mass index was highly correlated to angiotensinogen level across the population samples, ...
The central role of angiotensin I-converting enzyme in vertebrate pathophysiology.: Genomic epidemiologic data, increasingly supported by clinical outcomes resu
The renin-angiotensin system (RAS) is recognized by its pivotal role on cardiovascular regulation and more recently also on metabolism. Angiotensin-(1-7) has b...
Benter, I F.; Ferrario, C M.; Morris, Mariana; and Diz, D I., Antihypertensive actions of angiotensin-(1-7) in spontaneously hypertensive rats. (1995). College of Osteopathic Medicine Faculty Articles. 614 ...
RvD2 is a potent immunoresolvent and controller of leukocyte traffic and is protective in a wide range of disease models, including airway and gastrointestinal inflammation (8, 19). In the present study, we demonstrated that RvD2-DRV2 interaction protected mice from sepsis, preventing hypothermia, enhancing phagocytosis-based bacterial clearance, and increasing survival. In infectious exudates collected from sepsis, DRV2-KO gave increased levels of PG, LT, and TX, and reduced SPM (i.e., RvD1, RvD3, AT-RvD1, AT-RvD3) in infectious exudates (Fig. 2). These results are consistent with those found in E. coli peritoneal infections where selected SPM, including AT-RvD1, RvD2, RvD5, PD1, and AT-PD1, were significantly reduced in DRV2-KO mice compared with WT mice. DRV2-KO also gave increased amounts of TX (30), indicating that DRV2-KO is associated with heightened inflammatory status during bacterial infection. Of interest, mice deficient in an RvD1 receptor, namely ALX, also gave heightened disease ...
Discuss the medication that may have caused him to deteriorate - What is the enzyme that converts angiotensin I to angiotensin II and where is this normally
OBJECTIVE: To compare the acute hypotensive effects of three different methods of inhibiting the renin-angiotensin system in a primate model of cyclosporin-induced hypertension. DESIGN: The effects of maximally effective doses of an angiotensin I con
In the present study, we showed that ANG II markedly reduced ACE2 in cultured rat VSMCs through a regulatory process mediated by the angiotensin type 1 (AT1) receptor. Treatment of VSMCs with ANG-(1-7), the product of ACE2 hydrolysis of ANG II, did not affect ACE2 mRNA; however, ANG-(1-7) prevented the ANG II-mediated reduction in ACE2 mRNA. Addition of [d-Ala7]-ANG-(1-7), a selective AT(1-7) receptor antagonist, blocked the inhibitory actions of ANG-(1-7). These data are the first to demonstrate opposing transcriptional regulation of ACE2 by ANG II and ANG-(1-7) in VSMCs and suggest a complex interplay between these two peptides that is mediated by distinct receptor pathways. ANG-(1-7) prevented the ANG II-mediated reduction in VSMC ACE2 mRNA, and the inhibitory action of the heptapeptide was blocked by the addition of [d-Ala7]-ANG-(1-7). Since ACE2 preferentially converts ANG II to ANG-(1-7), downregulation of the enzyme by ANG II constitutes a positive feedback system that may favor ANG ...
LOPEZ VERRILLI, María A; RODRIGUEZ FERMEPIN, Martín; FERNANDEZ, Belisario E y GIRONACCI, Mariela M. Role of Angiotensin (1-7) in Neuronal Norepinephrine Reuptake in Hypertension. Rev. argent. cardiol. [online]. 2010, vol.78, n.2, pp. 151-155. ISSN 1850-3748.. We have previously demonstrated that angiotensin (Ang)-(1-7) decreases the release and synthesis of norepinephrine (NE) in spontaneously hypertensive rats (SHR). In the present study, we have investigated the effect of Ang-(1-7) on neuronal NE reuptake and the expression of NE trans-porter (NET), responsible for eliminating NE from the syn-aptic cleft. Although Ang-(1-7) does not have an acute effect on NE neuronal reuptake, it plays a role in stimulating the protein content of the NET in the long-term. Ang-(1-7) activates Mas receptor and stimulates protein synthesis de novo of the transporter. In this way, Ang-(1-7) would contribute to blood pressure control through the regulation of NE levels in the synaptic cleft.. Palabras clave : ...
Zestril is the drug that affect cardiovascular system. The drug active substance with the same name, belongs to the group of APF inhibitors. This drug is similar to Dirotone. In other words, Zestril impedes the transformation of Angiotensin I into Angiotensin II, which results in the pressure drop in the major vessels (mostly in the arteries). On the contrary, the blood flow to the capillaries is increasing. You can note the maximum reduction of blood pressure in about 6 hours after the drug intake. Zestril improves the condition of heart muscle. In the long-term use, hypertrophic myocardium returns to its natural state. Besides, this drug can reduce the excretion of protein with urine (due to the improved state of filtering tissue in kidneys).. ...
Altace (Ramipril) is used in the treatment of high blood pressure. Ramipril works by preventing the conversion of a chemical in your blood called angiotensin I into a more potent substance that inc...
Hi Angi,. Read your post and noticed you were from Upstate SC. I live in Sandy Springs (between Anderson and Clemson) I am a Lifetime member since 2005. Noticed that you are just a few pounds from your goal weight. Congratulations! You have really done well and will continue to do so, I know.. ...
mas mababa ang stress - delikado o nakakatulong? Ang usong produkto sa pagsusuri: Bago at pagkatapos na mga larawan, posibleng resulta at karanasan sa epekto at negatibong epekto.
The decapeptide is known as angiotensin I.. *Angiotensin I is then converted to an octapeptide, angiotensin II by angiotensin- ... Angiotensin II receptor antagonists, also known as angiotensin receptor blockers, can be used to prevent angiotensin II from ... It is believed that angiotensin I may have some minor activity, but angiotensin II is the major bio-active product. Angiotensin ... Angiotensin I is subsequently converted to angiotensin II by the angiotensin-converting enzyme (ACE) found on the surface of ...
Work on angiotensin blockers[edit]. Watkins left Johns Hopkins in 1973 for Harvard University where he researched the use of ... Angiotensin blockers were created in order to avoid the side effects of ACE inhibitors, which were previously the drug of ... In addition, his work on angiotensin blockers has helped many patients in need of treatment for congestive heart failure, even ... Two years after his research on angiotensin blockers at Harvard, Watkins returned to Johns Hopkins and joined the admissions ...
... is also thought to be the cause of the dry cough in some patients on widely prescribed angiotensin-converting enzyme ... In humans, bradykinin is broken down by three kininases: angiotensin-converting enzyme (ACE), aminopeptidase P (APP), and ... Kuoppala A, Lindstedt KA, Saarinen J, Kovanen PT, Kokkonen JO (April 2000). "Inactivation of bradykinin by angiotensin- ... in which case angiotensin II receptor antagonists (ARBs) are the next line of treatment. ...
... is an aminonucleoside antibiotic, derived from the Streptomyces alboniger bacterium,[1] that causes premature chain termination during translation taking place in the ribosome. Part of the molecule resembles the 3' end of the aminoacylated tRNA. It enters the A site and transfers to the growing chain, causing the formation of a puromycylated nascent chain and premature chain release.[2] The exact mechanism of action is unknown at this time but the 3' position contains an amide linkage instead of the normal ester linkage of tRNA. That makes the molecule much more resistant to hydrolysis and stops the ribosome. Puromycin is selective for either prokaryotes or eukaryotes. Also of note, puromycin is critical in mRNA display. In this reaction, a puromycin molecule is chemically attached to the end of an mRNA template, which is then translated into protein. The puromycin can then form a covalent link to the growing peptide chain allowing the mRNA to be physically linked to its translational ...
In humans, the IGF2 gene is located on chromosome 11p15.5, a region which contains numerous imprinted genes. In mice this homologous region is found at distal chromosome 7. In both organisms, Igf2 is imprinted, with expression resulting favourably from the paternally inherited allele. However, in some human brain regions a loss of imprinting occurs resulting in both IGF2 and H19 being transcribed from both parental alleles.[6] The protein CTCF is involved in repressing expression of the gene, by binding to the H19 imprinting control region (ICR) along with Differentially-methylated Region-1 (DMR1) and Matrix Attachment Region −3 (MAR3). These three DNA sequences bind to CTCF in a way that limits downstream enhancer access to the Igf2 region. The mechanism in which CTCF binds to these regions is currently unknown, but could include either a direct DNA-CTCF interaction or it could possibly be mediated by other proteins. In mammals (mice, humans, pigs), only the allele for insulin-like growth ...
"Randomized Trial of Icatibant for Angiotensin-Converting Enzyme Inhibitor-Induced Upper Airway Angioedema". The Journal of ...
... (GLP-2) is a 33 amino acid peptide with the sequence HADGSFSDEMNTILDNLAARDFINWLIQTKITD (see Proteinogenic amino acid) in humans. GLP-2 is created by specific post-translational proteolytic cleavage of proglucagon in a process that also liberates the related glucagon-like peptide-1 (GLP-1). GLP-2 is produced by the intestinal endocrine L cell and by various neurons in the central nervous system. Intestinal GLP-2 is co-secreted along with GLP-1 upon nutrient ingestion. When externally administered, GLP-2 produces a number of effects in humans and rodents, including intestinal growth, enhancement of intestinal function, reduction in bone breakdown and neuroprotection. GLP-2 may act in an endocrine fashion to link intestinal growth and metabolism with nutrient intake. GLP-2 and related analogs may be treatments for short bowel syndrome, Crohn's disease, osteoporosis and as adjuvant therapy during cancer chemotherapy. ...
Cholecystokinin tetrapeptide (CCK-4, Trp-Met-Asp-Phe-NH2) is a peptide fragment derived from the larger peptide hormone cholecystokinin. Unlike cholecystokin which has a variety of roles in the gastrointestinal system as well as central nervous system effects, CCK-4 acts primarily in the brain as an anxiogenic, although it does retain some GI effects, but not as much as CCK-8 or the full length polypeptide CCK-58. CCK-4 reliably causes severe anxiety symptoms when administered to humans in a dose of as little as 50μg,[1] and is commonly used in scientific research to induce panic attacks for the purpose of testing new anxiolytic drugs.[2][3][4][5] Since it is a peptide, CCK-4 must be administered by injection, and is rapidly broken down once inside the body so has only a short duration of action,[6] although numerous synthetic analogues with modified properties are known.[7][8][9][10][11][12][13][14][15][16][17] ...
... (INN) (code name MK-0974) is a calcitonin gene-related peptide receptor antagonist which was an investigational drug for the acute treatment and prevention of migraine, developed by Merck & Co..[1] In the acute treatment of migraine, it was found to have equal potency to rizatriptan[2] and zolmitriptan[3] A Phase IIa clinical trial studying telcagepant for the prophylaxis of episodic migraine was stopped on March 26, 2009 after the "identification of two patients with significant elevations in serum transaminases".[4] A memo to study locations stated that telcagepant had preliminarily been reported to increase the hepatic liver enzyme alanine transaminase (ALT) levels in "11 out of 660 randomized (double-blinded) study participants." All study participants were told to stop taking the medication.[5] On July 2011, Merck announced that it had discontinued development of telcagepant.[6] ...
The neuropeptide galanin elicits a range of biological effects by interaction with specific G-protein-coupled receptors. Galanin receptors are seven-trans membrane proteins shown to activate a variety of intracellular second-messenger pathways. GALR1 inhibits adenylyl cyclase via a G protein of the GI/GO family. GALR1 is widely expressed in the brain and spinal cord, as well as in peripheral sites such as the small intestine and heart.[5]. ...
Angiotensin. *Bombesin. *Calcitonin gene-related peptide. *Carnosine. *Cocaine- and amphetamine-regulated transcript ...
A decapeptide has ten amino acids (e.g., gonadotropin-releasing hormone & angiotensin I). ...
... , also called chorionic somatomammotropin, is a polypeptide placental hormone, part of the somatotropin family. Its structure and function is similar to that of growth hormone. It modifies the metabolic state of the mother during pregnancy to facilitate the energy supply of the fetus. For information on the human form, see human placental lactogen. Placental lactogen I and II were identified as prolactin-like molecules that can bind to prolactin receptor with high affinity and mimic the actions of prolactin. These hormones can contribute to lactogenesis, luteal maintenance and progesterone production (in rats) during the later stages of gestation. Placental lactogen I may be important in stimulating mammary cell proliferation and in stimulating some of the adaptations of the maternal lipid and carbohydrate metabolism. ...
Angiotensin. *Bombesin. *Calcitonin gene-related peptide. *Carnosine. *Cocaine- and amphetamine-regulated transcript ...
Angiotensin. *Bombesin. *Calcitonin gene-related peptide. *Carnosine. *Cocaine- and amphetamine-regulated transcript ...
The human CRHR2 gene contains 12 exons. Three major functional isoforms, alpha (411 amino acids), beta (438 amino acids), and gamma (397 amino acids), encoded by transcripts with alternative first exons,[7] differ only in the N-terminal sequence comprising the signal peptide and part of the extracellular domain (amino acids 18-108 of CRHR2 alpha); the unique N-terminal sequence of each isoform (34 amino acids in CRHR2 alpha; 61 amino acids in Hs CRHR2 beta; 20 amino acids in CRHR2 gamma) is followed by a sequence common to all isoforms (377 amino acids)[8] comprising most of the multi-pass transmembrane domain followed by a cytoplasmic domain of 47 amino acids. CRHR2 beta is expressed in human brain; CRHR2 alpha predominates in peripheral tissues. The N-terminal signal peptides of corticotropin-releasing hormone receptor 1 and CRHR2 beta are cleaved off in the endoplasmic reticulum to yield the mature receptors. In contrast, CRHR2 alpha contains a unique pseudo signal peptide that is not removed ...
Toy-Miou-Leong M, Cortes CL, Beaudet A, Rostène W, Forgez P (Mar 2004). "Receptor trafficking via the perinuclear recycling compartment accompanied by cell division is necessary for permanent neurotensin cell sensitization and leads to chronic mitogen-activated protein kinase activation". The Journal of Biological Chemistry. 279 (13): 12636-46. doi:10.1074/jbc.M303384200. PMID 14699144 ...
ProIAPP has been linked to Type 2 diabetes and the loss of islet β-cells.[24] Islet amyloid formation, initiated by the aggregation of proIAPP, may contribute to this progressive loss of islet β-cells. It is thought that proIAPP forms the first granules that allow for IAPP to aggregate and form amyloid which may lead to amyloid-induced apoptosis of β-cells. IAPP is cosecreted with insulin. Insulin resistance in Type 2 diabetes produces a greater demand for insulin production which results in the secretion of proinsulin.[25] ProIAPP is secreted simultaneously, however, the enzymes that convert these precursor molecules into insulin and IAPP, respectively, are not able to keep up with the high levels of secretion, ultimately leading to the accumulation of proIAPP. In particular, the impaired processing of proIAPP that occurs at the N-terminal cleavage site is a key factor in the initiation of amyloid.[25] Post-translational modification of proIAPP occurs at both the carboxy terminus and the ...
... the kisspeptin-angiotensin II pathway of producing aldosterone is increased.[17] Aldosterone that comes from the neighboring ...
CCK receptors significantly influence neurotransmission in the brain, regulating anxiety, feeding, and locomotion. CCK-B expression may correlate parallel to anxiety and depression phenotypes in humans. CCK-B receptors possess a complex regulation of dopamine activity in the brain. CCK-B activation appears to possess a general inhibitory action on dopamine activity in the brain, opposing the dopamine-enhancing effects of CCK-A. However, the effects of CCK-B on dopamine activity vary depending on location.[11] CCK-B antagonism enhances dopamine release in rat striatum.[12] Activation enhances GABA release in rat anterior nucleus accumbens.[13] CCK-B receptors modulate dopamine release, and influence the development of tolerance to opioids.[14] CCK-B activation decreases amphetamine-induced DA release, and contributes to individual variability in response to amphetamine.[15] In rats, CCK-B antagonism prevents the stress-induced reactivation of cocaine-induced conditioned place preference, and ...
The package insert for Gonal-F states that based on physio-chemical tests and bioassays that follitropin beta and follitropin alfa are indistinguishable. Two studies showed no difference.[5][6] However, a more recent study showed there may be a slight clinical difference, with the alfa form tending towards a higher pregnancy rate and the beta form tending towards a lower pregnancy rate, but with significantly higher estradiol (E2) levels.[7]. The package insert for Puregon states that structural analysis shows that the amino acid sequence of follitropin beta is identical to that of natural human follicle stimulating hormone (hFSH). Further, the ogliosaccharide side chains are very similar, but not completely identical to that of natural hFSH. However, these small differences do not affect the bioactivity compared to natural hFSH.. ...
The U.S. Food and Drug Administration (FDA) approved eptinezumab based primarily on evidence from two clinical trials (Trial 1/ NCT02559895 and Trial 2/ NCT02974153) of 1741 subjects with chronic or episodic migraine headaches.[6] Trials were conducted at 212 sites in United States, Georgia, Russia, Ukraine and European Union.[6] The benefit and side effects of eptinezumab were evaluated in two clinical trials of adult subjects 18 - 71 years of age with a history of migraine headaches.[6] The trials had similar designs.[6] Trial 1 enrolled subjects with a history of episodic migraine headaches and Trial 2 enrolled subjects with chronic migraine headaches.[6] Subjects were assigned to receive one of two doses of eptinezumab or placebo injections every three months for a total of twelve months in Trial 1, and for a total of 6 months in Trial 2.[6] Neither the subjects nor the health care providers knew which treatment was being given until the trial was completed.[6] The benefit of eptinezumab in ...
PTHrP is related in function to the "normal" parathyroid hormone. When a tumor secretes PTHrP, this can lead to hypercalcemia.[7] As this is sometimes the first sign of the malignancy, hypercalcemia caused by PTHrP is considered a paraneoplastic phenomenon. PTHR1 is responsible for most cases of humoral hypercalcemia of malignancy. PTHrP shares the same N-terminal end as parathyroid hormone and therefore it can bind to the same receptor, the Type I PTH receptor (PTHR1). PTHrP can simulate most of the actions of PTH including increases in bone resorption and distal tubular calcium reabsorption, and inhibition of proximal tubular phosphate transport. However, PTHrP is less likely than PTH to stimulate 1,25-dihydroxyvitamin D production. Therefore, PTHrP does not increase intestinal calcium absorption. ...
In industry, EDTA is mainly used to sequester metal ions in aqueous solution. In the textile industry, it prevents metal ion impurities from modifying colors of dyed products. In the pulp and paper industry, EDTA inhibits the ability of metal ions, especially Mn2+, from catalyzing the disproportionation of hydrogen peroxide, which is used in chlorine-free bleaching. In a similar manner, EDTA is added to some food as a preservative or stabilizer to prevent catalytic oxidative decoloration, which is catalyzed by metal ions.[4] In soft drinks containing ascorbic acid and sodium benzoate, EDTA mitigates formation of benzene (a carcinogen).[5] The reduction of water hardness in laundry applications and the dissolution of scale in boilers both rely on EDTA and related complexants to bind Ca2+, Mg2+, as well as other metal ions. Once bound to EDTA, these metal centers tend not to form precipitates or to interfere with the action of the soaps and detergents. For similar reasons, cleaning solutions often ...
Renin-angiotensin systemEdit. Hypovolemia leads to activation of the renin angiotensin system (RAS) and is detected by cells in ... Renin then enters the blood where it catalyzes a protein called angiotensinogen to angiotensin I. Angiotensin I is then almost ... Angiotensin II then travels in the blood until it reaches the posterior pituitary gland and the adrenal cortex where it causes ... This is also a result of the renin-angiotensin system activation.[medical citation needed] ...
ACE (Angiotensin converting enzyme) then removes a further two residues, converting angiotensin I into angiotensin II. ACE is ... Ng KK, Vane JR (1967). "Conversion of Angiotensin I to Angiotensin II". Nature. 216 (5117): 762-6. doi:10.1038/216762a0. PMID ... The conversion of the inactive angiotensin I to the potent angiotensin II was thought to take place in the plasma. However, in ... The inactivation of bradykinin and the conversion of angiotensin I to angiotensin II in the lungs was thought to be caused by ...
The conversion of angiotensin I to angiotensin II and the inactivation of bradykinin were thought to be mediated by the same ... Ng KK, Vane JR (November 1967). "Conversion of angiotensin I to angiotensin II". Nature. 216 (5117): 762-6. Bibcode:1967Natur. ... Captopril blocks the conversion of angiotensin I to angiotensin II and prevents the degradation of vasodilatory prostaglandins ... when he found the conversion of angiotensin I to angiotensin II took place in the pulmonary circulation instead of in the ...
... cleaves a further two amino acids from angiotensin I to form an octapeptide known as angiotensin II. Angiotensin II is a ... The angiotensin II-stimulated aldosterone released from the zona glomerulosa of the adrenal glands has an effect on ... Angiotensin II also acts on the smooth muscle in the walls of the arterioles causing these small diameter vessels to constrict ... This decapeptide is known as angiotensin I.[51] It has no known biological activity. However, when the blood circulates through ...
Because the glycocalyx is so prominent throughout the cardiovascular system, disruption to this structure has detrimental effects that can cause disease. Certain stimuli that cause atheroma may lead to enhanced sensitivity of vasculature. Initial dysfunction of the glycocalyx can be caused by hyperglycemia or oxidized low-density lipoproteins (LDLs), which then causes atherothrombosis. In microvasculature, dysfunction of the glycocalyx leads to internal fluid imbalance, and potentially edema. In arterial vascular tissue, glycocalyx disruption causes inflammation and atherothrombosis.[8] Experiments have been performed to test precisely how the glycocalyx can be altered or damaged. One particular study used an isolated perfused heart model designed to facilitate detection of the state of the vascular barrier portion, and sought to cause insult-induced shedding of the glycocalyx to ascertain the cause-and-effect relationship between glycocalyx shedding and vascular permeability. Hypoxic perfusion ...
Angiotensin-converting enzyme. 3.4.16. *Serine type carboxypeptidases: Cathepsin A. *DD-transpeptidase ...
The angiotensin II receptors, (AGTR1) and (AGTR2), are a class of G protein-coupled receptors with angiotensin II as their ... The angiotensin receptor is activated by the vasoconstricting peptide angiotensin II. The activated receptor in turn couples to ... The AT4 receptor is activated by the angiotensin II metabolite angiotensin IV, and may play a role in regulation of the CNS ... angiotensin II. The AT1 and AT2 receptors share a sequence identity of ~30%, but have a similar affinity for angiotensin II, ...
The decapeptide is known as angiotensin I.. *Angiotensin I is then converted to an octapeptide, angiotensin II by angiotensin- ... Angiotensin II receptor antagonists, also known as angiotensin receptor blockers, can be used to prevent angiotensin II from ... It is believed that angiotensin I may have some minor activity, but angiotensin II is the major bio-active product. Angiotensin ... Angiotensin I is subsequently converted to angiotensin II by the angiotensin-converting enzyme (ACE) found on the surface of ...
... angiotensin II, causes constriction of blood vessels. There are three forms of angiotensin. Angiotensin I is produced by the ... Angiotensin: Angiotensin, a peptide, one form of which, ... Angiotensin I is transformed into angiotensin II in the blood ... renin-angiotensin system. …of 10 amino acids) called angiotensin I. An enzyme in the serum called angiotensin-converting enzyme ... ACE) then converts angiotensin I into an octapeptide (consisting of eight amino acids) called angiotensin II. Angiotensin II ...
This peptide hormone constricts blood vessels, but, oddly, blocking the so-called angiotensin II receptor type 2 (AT2) appeared ... for new hypertension medications unearthed a mysterious new cell receptor that responded to a hormone known as angiotensin II. ...
The product of this enzymatic hydrolysis-the N-terminal heptapeptide sequence of angiotensin-is biologically inactive. ... The ACE2/Angiotensin-(1-7)/MAS Axis of the Renin-Angiotensin System: Focus on Angiotensin-(1-7) *Robson Augusto Souza Santos ... YANG, H., ERDÖS, E. & CHIANG, T. New Enzymatic Route for the Inactivation of Angiotensin. Nature 218, 1224-1226 (1968) doi: ... New Enzymatic Route for the Inactivation of Angiotensin. *H. Y. T. YANG1. , ...
Molecules that are dissolved in water may dissociate into charged ions. An acid is a substance that increases the number of H+ ions in a solution. A base is a substance that decreases the number of H+ ions in a solution. The concentration of H+ ions in a solution can be measured and is called the pH of the solution.. The pH of a solution can be measured using a scale that ranges from 0 to 14. A solution of pH = 7 is neutral, a solution of pH lower than 7 is acidic, and a solution of pH greater than 7 is basic (alkaline). The number of H+ ions increases as the pH number decreases (and vice versa). The difference between two successive numbers on the pH scale represents a ten-fold difference in the H+ ion concentration because the scale is a logarithmic scale (log of base 10). For example, a solution with a pH of 2 has 10 times more H+ ions as a solution with a pH of 3. A solution with a pH of 2 has 100 times more H+ ions as a solution with a pH of 4. ...
It is cleaved at the N-terminus by renin to result in angiotensin I, which will later be modified to become angiotensin II. ... It is part of the renin-angiotensin system, which regulates blood pressure. Angiotensin also stimulates the release of ... and angiotensin II levels. Asp-Arg-Val-Tyr-Ile-His-Pro-Phe-His-Leu , Val-Ile-... Angiotensin I (CAS# 11128-99-7), officially ... An oligopeptide, angiotensin is a hormone and a dipsogen. It is derived from the precursor molecule angiotensinogen, a serum ...
The controversy about whether ACE inhibitors and angiotensin blockers may affect COVID-19 infection continues, with hypotheses ... The controversy about whether angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) may ... which in turn results in excessive production of angiotensin II and less ACE2 to convert it the vasodilator angiotensin 1-7. ... They also note that ARBs enable the increase of available angiotensin II by competing with the same receptor and suggest that ...
Angiotensin II receptor blockers, or ARBs, are an option for people with heart failure. WebMD explains what they are and how ... Angiotensin II receptor blockers (also called ARBs) block the effects of a substance called angiotensin II. It causes blood ... Heart Failure and Angiotensin II Receptor Blockers Medically Reviewed by James Beckerman, MD, FACC on August 24, 2020 In this ...
Angiotensin converting enzyme inhibitors in pregnancy.. Mastrobattista JM1.. Author information. 1. Department of Obstetrics, ... Angiotensin converting enzyme (ACE) inhibitors are excellent antihypertensive agents and are becoming widely used as first-line ...
... angiotensin I) and two varieties (angiotensin II and angiotensin III) that elevate blood pressure and stimulate the adrenal ... Angiotensin ii definition, any of three oligopeptides occurring in plasma, an inactive form ( ... Angiotensin II is formed from inactive angiotensin I by the action of angiotensin-converting enzyme (or ACE). See also ACE ... angiotensin ii in Medicine Expand. angiotensin II n. An octapeptide that is a potent vasopressor and a powerful stimulus for ...
It does not generally exist simply as angiotensin, but rather as angiotensinogen, befor... ... Angiotensin is part of the renin-angiotensin-aldosterone system. ... angiotensin (thing). See all of angiotensin, no other writeups ... Angiotensin is part of the renin-angiotensin-aldosterone system. It does not generally exist simply as angiotensin, but rather ... before it is cleaved into angiotensin I by renin and then converted to angiotensin II by angiotensin converting enzyme which is ...
... ,ARUP Laboratories is a national reference laboratory and a worldwide leader in innovative ... Angiotensin II. 7. Angiotensin II EIA Kit. 8. Angiotensin Converting Enzyme, CSF. 9. SAFE-T-FILL Serum. 10. SAFE-T-FILL Serum ... ACE Kinetic Hypertension / Cardiac Evaluation, Cardiovascular 001-KK-ACKX Angiotensin Converting Enzyme. 4. Angiotensin II RIA ... ACE Kinetic Hypertension / Cardiac Evaluation, Cardiovascular 001-KK-ACK4 Angiotensin Converting Enzyme. 2. ACE Kinetic ...
Angiotensin IIIEdit. Asp , Arg-Val-Tyr-Ile-His-Pro-Phe. Angiotensin III has 40% of the pressor activity of angiotensin II, but ... Angiotensin IIEdit. Asp-Arg-Val-Tyr-Ile-His-Pro-Phe. Angiotensin I is converted to angiotensin II (AII) through removal of two ... Angiotensin IVEdit. Arg , Val-Tyr-Ile-His-Pro-Phe. Angiotensin IV is a hexapeptide that, like angiotensin III, has some lesser ... See also Renin-angiotensin system#Effects. Angiotensins II, III and IV have a number of effects throughout the body:. Adipic ...
... angiotensin I) and two varieties (angiotensin II and angiotensin III) that elevate blood pressure and stimulate the adrenal ... Angiotensin i definition, any of three oligopeptides occurring in plasma, an inactive form ( ... angiotensin amide, angiotensin i, angiotensin ii, angiotensin iii, angiotensin precursor ... Angiotensin II is formed from inactive angiotensin I by the action of angiotensin-converting enzyme (or ACE). See also ACE ...
Angiotensin receptor blockers can be used if there is a clinical indication for renin-angiotensin-aldosterone system blockade ... Angiotensin-converting-enzyme inhibitor-induced angioedema. Danica Quickfall, Baruch Jakubovic and Jonathan S. Zipursky ... Angiotensin-converting-enzyme (ACE) inhibitors are the leading cause of drug-induced angioedema ...
... angiotensin II. Inhibitors of ACE are a first line of therapy for hypertension, heart failure, myocardial infarction and ... has a critical role in cardiovascular function by cleaving the carboxy terminal His-Leu dipeptide from angiotensin I to produce ... Two putative active centers in human angiotensin I-converting enzyme revealed by molecular cloning. Proc. Natl Acad. Sci. USA ... The critical role of tissue angiotensin-converting enzyme as revealed by gene targeting in mice. J. Clin. Invest. 99, 2375-2385 ...
Angiotensin type-2 receptor-mediated hypotension in angiotensin type 1 receptor-blocked rats. Hypertension. 2001; 38: 1272-1277 ... The major biological actions of the renin-angiotensin system are mediated by angiotensin (Ang) II, which binds with equal ... Angiotensin type 2 receptor in resistance arteries of type 2 diabetic hypertensive patients. Hypertension. 2007; 49: 341-346. ... The subtype 2 (AT2) angiotensin receptor mediates renal production of nitric oxide in conscious rats. J Clin Invest. 1997; 100 ...
Helping you find trustworthy answers on Renin-Angiotensin System , Latest evidence made easy ... Find all the evidence you need on Renin-Angiotensin System via the Trip Database. ... Angiotensin-converting enzyme 2 cleaves angiotensin-II into the vasodilator peptide, angiotensin-(1-7), hence playing a pivotal ... role in the angiotensin-converting enzyme 2/angiotensin-(1-7) compensatory axis of the renin-angiotensin system. Angiotensin ...
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Inasmuch as the renin-angiotensin system can act as a protective mechanism again … ... it is of interest to establish whether angiotensin II also produces stimulation of new vessel formation. Angiotensin II or ... Neovascularization produced by angiotensin II J Lab Clin Med. 1985 Feb;105(2):141-5. ... Inasmuch as the renin-angiotensin system can act as a protective mechanism against local ischemia by activating preexisting ...
Angiotensin II Flow attention cardiovascular clinical application hypertension pathophysiology physiology Editors and ... The Angiotensin II AT2 Receptor Subtype Marc de Gasparo, Nigel R. Levens, Bruno Kamber, Pascal Furet, Steven Whitebread, ... Angiotensin II Receptor Antagonism in an Ovine Model of Heart Failure Comparison with ACE and Renin Inhibition ... Angiotensin Receptor Stimulation of Transforming Growth Factor-β in Rat Skin and Wound Healing ...
Proteopedia Angiotensin-converting_enzyme - the Angiotensin-Converting Enzyme Structure in Interactive 3D Angiotensin+ ... Angiotensin II binds to the type 1 angiotensin II receptor (AT1), which sets off a number of actions that result in ... Angiotensin-converting enzyme (EC 3.4.15.1), or ACE, is a central component of the renin-angiotensin system (RAS), which ... In addition, inhibiting angiotensin II formation diminishes angiotensin II-mediated aldosterone secretion from the adrenal ...
angiotensin amide synonyms, angiotensin amide pronunciation, angiotensin amide translation, English dictionary definition of ... angiotensin amide. n. Any of several polypeptide hormones, designated by Roman numerals, that are involved in the regulation of ... angiotensin I - a physiologically inactive form of angiotensin that is the precursor to angiotensin II ... angiotensin. (redirected from angiotensin amide). Also found in: Thesaurus, Medical, Encyclopedia. an·gi·o·ten·sin. (ăn′jē-ō- ...
Angiotensin converting enzyme (encoded by the gene DCP1, also known as ACE) catalyses the conversion of angiotensin I to the ... Sequence variation in the human angiotensin converting enzyme.. Rieder MJ1, Taylor SL, Clark AG, Nickerson DA. ... Because of its key function in the renin-angiotensin system, many association studies have been performed with DCP1. Nearly all ... physiologically active peptide angiotensin II, which controls fluid-electrolyte balance and systemic blood pressure. ...
Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are antihypertensive medicines used to treat high ... Angiotensin-converting enzyme (ACE) catalyzes the conversion of angiotensin I into angiotensin II in the lungs. Angiotensin II ... How do angiotensin-converting enzyme inhibitors and angiotensin receptor blockers work?. Angiotensin-converting enzyme ... Angiotensin receptor blockers. Alike ACE inhibitors, angiotensin receptor blockers (ARBs) are used to treat hypertension and ...
Second Edition updates new findings on the local renin-angiotensin systems (RAS) with a focus on the local RAASs of the ... Newer Insights into the Biochemical Physiology of the Renin-Angiotensin System: Role of Angiotensin-(1-7), Angiotensin ... The Local Cardiac Renin-Angiotensin Aldosterone System, Second Edition updates new findings on the local renin-angiotensin ... Intracellular Accumulation and Nuclear Trafficking of Angiotensin II and the Angiotensin II Type 1 Receptor ...
Giving ACE inhibitors or angiotensin receptor blockers to patients with advanced chronic kidney disease and hypertension may ... Angiotensin Drugs Help Advanced CKD Patients. by Todd Neale, Senior Staff Writer, MedPage Today December 17, 2013 ... Giving ACE inhibitors or angiotensin receptor blockers (ARBs) to patients with advanced chronic kidney disease (CKD) and ... Source Reference: Hsu T-W, et al "Renoprotective effect of renin-angiotensin-aldosterone system blockade in patients with ...
for angiotensin I (16 M). First-order kinetics will apply even at angiotensin I levels that are 10,000-fold higher than normal ... Other Angiotensins. Alternatively, angiotensin III (Ang 2-8) is produced from Ang II by the actions of aminopeptidase A, a zinc ... Angiotensin II is generated by the serial cleavage of angiotensinogen, first by renin and then by ACE. Angiotensin II exerts ... M. C. Chappell, N. T. Pirro, A. Sykes, and C. M. Ferrario, "Metabolism of angiotensin-(1-7) by angiotensin-converting enzyme," ...
... angiotensin receptor blockers (ARBs), and (possibly) aldosterone antagonists might either prevent new onset and recurrent ... Initial studies suggested that angiotensin converting enzyme (ACE) inhibitors, ... Actions of angiotensin II on the heart. *Angiotensin converting enzyme inhibitors and receptor blockers in acute myocardial ... Impact of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers on the long-term outcome after ...
  • The angiotensin II receptors, (AGTR1) and (AGTR2), are a class of G protein-coupled receptors with angiotensin II as their ligands. (wikipedia.org)
  • The AT1 and AT2 receptors share a sequence identity of ~30%, but have a similar affinity for angiotensin II, which is their main ligand. (wikipedia.org)
  • Angiotensin II is the major bioactive product of the renin-angiotensin system, binding to receptors on intraglomerular mesangial cells , causing these cells to contract along with the blood vessels surrounding them and causing the release of aldosterone from the zona glomerulosa in the adrenal cortex . (wikipedia.org)
  • Blood pressure also can be lowered using drugs that are designed to block the receptors to which angiotensin II must bind to exert its actions. (britannica.com)
  • The major biological actions of the renin-angiotensin system are mediated by angiotensin (Ang) II, which binds with equal affinity to Ang type 1 (AT 1 ) and type 2 (AT 2 ) receptors. (ahajournals.org)
  • Of particular importance is the attention given to the newly discovered AT 2 receptors, and the physiology and pathophysiology of angiotensin receptor subtypes. (springer.com)
  • These blockers work by inhibiting the angiotensin II receptors (type I and II), leading to functional inhibition of angiotensin II and subsequent reduction of the blood pressure. (news-medical.net)
  • It does this by binding to cell-surface proteins called angiotensin receptors (there's more than one type of these and they have a whole list of other downstream functions, but that takes us further afield). (sciencemag.org)
  • The confusion around the phrase "angiotensin receptors" has led to some people outside of the medical field wondering if the antagonist drugs (the sartans) would interfere with ACE-2, but that doesn't happen, either (there's another story with those, though - see below). (sciencemag.org)
  • There is no question that angiotensin II can play its enhancing effects on the sympathetic nervous system at various levels and that not only a presynaptic potentiation of norepinephrine secretion but also an amplification of the responsiveness of adrenergic receptors to neural stimuli is involved as indicated by the data of Lyons et al. (ahajournals.org)
  • It is certainly possible, on the basis of the in vitro findings of Kessler et al, R5 that this activity is increased by sympathetic influences also because of an enhanced effect of angiotensin II on its receptors. (ahajournals.org)
  • Such species like angiotensin III can then bind and interact with specific G protein coupled receptors like angiotensin receptor 1, or AT-1 1 where strong vasoconstricson can occur. (drugbank.ca)
  • Alternatively, angiotensin receptor blockers (ARBs) can be used to prevent angiotensin II from acting on angiotensin receptors . (bionity.com)
  • Within the renin-angio-tensin-aldosterone system (RAAS), increases in blood pressure are achieved when angiotensin I is converted to angiotensin II by angiotensin-converting enzyme (ACE), which then binds to AT 1 receptors located in various muscles and tissues such as vascular and myocardial tissue and in the liver. (uspharmacist.com)
  • Angiotensin receptor blockers (ARBs) work to decrease blood pressure by preventing angiotensin II from binding to AT 1 receptors. (uspharmacist.com)
  • The reported results should help with designing ligands for angiotensin receptors and possibly to other peptide GPCRs. (rcsb.org)
  • Two systems of nomenclature are used in reference to angiotensin-II receptor antagonists: one system employs Roman numerals, and the other is based on the amino acids that make up the A-I and A-II receptors (AT 1 receptor and AT 2 receptor). (aafp.org)
  • 2 Angiotensin-II receptor antagonists act by binding to specific membrane-bound receptors that displace A-II from its type 1-receptor subtype (AT 1 ). (aafp.org)
  • Ligand contact points in the angiotensin receptors. (mcmaster.ca)
  • Cell-surface G-protein-coupled receptors that mediate the effects of angiotensin II. (thefreedictionary.com)
  • Drugs that block the angiotensin receptors , (AT1R blockers) are prescribed to millions of people to lower high blood pressure. (thefreedictionary.com)
  • The chapters provide insights gained by the genetic manipulation of angiotensin II, assessment of its transcriptional and translational regulation, work on the angiotensin receptors , the status of the specific molecular components of the renin-angiotensin-aldosterone system under differing conditions, and functional responses to the angiotensins. (thefreedictionary.com)
  • The controversy about whether angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) may increase susceptibility to the COVID-19 virus infection continues unabated, with new commentaries about this appearing almost daily. (medscape.com)
  • In one prominent report published as a letter to The Lancet Respiratory Medicine on March 11, Lei Feng, MD, PhD, University Hospital Basel, Switzerland, and colleagues write: "The expression of ACE2 is substantially increased in patients with type 1 or type 2 diabetes , who are treated with ACE inhibitors and angiotensin II type-I receptor blockers (ARBs). (medscape.com)
  • Angiotensin II receptor blockers (also called ARBs) block the effects of a substance called angiotensin II. (webmd.com)
  • Renin - Angiotensin System Blockade Improves Cardiac Indices in Acromegaly Patients Blockade of the angiotensin-renin system , with angiotensin converting enzyme inhibitors (ACEi) and angiotensin receptor blockers (ARBs), has been shown to improve cardiac outcomes following myocardial infarction and delay progression of heart failure. (tripdatabase.com)
  • Alike ACE inhibitors, angiotensin receptor blockers (ARBs) are used to treat hypertension and related comorbid conditions. (news-medical.net)
  • Giving ACE inhibitors or angiotensin receptor blockers (ARBs) to patients with advanced chronic kidney disease (CKD) and hypertension may prevent the start of long-term dialysis and could delay death, Taiwanese researchers found. (medpagetoday.com)
  • Initial studies suggested that angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), and (possibly) aldosterone antagonists might either prevent new onset and recurrent atrial fibrillation (AF) or reduce the rate of major adverse cardiovascular outcomes in these patients. (uptodate.com)
  • In this topic ACE inhibitors and ARBs collectively will be referred to as 'angiotensin inhibition. (uptodate.com)
  • While angiotensin receptor blockers (ARBs) can reprogram CAFs from an active to a quiescent state, their ability to change the cells' immunomodulatory functions is unknown. (news-medical.net)
  • It covers topics related to angiotensin II receptor blockers (ARBs) and nephropathy. (diabetesjournals.org)
  • As a novel aspect connecting the importance of SNS and RAS activation, we and other investigators have recently demonstrated that angiotensin II type 1 receptor (AT 1 R) blockers (ARBs) improve SNS activation in patients with MetS. (hindawi.com)
  • In the pathogenesis of MetS, renin-angiotensin system (RAS) is activated in various organs and tissues [ 3 - 6 ], and RAS inhibitors, such as angiotensin converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs), are preferred for the treatments of hypertension with MetS because of the prominent depressor effect with the improvement of insulin resistance [ 7 - 9 ]. (hindawi.com)
  • The protective effect observed with angiotensin receptor blockers (ARBs) and angiotensin converting enzyme inhibitors (ACEIs) could be as the result of inhibition of Ang II signaling. (frontiersin.org)
  • Angiotensin receptor blockers (ARBs) are potential options for the treatment of high blood pressure. (uspharmacist.com)
  • newer angiotensin receptor blockers (ARBs) and older angiotensin - converting enzyme (ACE) inhibitors. (everydayhealth.com)
  • What Are ARBs ( Angiotensin Receptor Blockers)? (everydayhealth.com)
  • Angiotensin receptor blockers (ARBs) have similar effects and side-effects to ACE inhibitors, except that they do not cause cough. (edren.org)
  • Two FDA officials are quarreling in public about their different views about the safety of angiotensin-receptor blockers (ARBs), according to a story by Thomas Burton in Friday's Wall Street Journal. (cardiobrief.org)
  • Angiotensin receptor blockers (ARBs) selectively block the binding of angiotensin II to the AT1 receptor. (oncologynurseadvisor.com)
  • Angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) are the preferred agents for lowering blood pressure and decreasing proteinuria. (medscape.com)
  • Plasma renin then carries out the conversion of angiotensinogen , released by the liver, to angiotensin I . [2] Angiotensin I is subsequently converted to angiotensin II by the angiotensin-converting enzyme (ACE) found on the surface of vascular endothelial cells, predominantly those of the lungs. (wikipedia.org)
  • Angiotensin I is then converted to an octapeptide , angiotensin II by angiotensin-converting enzyme (ACE), [7] which is thought to be found mainly in endothelial cells of the capillaries throughout the body, within the lungs and the epithelial cells of the kidneys. (wikipedia.org)
  • Angiotensin I is transformed into angiotensin II in the blood by the action of angiotensin-converting enzyme (ACE). (britannica.com)
  • Angiotensin-converting enzyme (EC 3.4.15.1), or ACE, is a central component of the renin-angiotensin system (RAS), which controls blood pressure by regulating the volume of fluids in the body. (wikipedia.org)
  • ACE is also known by the following names: dipeptidyl carboxypeptidase I peptidase P dipeptide hydrolase peptidyl dipeptidase angiotensin converting enzyme kininase II angiotensin I-converting enzyme carboxycathepsin dipeptidyl carboxypeptidase "hypertensin converting enzyme" peptidyl dipeptidase I peptidyl-dipeptide hydrolase peptidyldipeptide hydrolase endothelial cell peptidyl dipeptidase peptidyl dipeptidase-4 PDH peptidyl dipeptide hydrolase DCP CD143 ACE hydrolyzes peptides by the removal of a dipeptide from the C-terminus. (wikipedia.org)
  • Kininase II is the same as angiotensin-converting enzyme. (wikipedia.org)
  • Angiotensin converting enzyme inhibitors in pregnancy. (nih.gov)
  • Angiotensin converting enzyme (ACE) inhibitors are excellent antihypertensive agents and are becoming widely used as first-line therapy for chronic hypertension in women of reproductive age owing to their efficacy and few side effects. (nih.gov)
  • Angiotensin II is formed from inactive angiotensin I by the action of angiotensin-converting enzyme (or ACE ). (dictionary.com)
  • It does not generally exist simply as angiotensin , but rather as angiotensinogen , before it is cleaved into angiotensin I by renin and then converted to angiotensin II by angiotensin converting enzyme which is located mostly in the lungs . (everything2.com)
  • Angiotensinogen and angiotensin converting enzyme are normally present in large amounts in the system, but cannot be activated and used, respectively, until renin is present. (everything2.com)
  • 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). (wikipedia.org)
  • Angiotensin-converting enzyme (ACE) has a critical role in cardiovascular function by cleaving the carboxy terminal His-Leu dipeptide from angiotensin I to produce a potent vasopressor octapeptide, angiotensin II. (nature.com)
  • Two putative active centers in human angiotensin I-converting enzyme revealed by molecular cloning. (nature.com)
  • Williams, T. A., Corvol, P. & Soubrier, F. Identification of two active site residues in human angiotensin I-converting enzyme. (nature.com)
  • RXP 407, a selective inhibitor of the N-domain of angiotensin I-converting enzyme, blocks in vivo the degradation of hemoregulatory peptide acetyl-Ser-Asp-Lys-Pro with no effect on angiotensin I hydrolysis. (nature.com)
  • The critical role of tissue angiotensin-converting enzyme as revealed by gene targeting in mice. (nature.com)
  • Ehlers, M. R. W., Fox, E. A., Strydom, D. J. & Riordan, J. F. Molecular cloning of human testicular angiotensin-converting enzyme: the testis isozyme is identical to the C-terminal half of endothelial angiotensin-converting enzyme. (nature.com)
  • Identification of N -linked glycosylation sites in human testis angiotensin-1 converting enzyme and expression of an active deglycosylated form. (nature.com)
  • Ehlers, M. R. W. & Riordan, J. F. Angiotensin-converting enzyme: zinc- and inhibitor-binding stoichiometries of the somatic and testis isozymes. (nature.com)
  • Bünning, P. & Riordan, J. F. Activation of angiotensin converting enzyme by monovalent anions. (nature.com)
  • Angiotensin converting enzyme inhibitors (ACEi) and angiotensin receptor blockers (ARB) are increasingly used in uremic patients (pts). (tripdatabase.com)
  • Blockade of the renin - angiotensin -aldosterone system (RAAS) with angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARB) has been shown to decrease incident atrial fibrillation (AF). (tripdatabase.com)
  • Sequence variation in the human angiotensin converting enzyme. (nih.gov)
  • Angiotensin converting enzyme (encoded by the gene DCP1, also known as ACE) catalyses the conversion of angiotensin I to the physiologically active peptide angiotensin II, which controls fluid-electrolyte balance and systemic blood pressure. (nih.gov)
  • Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are antihypertensive medicines used to treat high blood pressure. (news-medical.net)
  • How do angiotensin-converting enzyme inhibitors and angiotensin receptor blockers work? (news-medical.net)
  • Angiotensin-converting enzyme (ACE) catalyzes the conversion of angiotensin I into angiotensin II in the lungs. (news-medical.net)
  • The discovery of the angiotensin-converting enzyme ACE2-angiotensin (1-7)-Mas receptor axis that exerts vasodilator, antiproliferative, and antifibrotic actions opposed to those of the ACE-Ang II-AT 1 receptor axis has led to the hypothesis that a decrease in the expression or activity of angiotensin (1-7) renders the systems more susceptible to the pathological actions of Ang II. (hindawi.com)
  • The hemodynamic effects of angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARB) result in improved ventricular function and also reductions in LA pressure and wall stress [ 2 ]. (uptodate.com)
  • That small peptide is then made even smaller by angiotensin-converting enzyme 1 (ACE-1), and interestingly, no one's ever found a function for angiotensin-1 other than to sit around and get cleaved in this way. (sciencemag.org)
  • Morganti A, Grassi G, Giannattasio C, Bolla G, Turolo L, Saino A, Sala C, Mancia G, Zanchetti A. Effect of angiotensin converting enzyme inhibition on cardiovascular regulation during reflex sympathetic activation in sodium replete patients with essential hypertension. (ahajournals.org)
  • Alpha-linolenic acid inhibits angiotensin-converting enzyme activity in hypertensive rats. (greenmedinfo.com)
  • Gynura procumbens inhibit angiotensin-converting enzyme in spontaneously hypertensive rats. (greenmedinfo.com)
  • Pomegranate juice reduces blood pressure by inhibiting Angiotensin Converting Enzyme (ACE) activity in diabetic rats. (greenmedinfo.com)
  • Ang II is formed by cleavage of Ang I by the angiotensin-converting enzyme (ACE) or chymases. (anaspec.com)
  • Angiotensin I is then converted to angiotensin II by angiotensin-converting enzyme (ACE), [1] which is found mainly in lung capillaries . (bionity.com)
  • Inhibitors of angiotensin-converting enzyme (ACE inhibitors) are often used to reduce the formation of the more potent angiotensin II. (bionity.com)
  • Angiotensin-converting enzyme 2 (ACE2), a first homolog of ACE, regulates the renin-angiotensin system by counterbalancing ACE activity. (nih.gov)
  • 6. The method of claim 1, wherein said angiotensin-converting enzyme inhibitor of Formula I is administered in a sub-anti-hypertensive dose. (google.com)
  • Enalapril: a new angiotensin converting enzyme inhibitor. (webmd.com)
  • Hyperkalemia in azotemic patients during angiotensin-converting enzyme inhibition and aldosterone reduction with captopril. (webmd.com)
  • In the central nervous system, angiotensinogen is synthesized by astrocytes and subsequently cleaved by renin, angiotensin converting enzyme (ACE) and aminopeptidases or ACE2 and Neprilysin ( Bodiga and Bodiga, 2013 ). (frontiersin.org)
  • The circulating RAS comprises kidney-derived renin acting on liver-derived angiotensinogen to generate angiotensin (Ang) I that is converted to Ang II by angiotensin converting enzyme (ACE). (frontiersin.org)
  • Angiotensin-converting enzyme inhibitors--when to use? (biomedsearch.com)
  • In practice, angiotensin-converting enzyme inhibitors have been shown to given considerable relief to patients with severe heart failure, but in patients who are only moderately ill these drugs may have less effect than increasing the dose of diuretics. (biomedsearch.com)
  • Vasodilators in general probably reduce the fatality of patients with heart failure, but the effect is not specific to angiotensin-converting enzyme inhibitors. (biomedsearch.com)
  • ACE inhibitors, or angiotensin - converting enzyme inhibitors, treat high blood pressure by relaxing blood. (everydayhealth.com)
  • Angiotensin - converting enzyme inhibitors - commonly called ACE inhibitors - prevent an enzyme in your. (everydayhealth.com)
  • diuretics and angiotensin converting enzyme inhibitors (ACE. (everydayhealth.com)
  • converting enzyme (ACE) converts the hormone angiotensin I into. (everydayhealth.com)
  • Angiotensin converting enzyme inhibitors cause cough in some patients, but the mechanism of this effect is not known. (bmj.com)
  • Nine patients in whom angiotensin converting enzyme inhibitors had not been associated with cough served as controls. (bmj.com)
  • The benefit of these medications over angiotensin-converting-enzyme (ACE) inhibitors has not been proven aside from a reduction in dry cough. (cmaj.ca)
  • 1 Although angiotensin-receptor blockers were effective in reducing mortality and morbidity associated with hypertension in one large trial, patients in the control group were not given an angiotensin-converting-enzyme (ACE) inhibitor. (cmaj.ca)
  • Note: ACE = angiotensin-converting enzyme, ARB = angiotensin-receptor blocker. (cmaj.ca)
  • The angiotensin-converting enzyme (ACE)-related carboxypeptidase, ACE2, is a type I integral membrane protein of 805 amino acids that contains one HEXXH + E zinc-binding consensus sequence. (rcsb.org)
  • 3. angiotensin-converting enzyme inhibitor (n. (synonym.com)
  • Quantitative RT-PCR analyses showed an up-regulation of renin, angiotensin-converting enzyme, as well as AT1R in the inflamed spinal cord and the immune system, including antigen presenting cells (APC). (pnas.org)
  • Treatment with the renin inhibitor aliskiren, the angiotensin II converting-enzyme inhibitor enalapril, as well as preventive or therapeutic application of the AT1R antagonist losartan, resulted in a significantly ameliorated course of MOG-EAE. (pnas.org)
  • The purpose of this study is measure the alterations in renal blood oxygenation after angiotensin II converting enzyme inhibition. (clinicaltrials.gov)
  • If surgical repair must be postponed, diuretics and afterload reducers, such as angiotensin-converting enzyme (ACE) inhibitors or calcium channel blockers, have proved helpful in adults and children. (medscape.com)
  • Moreover, alterations in the expression of angiotensin-converting enzyme-1, angiotensin-converting enzyme-2, and angiotensin-converting enzyme-3 might be one of the most important mechanisms underlying both female and male infertility. (mdpi.com)
  • However, as a pseudogene in humans, further studies are needed to explore whether the abnormal angiotensin-converting enzyme-3 gene could result in the problems of human reproduction. (mdpi.com)
  • unlike angiotensin-converting enzyme inhibitors, they do not inhibit bradykinin metabolism or enhance prostaglandin synthesis. (aafp.org)
  • Cough occurs much less often with these agents than with angiotensin-converting enzyme inhibitors, and they do not adversely affect lipid profiles or cause rebound hypertension after discontinuation. (aafp.org)
  • Renin, an enzyme produced primarily by the juxtaglomerular cells of the kidney, catalyzes the conversion of angiotensinogen into an inactive substance, angiotensin I (A-I). Angiotensin-converting enzyme (ACE) then converts A-I to the physiologically active angiotensin II (A-II), which causes potent vasoconstriction, aldosterone secretion and sympathetic activation. (aafp.org)
  • Components of the renin-angiotensin-aldosterone system and sites at which angiotensin-converting enzyme (ACE) inhibitors work and angiotensin-II receptor antagonists interrupt the type 1-receptor subtype (AT 1 ) of angiotensin II. (aafp.org)
  • Aim: The aim of this study was to evaluate the association with angiotensin converting enzyme gene polymorphism and changes in its enzyme serum level in preeclamptic patients compared to non preeclamptic control group together with studying the changes in umbilical artery and uterine artery Doppler. (scirp.org)
  • The story of angiotensin converting enzyme (ACE) inhibitors started approximately 50 years ago, when it was discovered that human plasma incubated with the venom of the Brazilian viper, Bothrops Jararaca , generated a hypotensive compound. (bmj.com)
  • The observation was then made by Vane that these peptides could also block the conversion of angiotensin I into angiotensin II via the angiotensin converting enzyme. (bmj.com)
  • Dipeptidyl peptidase-4 inhibitors can inhibit angiotensin converting enzyme. (medworm.com)
  • 172638 Authors: Abouelkheir M, El-Metwally TH Abstract Angiotensin-1 converting enzyme inhibitors (ACEIs) improve insulin sensitivity. (medworm.com)
  • Days Performed: Mon-Sat The use of angiotensin converting enzyme (ACE) - inhibiting antihypertensive drugs will cause decreased ACE values. (akronchildrens.org)
  • In the present study, we investigated the inhibitory effects of four tea catechins, including (−)-epicatechin (EC), (−)-epigallocatechin (EGC), (−)-epicatechin gallate (ECg) and (−)-epigallocatechin gallate (EGCg), on angiotensin converting enzyme (ACE) activity in vitro . (go.jp)
  • Angiotensin converting enzyme inhibitors are used in less than one half of transplant recipients. (bioportfolio.com)
  • Preliminary data suggest that angiotensin converting enzyme inhibitors retard the atherosclerotic plaque development that is the hallmark of cardiac allograft vasculopathy. (bioportfolio.com)
  • The objective of this project is to investigate the role of an angiotensin converting enzyme inhibitor, ramipril, in preventing the development of cardiac allograft vasculopathy. (bioportfolio.com)
  • and optionally a therapeutically effective amount of at least one member of the group consisting of an angiotensin converting enzyme inhibitor, an angiotensin (II) receptor 1 blocker, and an aldosterone blocker. (freepatentsonline.com)
  • Angiotensinogen is an α-2-globulin synthesized in the liver and is a precursor for angiotensin, but has also been indicated as having many other roles not related to angiotensin peptides. (wikipedia.org)
  • As shown, it is capable of clipping both angiotensin-I and angiotensin-II down further, to even small peptides (angiotensin 1-9 and 1-7) that have activities of their own. (sciencemag.org)
  • These classical functions of RAS are mediated by angiotensin effector peptides including Ang II, III and 1-7 ( Atlas, 2007 ). (frontiersin.org)
  • However, tissues are the main site of production of angiotensin peptides by the circulating RAS, whereby plasma-derived renin acts on plasma-derived angiotensinogen to generate Ang I, which is converted to Ang II by endothelial ACE ( 1 - 4 ). (frontiersin.org)
  • Drugs that inhibit ACE, and thus block the conversion of angiotensin I to angiotensin II, are used to lower blood pressure in patients with hypertension . (britannica.com)
  • More than two decades ago, drugmakers searching for new hypertension medications unearthed a mysterious new cell receptor that responded to a hormone known as angiotensin II. (nature.com)
  • Intrarenal renin - angiotensin system activation in end-stage renal disease 28179627 2018 07 30 2018 12 02 1348-4214 40 4 2017 04 Hypertension research : official journal of the Japanese Society of Hypertension Hypertens. (tripdatabase.com)
  • Are Local Renin-Angiotensin Systems the Focal Points for Understanding Salt Sensitivity in Hypertension? (springer.com)
  • Angiotensin II represents a key molecule in hypertension and cerebrovascular pathology. (hindawi.com)
  • Mechanisms proposed to explain the benefit of angiotensin blockade found in the early studies included the direct effects of angiotensin blockade on the structural and electrical properties of the atria, as well as the indirect influence of improved control of heart failure and hypertension (in patients with these conditions), both of which are known risk factors for atrial fibrillation (AF) [ 1 ]. (uptodate.com)
  • Renin-angiotensin system (RAS) is activated in metabolic syndrome (MetS), and RAS inhibitors are preferred for the treatments of hypertension with MetS. (hindawi.com)
  • Angiotensin II has been investigated for the treatment, basic science, and diagnostic of Hypertension, Renin Angiotensin System, and Idiopathic Membranous Nephropathy. (drugbank.ca)
  • The LIFE trial (Cardiovascular morbidity and mortality in the Losartan Intervention For Endpoint reduction in hypertension study) compared losartan with atenolol, a beta-blocker, to determine whether selective blocking of angiotensin II improves left ventricular hypertrophy (LVH) beyond reducing blood pressure over 4 years. (uspharmacist.com)
  • Meta-analyses that included several randomized trials failed to show superiority of angiotensin-receptor blockers over ACE inhibitors for the treatment of hypertension, 6 heart failure 7 or the secondary prevention of coronary artery disease. (cmaj.ca)
  • It exerts its various actions on the cardiovascular and renal system, mainly via interaction with the angiotensin II type-1 receptor (AT1R), which contributes to blood pressure regulation and development of hypertension but may also mediate effects on the immune system. (pnas.org)
  • Clinical trials indicate that angiotensin-II receptor antagonists are effective and safe in the treatment of hypertension. (aafp.org)
  • Since the first angiotensin-II receptor antagonists were introduced a few years ago, numerous clinical trials have been conducted on their use in patients with hypertension and their potential use in patients with congestive heart failure. (aafp.org)
  • The angiotensin-II receptor antagonists that have been labeled for use in hypertension by the U.S. Food and Drug Administration (FDA) are losartan (Cozaar), valsartan (Diovan), irbesartan (Avapro), candesartan (Atacand) and telmisartan (Micardis). (aafp.org)
  • The renin-angiotensin-aldosterone system plays an integral role in the pathophysiology of hypertension because it affects the regulation of fluid volume, electrolyte balance and blood volume. (aafp.org)
  • The enormous success of ACE inhibitors in hypertension and heart failure spurred hope that adding a second drug to block the renin-angiotensin system would yield improved outcomes. (cardiobrief.org)
  • Recent studies suggest that hypertension induced by angiotensin II (AngII) results primarily from the renal effects of this hormone. (pnas.org)
  • It has been theorized that dual blockade of the renin-angiotensin-aldosterone system (RAAS) might prove even more beneficial, but these hopes have not been realized. (forbes.com)
  • Hsu and colleagues provide reassuring information complementing the data from randomized clinical trials that renin-angiotensin-aldosterone system (RAAS) blockade can be safely implemented even in advanced chronic kidney disease," according to Meyeon Park, MD , and Chi-yuan Hsu, MD , of the University of California San Francisco. (medpagetoday.com)
  • 1996). Effects of angiotensin II receptor blockade during exercise: comparison of losartan and saralasin. (exrx.net)
  • Although definitive evidence supporting dual blockade of the renin-angiotensin system has never been found, more than 200,000 patients in the US currently receive this therapy. (cardiobrief.org)
  • What is the role of renin-angiotensin blockade in the treatment of immunoglobulin A (IgA) nephropathy? (medscape.com)
  • Throughout the body, angiotensin II is a potent vasoconstrictor of arterioles . (wikipedia.org)
  • It converts the hormone angiotensin I to the active vasoconstrictor angiotensin II. (wikipedia.org)
  • Angiotensin II is a potent vasoconstrictor in a substrate concentration-dependent manner. (wikipedia.org)
  • The most important is known as angiotensin II, a powerful vasoconstrictor that stimulates steroid production by the adrenal glands, reduces fluid loss from the kidneys, and also functions as a neurotransmitter. (dictionary.com)
  • Angiotensin II is an active vasoconstrictor that narrows the blood vessels and increases systemic blood pressure. (news-medical.net)
  • Kessler K, Harakal C. Potentiation of the vasoconstrictor effect of angiotensin by catecholamines in vitro. (ahajournals.org)
  • As of December 21, 2017 the FDA approved La Jolla Pharmaceutical's Giapreza (angiotensin II) Injection for Intravenouse Infusion for the indication of acting as a vasoconstrictor to increase blood pressure in adults with septic or other distributive shock. (drugbank.ca)
  • Angiotensin II is a vasoconstrictor indicated for increasing blood pressure in adults with septic or other distributive shock Label . (drugbank.ca)
  • It prevents the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion. (medscape.com)
  • In the Veterans Affairs Nephropathy in Diabetes (VA NEPHRON-D) trial, Linda Fried and colleagues randomized type 2 diabetics with proteinuric kidney disease already receiving the angiotensin-receptor blocker losartan to either the ACE inhibitor lisinopril or placebo. (forbes.com)
  • ACE is a target of ACE inhibitor drugs, which decrease the rate of Angiotensin II production. (wikipedia.org)
  • So you can see how an ACE-1 inhibitor could be good for high blood pressure, by blocking any formation of angiotensin II, and a renin inhibitor would be as well, by blocking the whole process a bit further upstream, and something that blocked that last binding step (an antagonist of the angiotensin receptor) would also probably work. (sciencemag.org)
  • 14.Phakdeekitcharoen B, Leelasa-nguan P. Effects of an ACE inhibitor or angiotensin receptor blocker on potassium in CAPD patients. (webmd.com)
  • Angiotensin II inhibitors with calcium channel blocking agents is a combination medicine containing both an angiotensin II inhibitor and a calcium channel blocker. (drugs.com)
  • The angiotensin II inhibitor stops the activation of the angiotensin II receptor which results in vasodilation, a reduction of aldosterone production and reduced vasopressin. (drugs.com)
  • for the study patients these and the cough index were measured twice before rechallenge for two weeks with an angiotensin enzyme inhibitor and once afterwards. (bmj.com)
  • A competitive ACE inhibitor, it reduces angiotensin II levels, decreasing aldosterone secretion. (medscape.com)
  • Adding a non-steroidal anti-inflammatory drug (NSAID) to dual antihypertensive therapy (a diuretic plus either an ACE inhibitor or an angiotensin receptor blocker) is associated with an increase in risk for kidney injury, according to a large new retrospective study published in BMJ. (cardiobrief.org)
  • Instead, they block the effects of angiotensin, preventing the hormone from narrowing the blood vessels. (heart.org)
  • The Local Cardiac Renin-Angiotensin Aldosterone System, Second Edition updates new findings on the local renin-angiotensin systems (RAS) with a focus on the local RAASs of the cardiovascular system and kidney. (springer.com)
  • It is suggested that this central effect also contributes to the cardiovascular response to endogenous angiotensin. (bmj.com)
  • There is also no question that the enhancing effect of angiotensin II on sympathetic cardiovascular influences is reciprocated because sympathetic nerve activity is an important determinant of renal secretion of renin R3 R4 and thus of the activity of the renin-angiotensin system. (ahajournals.org)
  • The octapeptide angiotensin II (Ang II) exerts a wide range of effects on the cardiovascular system. (anaspec.com)
  • Renin Angiotensin System (RAS) is a hormonal system that regulates blood pressure and fluid balance through a coordinated action of renal, cardiovascular, and central nervous systems. (frontiersin.org)
  • Interpretation Had access to angiotensin-receptor blockers been restricted, the potential cost savings to the Canadian health care system might have been more than $77 million in 2006, likely without any adverse effect on cardiovascular health. (cmaj.ca)
  • Angiotensin II, one of the most potent neurohormones in this system, is known to cause vasoconstriction, sodium retention, cardiac hypertrophy, cell death, endothelial dysfunction and other detrimental cardiovascular effects. (oncologynurseadvisor.com)
  • Likewise it converts the inactive decapeptide angiotensin I to the octapeptide angiotensin II by removing the dipeptide His-Leu. (wikipedia.org)
  • ACE-1 takes off two more amino acids to give you the octapeptide known as angiotensin-II, and that one has profound effects on raising blood pressure (it has many other functions as well). (sciencemag.org)
  • Human heart chymase, a chymotrypsin-like serine proteinase, hydrolyzes the Phe8-His9 bond to yield the octapeptide hormone angiotensin II and His-Leu. (anaspec.com)
  • Angiotensin II (AngII: Asp-Arg-Val-Tyr-Ile-His-Pro-Phe) is an octapeptide hormone playing an important role in the regulation of blood pressure. (mcmaster.ca)
  • Saino et al 1 and Lyons et al 2 published provocative findings regarding the vascular level interaction of the sympathetic and renin-angiotensin systems. (ahajournals.org)
  • It would be important, however, to device a way to see whether this is the case also in vivo and what is the relative importance of this mechanism in the overall positive feed-back interaction between the sympathetic and the renin-angiotensin systems. (ahajournals.org)
  • Comparative Analysis of Renin - Angiotensin System (RAS)-Related Gene Expression Between Hypertensive and Normotensive Rats BACKGROUND The renal renin - angiotensin system (RAS) is physiologically important for blood pressure regulation. (tripdatabase.com)
  • Intrarenal renin - angiotensin system activation in end-stage renal disease. (tripdatabase.com)
  • Angiotensin II is under investigation for the treatment of Sepsis, Septic Shock, Diabetes Mellitus, and Acute Renal Failure. (drugbank.ca)
  • Angiotensin II regulation of renal vascular ENaC proteins. (biomedsearch.com)
  • In renal epithelial tissue, ENaC expression is regulated by angiotensin II (Ang II). (biomedsearch.com)
  • This study evaluates prospectively the effects of an anti-angiotensin II regimen on renal outcome in patients with mesangioproliferative glomerulonephritis followed-up for 10 years. (clinicaltrials.gov)
  • The understanding of kidney adaptive mechanisms to renin angiotensin system effects in healthy subjects will be useful for the early detection of renal disease and for the development of new therapies to decrease the progression of the disease and its consequences. (clinicaltrials.gov)
  • Because the renal consequences of WNK4 carrying pseudoaldosteronism type II mutations resemble the response to intravascular volume depletion (promotion of salt reabsorption without K + secretion), a condition that is associated with high angiotensin II (AngII) levels, it has been proposed that AngII signaling might affect WNK4 modulation of the NCC. (pnas.org)
  • Angiotensin I is produced by the action of renin (an enzyme produced by the kidneys ) on a protein called angiotensinogen, which is formed by the liver . (britannica.com)
  • Plasma angiotensinogen levels are increased by plasma corticosteroid, estrogen, thyroid hormone, and angiotensin II levels. (wikipedia.org)
  • Angiotensin I (CAS# 11128-99-7), officially called proangiotensin, is formed by the action of renin on angiotensinogen. (wikipedia.org)
  • Angiotensin I ( CAS # 11128-99-7) is formed by the action of renin on angiotensinogen . (wikipedia.org)
  • eng R01 DK072408 DK NIDDK NIH HHS United States Journal Article Comment 2017 02 09 England Hypertens Res 9307690 0916-9636 11002-13-4 Angiotensinogen 11128-99-7 Angiotensin II EC 3.4.23.15 Renin IM Hypertens Res. (tripdatabase.com)
  • Angiotensin I, itself a decapeptide with weak biological activity, is produced from angiotensinogen and then quickly converted to angiotensin II by angiotensin converting enzymes (ACE). (drugbank.ca)
  • Renin cleaves an inactive peptide called angiotensinogen , converting it into angiotensin I . (bionity.com)
  • That results in the decreased formation of angiotensin II and decreased metabolism of bradykinin, which leads to systematic dilation of the arteries and veins and a decrease in arterial blood pressure. (wikipedia.org)
  • AngII (angiotensin II), which induces oxidative stress and inflammation, is also implicated in the progression of atherosclerosis. (mendeley.com)
  • Angiotensin II (AngII) via AT1 receptor is reported to increase brain Aβ level via different mechanisms including increasing amyloid precursor protein (APP) mRNA, β-secretase activity, and presenilin expression. (frontiersin.org)
  • The novelty of the medication lies in the fact that it is the first and only use of synthetic human angiotensin II to help maintain body blood pressure. (drugbank.ca)
  • 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). (wikipedia.org)
  • It is concluded that angiotensin II not only facilitates the activation of preexisting collateral vascular pathways but also has angiogenic properties and therefore could play an active role not only in the fast but also in the slow phase of the development of collateral circulation. (nih.gov)
  • In this study, we tested the role of α7nAChR in angiotensin II (Ang II)-induced senescence of vascular smooth muscle cells (VSMCs). (ingentaconnect.com)
  • Saralasin, a partial agonist angiotensin II receptor, does not appear to affect mean arterial pressure (MAP) and systemic vascular resistance (SVR) during exercise. (exrx.net)
  • Activation of the type 1 angiotensin II receptor (AT1) triggers proinflammatory signaling through pathways independent of classical Gq signaling that regulate vascular homeostasis. (jci.org)
  • By developing native and glycosylated forms of the angiotensin-(1-7) peptide for vascular cognitive impairment, ProNeurogen hopes to plug a treatment gap that repurposed Alzheimer's disease drugs have failed to fill. (biocentury.com)
  • These patients are often being treated with ACE-1 inhibitors or angiotensin-receptor antagonists. (sciencemag.org)
  • 13.Fujii H, Nakahama H, Yoshihara F, Nakamura S, Inenaga T, Kawano Y. Life-threatening Hyperkalemia during a Combined Therapy with the Angiotensin Receptor Blocker Candesartan and Spironolactone. (webmd.com)
  • The purpose of this study is to determine whether a treatment for diabetic nephropathy, the angiotensin receptor blocker candesartan, modifies mediators of kidney injury independent of blood pressure and the relationships to drug dose. (clinicaltrials.gov)
  • NEW ORLEANS, Nov. 11 -- The angiotensin-receptor blocker irbesartan (Avapro) holds no benefit for heart failure patients with preserved left ventricular ejection fraction, researchers found. (medpagetoday.com)
  • Although they offer some tantalizing signals and still some persistent concerns about crossover," she said, "they deliver a pretty consistent message and really don't justify adding an ACE or an ARB [angiotensin-receptor blocker] for a patient with heart failure and preserved ejection fraction if the blood pressure is already controlled. (medpagetoday.com)
  • The treatment of a large proportion of patients with multiple inhibitors of the renin-angiotensin-aldosterone system might have left little room for further benefit from the addition of an angiotensin-receptor blocker," the researchers said. (medpagetoday.com)
  • Barry Brenner, Boston, MA, discussed the Reduction of Endpoints in NIDDM with the Angiotensin II Antagonist Losartan (RENAAL) trial of 1,513 patients with type 2 diabetes and nephropathy from 250 centers in 29 countries. (diabetesjournals.org)
  • [4] Angiotensin II also stimulates the secretion of the hormone aldosterone [4] from the adrenal cortex . (wikipedia.org)
  • In addition, inhibiting angiotensin II formation diminishes angiotensin II-mediated aldosterone secretion from the adrenal cortex, leading to a decrease in water and sodium reabsorption and a reduction in extracellular volume. (wikipedia.org)
  • Angiotensin II also increases Aldosterone secretion, therefore, it acts as an endocrine , autocrine / paracrine , and intracrine hormone. (wikipedia.org)
  • Interruption of the renin-angiotensin system in hypertensive patients by captopril induces sustained reduction in aldosterone secretion, potassium retention and natruiresis. (webmd.com)
  • This conversion from angiotensin I to angiotensin II and subsequent receptor binding leads to increases in vasoconstriction, aldosterone secretion, and sympa-thetic activation. (uspharmacist.com)
  • 1 , 4 Angiotensin-II receptor blockers antagonize A-II-induced biologic actions, including smooth muscle contraction, sympathetic pressor mechanisms and aldosterone secretion. (aafp.org)
  • The AT1 receptor is the best elucidated angiotensin receptor. (wikipedia.org)
  • The renin-angiotensin system ( RAS ) or the renin-angiotensin-aldosterone system ( RAAS ) is a hormone system that regulates blood pressure and fluid balance . (wikipedia.org)
  • Our program will also push beyond the barriers of our current understanding of the RAAS by inviting speakers who have not previously attended the Angiotensin GRC. (grc.org)
  • Angiotensin II is a naturally occurring peptide hormone of the renin-angiotensin-aldosterone-system (RAAS) that has the capacity to cause vasoconstriction and an increase in blood pressure in the human body. (drugbank.ca)
  • The renin-angiotensin system (RAS) or the renin-angiotensin-aldosterone system (RAAS) is a hormone system that helps regulate long-term blood pressure and extracellular volume in the body. (bionity.com)
  • Activation of the renin-angiotensin-aldosterone system (RAAS) plays an important role in development and progression of heart failure (HF). (oncologynurseadvisor.com)
  • The renin-angiotensin-aldosterone system (RAAS) is a key modulator of blood pressure. (pnas.org)
  • COVID-19 and Angiotensin Drugs: Help or Harm? (medscape.com)
  • It is part of the renin-angiotensin system , which is a major target for drugs that raises blood pressure. (wikipedia.org)
  • Angiotensin II receptor blockers, also known as ARB blockers or angiotensin 2 receptor blockers, are drugs used to treat high blood pressure and heart failure. (heart.org)
  • Angiotensin II receptor blockers are often used in patients who cannot tolerate a common type of drugs known as ACE inhibitors. (heart.org)
  • We show that this type of immunosuppression may be reversed by reprogramming the microenvironment with drugs called angiotensin receptor blockers. (news-medical.net)
  • The angiotensin receptor blockers came next (drugs with the -sartan suffix), and there are several of them. (sciencemag.org)
  • are there any angiotensin drugs that dont include hydrochothiazide? (drugs.com)
  • Patients are more likely to continue to take angiotensin-receptor blockers compared with other classes of blood pressure drugs, according to the findings of a meta-analysis by US researchers. (pulsetoday.co.uk)
  • The findings don't close the book on angiotensin-receptor blockers and other drugs in the class, though, Drs. Jessup and Massie agreed. (medpagetoday.com)
  • A peptide analog to angiotensin II that is used as a vasopressor in the treatment of certain types of shock and circulatory collapse. (dictionary.com)
  • Any of several polypeptide hormones, designated by Roman numerals, that are involved in the regulation of blood pressure, especially one of them, angiotensin II, which is a strong vasopressor. (thefreedictionary.com)
  • Consequently, angiotensin II demonstrates its strong vasopressor activity when it is rapidly degraded by aminopeptidases A and M into further entities like angiotensin III and angiotensin IV, respectively. (drugbank.ca)
  • Angiotensin-receptor blockers and ACE inhibitors are already widely used for the treatment of heart failure with preserved ejection fraction, Dr. Redfield said. (medpagetoday.com)
  • Inhibitors of the renin-angiotensin-aldosterone system have improved outcomes, though not mortality, in patients with heart failure with a low left ventricular ejection fraction. (medpagetoday.com)
  • [3] Angiotensin II is a potent vasoconstrictive peptide that causes blood vessels to narrow, resulting in increased blood pressure. (wikipedia.org)
  • Angiotensin II acts directly on blood vessels, causing their constriction and thereby raising blood pressure . (britannica.com)
  • Angiotensin is a peptide hormone that causes vasoconstriction and an increase in blood pressure. (wikipedia.org)
  • It is part of the renin-angiotensin system, which regulates blood pressure. (wikipedia.org)
  • This peptide hormone constricts blood vessels, but, oddly, blocking the so-called angiotensin II receptor type 2 (AT2) appeared to have no effect on blood pressure, so the target was largely ignored by drug developers. (nature.com)
  • Angiotensin II binds to the type 1 angiotensin II receptor (AT1), which sets off a number of actions that result in vasoconstriction and therefore increased blood pressure. (wikipedia.org)
  • ACE inhibitors reduce the level of angiotensin II by inhibiting the enzyme, leading to the widening of the blood vessels (vasodilation) and subsequent reduction of the systemic blood pressure. (news-medical.net)
  • The renin-angiotensin system is often manipulated clinically to treat high blood pressure . (bionity.com)
  • Angiotensin also stimulates the release of aldosterone from the adrenal cortex to promote sodium retention by the kidneys. (wikipedia.org)
  • Angiotensin also stimulates the release of aldosterone , another hormone, from the adrenal cortex . (wikipedia.org)
  • Angiotensin I appears to have no direct biological activity and exists solely as a precursor to angiotensin II. (wikipedia.org)
  • Sources of data for model parameters included IMS Health Canada data collected from one-third of all retail pharmacies for the cost and use of angiotensin-receptor blockers and ACE inhibitors in each province, as well as published studies for administrative costs and incidence of dry cough. (cmaj.ca)
  • ACE inhibitors and angiotensin-receptor blockers have been found to effectively slow progression of kidney disease. (forbes.com)
  • 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. (wikipedia.org)
  • While the enzyme inhibitors work by reducing the level of angiotensin II in the body, the receptor blockers inhibit the function of angiotensin II by directly blocking the specific receptor. (news-medical.net)
  • In rats, high dose of sitagliptin was able to inhibit ACE activity and reduce angiotensin II levels while linagliptin has only a mild effect. (medworm.com)
  • Indeed, it has been demonstrated that, upon acting on the AT1 receptor, angiotensin II activates matrix metalloproteases that release the epidermal growth factor (EGF), binding to its receptor promotes the activation of mammalian target of rapamycin (mTOR) and ribosomal S6 kinase-1, both of which inhibit phosphatidylinositol 3-kinase insulin signaling, thus favoring insulin resistance ( 2 - 4 ). (scielo.br)
  • At a symposium at the 61st Scientific Sessions of the ADA in June 2001, the results of three recent diabetic nephropathy trials with angiotensin II subtype 1 receptor antagonists were presented. (diabetesjournals.org)
  • Abcam's Angiotensin A in vitro competitive ELISA (Enzyme-Linked Immunosorbent Assay) kit is designed for the accurate quantitative measurement of Angiotensin A in plasma and serum. (abcam.com)
  • Dose‐response curves from human plasma and serum diluted into assay buffer were compared to the Angiotensin A standard curve. (abcam.com)
  • Doppler study of umbilical and uterine arteries and the detection of Angiotensin converting gene polymorphism by PCR with Estimation of serum ACE in serum by ELISA technique. (scirp.org)
  • Angiotensin was isolated in the late 1930s (first named 'angiotonin' or 'hypertensin') and subsequently characterized and synthesized by groups at the Cleveland Clinic and Ciba laboratories. (wikipedia.org)
  • Angiotensin was independently isolated in Indianapolis and Argentina in the late 1930s (as 'angiotonin' and 'hypertensin', respectively) and subsequently characterised and synthesized by groups at the Cleveland Clinic and Ciba laboratories in Basel, Switzerland. (wikipedia.org)
  • The suggestion is that higher local concentrations of either angiotensin II or perindoprilat are achieved when a vessel is noradrenergically preconstricted by infused norepinephrine or lower body negative pressure. (ahajournals.org)
  • Interestingly, some clinical studies have demonstrated that treatment with either angiotensin I-converter enzyme inhibitors (ACEI) or angiotensin II receptor antagonist (ARA) reduces the incidence of diabetes mellitus in high risk patients ( 5 , 6 ). (scielo.br)
  • 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. (wikipedia.org)
  • In the kidneys, angiotensin II constricts glomerular arterioles, having a greater effect on efferent arterioles than afferent. (wikipedia.org)
  • In addition, angiotensin II increases blood osmolality and volume by inducing water and sodium retention in the kidneys. (news-medical.net)
  • Angiotensin is a short peptide hormone that causes constriction of the efferent arteriole at the glomerulus, leading to increased glomerular filtration pressure. (edren.org)
  • Design and Synthesis of Angiotensin IV Peptidomimetics Targeting the Insulin-Regulated Aminopeptidase (IRAP) (Ph.D. thesis). (wikipedia.org)
  • Angiotensin II and ET-1, both at 10 nmol/L, induced myocyte hypertrophy, as demonstrated by increased protein content and synthesis, [Ca 2+ ] i levels, protein kinase C (PKC) activity and phosphorylation of extracellular signal-regulated kinase, c-Jun N-terminal kinase and mitogen-activated protein kinase (MAPK) p38 (p38). (ingentaconnect.com)
  • One is in the synthesis of angiotensin II, which has vasoconstrictive properties, promotes retention of sodium and water, and promotes cell growth. (bmj.com)
  • The AT4 receptor is activated by the angiotensin II metabolite angiotensin IV, and may play a role in regulation of the CNS extracellular matrix, as well as modulation of oxytocin release. (wikipedia.org)
  • Angiotensin III is a metabolite of angiotensin II and shares similar, though less potent, actions. (britannica.com)
  • See 'The electrocardiogram in atrial fibrillation' and 'Actions of angiotensin II on the heart' and 'Epidemiology of and risk factors for atrial fibrillation' . (uptodate.com)
  • Angiotensin also has direct effects on many other cells, including the podocyte, and it is likely that some of its effects depend on these other actions too. (edren.org)
  • Most of these actions are mediated through angiotensin II type 1 (AT1) receptor. (oncologynurseadvisor.com)