Angiotensin I: 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.Angiotensin II: 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.Receptor, Angiotensin, Type 1: 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.Receptors, Angiotensin: Cell surface proteins that bind ANGIOTENSINS and trigger intracellular changes influencing the behavior of cells.Angiotensins: 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.Peptidyl-Dipeptidase A: 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.Receptor, Angiotensin, Type 2: 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.Angiotensin III: 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%).Renin: 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.Angiotensin Receptor Antagonists: Agents that antagonize ANGIOTENSIN RECEPTORS. Many drugs in this class specifically target the ANGIOTENSIN TYPE 1 RECEPTOR.Angiotensin-Converting Enzyme Inhibitors: 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.Angiotensin II Type 1 Receptor Blockers: 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.Teprotide: 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.Renin-Angiotensin System: 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.Captopril: 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.Losartan: An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.Saralasin: 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.Angiotensinogen: 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.TetrazolesBlood Pressure: PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.Enalaprilat: 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.Cilazapril: 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.Biphenyl CompoundsAngiotensin II Type 2 Receptor Blockers: Agents that antagonize the ANGIOTENSIN II TYPE 2 RECEPTOR.1-Sarcosine-8-Isoleucine Angiotensin II: An ANGIOTENSIN II analog which acts as a highly specific inhibitor of ANGIOTENSIN TYPE 1 RECEPTOR.Bradykinin: 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.Enalapril: An angiotensin-converting enzyme inhibitor that is used to treat HYPERTENSION and HEART FAILURE.Chymases: 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.Lisinopril: One of the ANGIOTENSIN-CONVERTING ENZYME INHIBITORS (ACE inhibitors), orally active, that has been used in the treatment of hypertension and congestive heart failure.Imidazoles: 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).Aldosterone: 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.Vasoconstrictor Agents: Drugs used to cause constriction of the blood vessels.Hypertension: 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.Kidney: Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.Antihypertensive Agents: 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.Oligopeptides: Peptides composed of between two and twelve amino acids.Benzimidazoles: Compounds with a BENZENE fused to IMIDAZOLES.3-Mercaptopropionic Acid: An inhibitor of glutamate decarboxylase. It decreases the GAMMA-AMINOBUTYRIC ACID concentration in the brain, thereby causing convulsions.Neprilysin: 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.Thiorphan: A potent inhibitor of membrane metalloendopeptidase (ENKEPHALINASE). Thiorphan potentiates morphine-induced ANALGESIA and attenuates naloxone-precipitated withdrawal symptoms.Rats, Sprague-Dawley: 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.Vasoconstriction: The physiological narrowing of BLOOD VESSELS by contraction of the VASCULAR SMOOTH MUSCLE.Dose-Response Relationship, Drug: The relationship between the dose of an administered drug and the response of the organism to the drug.Rats, Inbred SHR: A strain of Rattus norvegicus with elevated blood pressure used as a model for studying hypertension and stroke.Hypertension, Renal: Persistent high BLOOD PRESSURE due to KIDNEY DISEASES, such as those involving the renal parenchyma, the renal vasculature, or tumors that secrete RENIN.Rats, Inbred WKY: A strain of Rattus norvegicus used as a normotensive control for the spontaneous hypertensive rats (SHR).Pyridines: Compounds with a six membered aromatic ring containing NITROGEN. The saturated version is PIPERIDINES.Rats, Inbred Strains: 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.Diet, Sodium-Restricted: A diet which contains very little sodium chloride. It is prescribed by some for hypertension and for edematous states. (Dorland, 27th ed)Norepinephrine: 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.Muscle, Smooth, Vascular: The nonstriated involuntary muscle tissue of blood vessels.Radioimmunoassay: 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.Nephrectomy: Excision of kidney.PyridazinesRenal Circulation: The circulation of the BLOOD through the vessels of the KIDNEY.Drinking: The consumption of liquids.Placental Function Tests: Methods used for the assessment of placental function.Juxtaglomerular Apparatus: 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.Bethanidine: A guanidinium antihypertensive agent that acts by blocking adrenergic transmission. The precise mode of action is not clear.Dipeptides: Peptides composed of two amino acid units.Hypertension, Renovascular: Hypertension due to RENAL ARTERY OBSTRUCTION or compression.Rabbits: 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.Ramipril: A long-acting angiotensin-converting enzyme inhibitor. It is a prodrug that is transformed in the liver to its active metabolite ramiprilat.Aorta: The main trunk of the systemic arteries.Serine Endopeptidases: Any member of the group of ENDOPEPTIDASES containing at the active site a serine residue involved in catalysis.Time Factors: Elements of limited time intervals, contributing to particular results or situations.Hemodynamics: The movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM.Myocardium: 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.Angiotensin Amide: The octapeptide amide of bovine angiotensin II used to increase blood pressure by vasoconstriction.Cells, Cultured: 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.Rats, Wistar: A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.Dogs: 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)Protease Inhibitors: Compounds which inhibit or antagonize biosynthesis or actions of proteases (ENDOPEPTIDASES).Receptors, Bradykinin: 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, Messenger: 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.Vascular Resistance: 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.Chromatography, High Pressure Liquid: Liquid chromatographic techniques which feature high inlet pressures, high sensitivity, and high speed.Blood Vessels: Any of the tubular vessels conveying the blood (arteries, arterioles, capillaries, venules, and veins).Heart Rate: The number of times the HEART VENTRICLES contract per unit of time, usually per minute.Furosemide: A benzoic-sulfonamide-furan. It is a diuretic with fast onset and short duration that is used for EDEMA and chronic RENAL INSUFFICIENCY.Perindopril: An angiotensin-converting enzyme inhibitor. It is used in patients with hypertension and heart failure.Peptide Fragments: Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.Perinephritis: Inflammation of the connective and adipose tissues surrounding the KIDNEY.Sodium Chloride: A ubiquitous sodium salt that is commonly used to season food.Sodium: A member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23.Arteries: The vessels carrying blood away from the heart.Proline: 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.Renal Artery: A branch of the abdominal aorta which supplies the kidneys, adrenal glands and ureters.Perfusion: Treatment process involving the injection of fluid into an organ or tissue.Aorta, Thoracic: The portion of the descending aorta proceeding from the arch of the aorta and extending to the DIAPHRAGM, eventually connecting to the ABDOMINAL AORTA.Kidney Cortex: The outer zone of the KIDNEY, beneath the capsule, consisting of KIDNEY GLOMERULUS; KIDNEY TUBULES, DISTAL; and KIDNEY TUBULES, PROXIMAL.Endothelium: A layer of epithelium that lines the heart, blood vessels (ENDOTHELIUM, VASCULAR), lymph vessels (ENDOTHELIUM, LYMPHATIC), and the serous cavities of the body.Hypertension, Malignant: 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.Endopeptidases: A subclass of PEPTIDE HYDROLASES that catalyze the internal cleavage of PEPTIDES or PROTEINS.Kinetics: The rate dynamics in chemical or physical systems.Mesenteric Arteries: Arteries which arise from the abdominal aorta and distribute to most of the intestines.Valine: 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.Endothelium, Vascular: Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.Natriuresis: Sodium excretion by URINATION.Phosphinic Acids: Inorganic or organic derivatives of phosphinic acid, H2PO(OH). They include phosphinates and phosphinic acid esters.Carboxypeptidases: Enzymes that act at a free C-terminus of a polypeptide to liberate a single amino acid residue.Cathepsin G: A serine protease found in the azurophil granules of NEUTROPHILS. It has an enzyme specificity similar to that of chymotrypsin C.Hydrolysis: The process of cleaving a chemical compound by the addition of a molecule of water.Vasodilation: The physiological widening of BLOOD VESSELS by relaxing the underlying VASCULAR SMOOTH MUSCLE.Kidney Glomerulus: A cluster of convoluted capillaries beginning at each nephric tubule in the kidney and held together by connective tissue.Substrate Specificity: A characteristic feature of enzyme activity in relation to the kind of substrate on which the enzyme or catalytic molecule reacts.Renal Artery Obstruction: 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).Enzyme Inhibitors: Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.Cardiomegaly: 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.Benzoates: Derivatives of BENZOIC ACID. Included under this heading are a broad variety of acid forms, salts, esters, and amides that contain the carboxybenzene structure.Lung: Either of the pair of organs occupying the cavity of the thorax that effect the aeration of the blood.Nitric Oxide: 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.Amino Acid Sequence: 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.Molecular Sequence Data: 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.Serine Proteinase Inhibitors: Exogenous or endogenous compounds which inhibit SERINE ENDOPEPTIDASES.Indomethacin: 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.Heart: The hollow, muscular organ that maintains the circulation of the blood.Indoles: 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.Peptides: 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.Regional Blood Flow: The flow of BLOOD through or around an organ or region of the body.NADPH Oxidase: 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.Kallikreins: 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).Glomerular Filtration Rate: 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.Analysis of Variance: A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.Hypertrophy: 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).Vasopressins: 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.Hydralazine: A direct-acting vasodilator that is used as an antihypertensive agent.Vasodilator Agents: Drugs used to cause dilation of the blood vessels.Subfornical Organ: A structure, situated close to the intraventricular foramen, which induces DRINKING BEHAVIOR after stimulation with ANGIOTENSIN II.Adrenal Glands: 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.Veins: The vessels carrying blood away from the capillary beds.Edetic Acid: 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, Intravenous: Injections made into a vein for therapeutic or experimental purposes.Hindlimb: 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)Fibrosis: Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury.Tissue Distribution: 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.Body Weight: The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.Propranolol: 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.Disease Models, Animal: 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.Signal Transduction: 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.Isoproterenol: 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.Glutamyl Aminopeptidase: 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.Polymorphism, Genetic: 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.Sympathetic Nervous System: 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.Muscle Contraction: 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.Reference Values: 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.Kidney Tubules, Proximal: 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.Swine: 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).Arginine Vasopressin: 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.ThiazepinesCathepsins: 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.EthersSodium Chloride, Dietary: Sodium chloride used in foods.Biological Assay: 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.Sheep: 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.Guinea Pigs: 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.Double-Blind Method: 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.Cricetinae: A subfamily in the family MURIDAE, comprising the hamsters. Four of the more common genera are Cricetus, CRICETULUS; MESOCRICETUS; and PHODOPUS.Proteinuria: The presence of proteins in the urine, an indicator of KIDNEY DISEASES.Osmolar Concentration: 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.Cattle: 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.Infusion Pumps, Implantable: 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.Mice, Knockout: 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.Phenylephrine: An alpha-1 adrenergic agonist used as a mydriatic, nasal decongestant, and cardiotonic agent.Zona Glomerulosa: 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.Mice, Inbred C57BLAldosterone Synthase: 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.Calcium: 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.Kinins: 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)

*Angiotensin-converting enzyme 2

"A novel angiotensin-converting enzyme-related carboxypeptidase (ACE2) converts angiotensin I to angiotensin 1-9". Circulation ... "A novel angiotensin-converting enzyme-related carboxypeptidase (ACE2) converts angiotensin I to angiotensin 1-9". Circulation ... Angiotensin converting enzyme 2 (ACE 2) is an exopeptidase that catalyses the conversion of angiotensin I to the nonapeptide ... Keidar S, Kaplan M, Gamliel-Lazarovich A (Feb 2007). "ACE2 of the heart: From angiotensin I to angiotensin (1-7)". ...

*Teprotide

It is an angiotensin converting enzyme inhibitor (ACE inhibitor), which inhibits the conversion of angiotensin I to angiotensin ... It was found that teprotide inhibits the enzyme that converts angiotensin I to angiotensin II. From this researchers conducted ... Cushman, D.W.; M.A. Ondetti (April 1991). "History of the design of captopril and related inhibitors of angiotensin converting ... by administering teprotide to dogs and rats and observing that it inhibited the vasopressor response induced by angiotensin I. ...

*Captopril suppression test

Aldosterone production is suppressed by captopril through the renin-angiotensin-aldosterone system. CST results are used to ...

*Angiotensin II receptor blocker

"Angiotensin FDA Drug Safety Communication: No increase in risk of cancer with certain blood pressure drugs--Angiotensin ... Angiotensin II receptor blockers (ARBs), also known as angiotensin II receptor antagonists , AT1 receptor antagonists or ... They block the activation of AT1 receptors, preventing the binding of angiotensin II. Angiotensin II receptor blockers are used ... Gales BJ, Bailey EK, Reed AN, Gales MA (February 2010). "Angiotensin-converting enzyme inhibitors and angiotensin receptor ...

*Angiotensin II receptor type 1

... or AT1 receptor is the best characterized angiotensin receptor. It has vasopressor effects and ... The angiotensin receptor is activated by the vasoconstricting peptide angiotensin II. The activated receptor in turn couples to ... angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are associated with fewer traumatic stress symptoms ... Angiotensin II receptor type 1 has been shown to interact with Zinc finger and BTB domain-containing protein 16. The protein's ...

*Angiotensin II receptor

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, ...

*Captopril challenge test

... an angiotensin converting enzyme inhibitor. It is used to assist in the diagnosis of renal artery stenosis. It is not generally ...

*Renin inhibitor

This leads to the product angiotensin I (Ang I) which is a decapeptide. Ang I is broken down by the angiotensin-converting ... Ferrario, C. M.; Iyer, S. N. (1998). "Angiotensin-(1-7): A bioactive fragment of the renin-angiotensin system". Regulatory ... design Angiotensin Angiotensin II receptor antagonist Beta blocker Circulatory system Discovery and development of angiotensin ... namely the conversion of angiotensinogen to angiotensin I. This leads to a totality in absence of Angiotensin II based on the ...

*Angiotensin II receptor type 2

... has been shown to interact with MTUS1. Angiotensin II receptor GRCh38: Ensembl release 89: ... "The angiotensin II type 2 receptor causes constitutive growth of cardiomyocytes and does not antagonize angiotensin II type 1 ... Angiotensin II receptor type 2, also known as the AT2 receptor is a protein that in humans is encoded by the AGTR2 gene. ... Angiotensin II is a potent pressor hormone and a primary regulator of aldosterone secretion. It is an important effector ...

*Angiotensin

It is part of the renin-angiotensin system, which is a major target for drugs that raises blood pressure. Angiotensin also ... It plays an important role in the renin-angiotensin system. Angiotensin was independently isolated in Indianapolis and ... Asp-Arg-Val-Tyr-Ile-His-Pro-Phe-His-Leu-Val-Ile-... Asp-Arg-Val-Tyr-Ile-His-Pro-Phe-His-Leu , Val-Ile-... Angiotensin I (CAS# ... Angiotensin is an oligopeptide and is a hormone and a powerful dipsogen. It is derived from the precursor molecule ...

*Angiotensin (1-7)

Action of the ACE on Angiotensin 1-9. Action of the neprilysinon Angiotensin 1-9. Action of the ACE2 on Angiotensin II. The ... Zisman, L. S. (7 October 2003). "Angiotensin-(1-7) Formation in the Intact Human Heart: In Vivo Dependence on Angiotensin II as ... Santos, R. A. S.; Ferreira, A. J.; Verano-Braga, T.; Bader, M. (23 October 2012). "Angiotensin-converting enzyme 2, angiotensin ... Action of the neprilysin on Angiotensin I. Action of the Prolyl endopeptidase on Angiotensin I. ...

*Angiotensin-converting enzyme

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 ...

*Renin-angiotensin system

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 ... Angiotensin I is subsequently converted to angiotensin II by the enzyme angiotensin-converting enzyme (ACE) found in the lungs ... It is believed that angiotensin I may have some minor activity, but angiotensin II is the major bio-active product. Angiotensin ...

*Discovery and development of angiotensin receptor blockers

The angiotensin receptor blockers (ARBs), also called angiotensin (AT1) receptor antagonists or sartans, are a group of ... "The distribution of angiotensin II type 1 receptors, and the tissue renin-angiotensin systems" (PDF), Molecular Medicine Today ... Renin and Angiotensin; Jackson E.K., 789-821) Editors; Brunton L.L., Lazo J.S., Parker K.L. New York McGraw Hill 2006. ISBN 0- ... Two more angiotensin receptors have been described, AT3 and AT4, but their role is still unknown. AT1 receptors are mainly ...

*Journal of the Renin-Angiotensin-Aldosterone System

... is a peer-reviewed academic journal that publishes papers in the field of ... Journal of the Renin-Angiotensin-Aldosterone System is abstracted and indexed in, among other databases: SCOPUS, and the Social ... Journal of the Renin-Angiotensin-Aldosterone System is a resource for biomedical professionals, including basic scientists and ... Journal of the Renin-Angiotensin-Aldosterone System also publishes research on other peptides, such as vasopressin, the ...

*DMOZ - Health: Pharmacy: Drugs and Medications: Antihypertensives: Angiotensin Antagonists

"Health ... Angiotensin Antagonists" search on: AOL - Ask - Bing - DuckDuckGo - Gigablast - Google - ixquick - Yahoo - Yandex - ...

*Angiotensinamide

It is a derivative of angiotensin II. Angiotensin. ... Angiotensinamide (INN; BAN and USAN angiotensin amide) is a ...

*Rajko Igić

Škrbić R, *Igić R. Seven decades of angiotensin (1939-2009). Peptides 2009;30:1945-50. Igić R, Škrbić R. The renin-angiotensin ... His research career centered on the [Renin Angiotensin System , renin-angiotensin system]. While at the University in Tuzla in ... Angiotensin I converting enzyme activity in the choroid plexus and in the retinal. In: Buckley JP, Ferrario CM, eds. Central ... Metabolism of angiotensin I by guinea pig aqueous humor. Can J Physiol Pharmacol 2001;79:627-30. Igić R, Behnia R. Properties ...

*Captopril

The conversion of angiotensin I to angiotensin II and the inactivation of bradykinin were thought to be mediated by the same ... The first breakthrough was made by Kevin K.F. Ng in 1967, when he found the conversion of angiotensin I to angiotensin II took ... Ng, KKF; Vane, JR (1967). "Conversion of angiotensin I to angiotensin II". Nature. 216: 762-766. doi:10.1038/216762a0. PMID ... Ng and Vane found the conversion of angiotensin I to angiotensin II was inhibited during its passage through the pulmonary ...

*Impedance cardiography

Angiotensin-converting-enzyme; ARB = Angiotensin-receptor-blocker). Afterload also increases with increasing blood viscosity, ...

*Cathepsin G

Reilly CF, Tewksbury DA, Schechter NM, Travis J (August 1982). "Rapid conversion of angiotensin I to angiotensin II by ... Other functions of cathepsin G have been reported, including cleavage of receptors, conversion of angiotensin Ⅰ to angiotensin ... Klickstein LB, Kaempfer CE, Wintroub BU (December 1982). "The granulocyte-angiotensin system. Angiotensin I-converting activity ...

*Una Ryan

Ryan, Una; Ryan, James W (April 1980). "Angiotensin-Converting Enzyme: II. Pulmonary Endothelial Cells in Culture". ... taking up a Howard Hughes Fellowship at the University of Miami to study angiotensin-converting enzymes. After completion of ...

*Reabsorption

3. Renin causes production of Angiotensin I. 4. Angiotensin Converting Enzyme (ACE) converts Angiotensin I to Angiotensin II. 5 ... Renin-angiotensin system: 1. The kidneys sense low blood pressure. 2. Release renin into the blood. ... Angiotensin II stimulates the release of Aldosterone, ADH, and thirst. 6. Aldosterone causes kidneys to reabsorb sodium; ADH ...

*Glossary of diabetes

ACE inhibitor Angiotensin conversion enzyme. A class of drugs used to decrease hypertension, mainly by interfering with the ... Insulin is a hormone as are glucagon, adrenaline, and angiotensin II. Human insulin Man-made insulins that is identical to the ...

*Prostasomes

... angiotensin converting enzyme (ACE, CD143); tissue factor TF (CD142, thromboplastin); decay accelerating factor (CD55); ...
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-(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 ...
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)]
... Braz J Med Biol Res [online]. 1997, vol.30, n.4, pp.503-513. ISSN 1414-431X. http://dx.doi.org/10.1590/S0100-879X1997000400012.. The heptapeptide angiotensin-(1-7) is considered to be a biologically active endproduct of the renin-angiotensin system. This angiotensin, which is devoid of the most known actions of angiotensin II such as induction of drinking behavior and vasoconstriction, has several selective effects in the brain and periphery. In the present article we briefly review recent evidence for a physiological role of angiotensin-(1-7) in the control of hydroelectrolyte balance. Keywords : angiotensin antagonists; angiotensin II; hydroelectrolyte balance; renin-angiotensin system; kidney; water transport. ...
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
Ac-Angiotensinogen (1-14) (Porcine), 1 mg. Renin cleavage of Ac-DRVYIHPFHLLVYS yields N-terminally acetylated angiotensin I and LVYS.
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Peptides , Bradykinins , [Des-Pro2]-Bradykinin; Angiotensin I Converting Enzyme (ACE I) Inhibitor; This peptide is an inhibitor for Angiotensin I Converting Enzyme (ACE I), derived from Bradykinin. ACE I partially suppresses the renin-angiotensin-aldosterone system (RAAS), which regulates blood pressure and may mediate hypertension. ACE I converts angiotensin I to the biologically active peptide angiotensin II using a zinc- and chloride- dependent mechanism.; RPPGFSPFR; H-Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg-OH
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
Definition : Immunoassay reagents intended to perform qualitative and/or quantitative analyses on a body fluid sample (e.g., serum) to determine the level of one or both of the vasopressor hormones angiotensin I and/or angiotensin II. Angiotensin I, a decapeptide, is produced in the blood by the hydrolization of angiotensinogen (previously produced in the liver) by renin; it is rapidly converted into angiotensin II, an octapeptide, by a circulating angiotensin-converting enzyme. Angiotensin II is a powerful vasoconstrictor that also stimulates the cells of the zona glomerulosa to produce aldosterone.. Entry Terms : "Peptidyl-Dipeptidase A Determination Reagents" , "Angiotensin I/II Determination Reagents" , "Reagents, Immunoassay, Renal Metabolism, Angiotensin I/II". UMDC code : 19879 ...
Transgenic (TG) rats carrying the mouse Ren-2 gene (Ren-2d)27 are a newly established monogenetic model in hypertension research. To gain an insight into the mechanisms of this form of hypertension we determined the effects of a 13-day therapy with losartan (10 mg/kg) or lisinopril (20 mg/kg) on the blood pressure (BP) and plasma levels of angiotensin (ANG) peptides of mature female TG hypertensive and Sprague-Dawley (SD) rats. The contribution of endothelium-derived nitric oxide (NO) to the maintenance of their hypertension and the response to therapy was evaluated by systemic injection of either NG-monomethyl-L-arginine (L-NMMA) or endothelin-1. Hypertension in TG rats was associated with decreased plasma ANG I, no differences in plasma ANG II, and plasma ANG-(1-7) near the detectable level. Lisinopril lowered BP more than losartan in both TG hypertensive and normotensive controls. In both strains, the chronic fall in BP produced by lisinopril was accompanied by significant increases in plasma ...
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 ...
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.. ...
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. ...
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] ...
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 ...
The central role of angiotensin I-converting enzyme in vertebrate pathophysiology.: Genomic epidemiologic data, increasingly supported by clinical outcomes resu
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 ...
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).. ...
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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...
Looking for online definition of Angiotensin I-Converting Enzyme in the Medical Dictionary? Angiotensin I-Converting Enzyme explanation free. What is Angiotensin I-Converting Enzyme? Meaning of Angiotensin I-Converting Enzyme medical term. What does Angiotensin I-Converting Enzyme mean?
TY - JOUR. T1 - Evidence that the vasodilator angiotensin-(1-7)-Mas axis plays an important role in erectile function. AU - Da Costa Gonçalves, Andrey C.. AU - Leite, Romulo. AU - Fraga-Silva, Rodrigo A.. AU - Pinheiro, Sergio V.. AU - Reis, Augusto B.. AU - Reis, Fernando M.. AU - Touyz, Rhian M.. AU - Webb, R Clinton. AU - Alenina, Natalia. AU - Bader, Michael. AU - Santos, Robson A.S.. PY - 2007/10/1. Y1 - 2007/10/1. N2 - The vasodilator/antiproliferative peptide angiotensin-(1-7) [ANG-(1-7)] is released into the corpus cavernosum sinuses, but its role in erectile function has yet to be defined. In this study, we sought to determine whether ANG-(1-7) and its receptor Mas play a role in erectile function. The ANG-(1-7) receptor Mas was immunolocalized in rat corpus cavernosum by confocal microscopy. Infusion of ANG-(1-7) into corpus cavernosum at a rate of 15.5 pmol · kg-1 · min-1 potentiated the elevation of the corpus cavernosum pressure induced by electrical stimulation of the major ...
Our results demonstrate that in vitro blockade of ACE is insufficient to prevent the contraction of human subcutaneous resistance arteries to Ang I. Because our preliminary experiments showed that this response is completely blocked by losartan, we assume that contraction to Ang I represents the effect of Ang II generated locally and acting on the Ang II type I receptor. Thus, treatment with an ACEI appears to be unable to prevent conversion of Ang I to Ang II in human resistance arteries. In the rabbit, in contrast, ACEI administration fully prevented Ang I-induced contraction.. Because ACE is identical to kininase II, the enzyme responsible for the degradation of kinins, it has been suggested that potentiation of BK may be partly responsible for the actions of ACEI. Thus, plasma kinin concentrations are increased in humans by quinapril, and ACEI-induced coronary artery vasodilation in dogs and humans has been shown to be mediated by BK.16 17 18 We investigated the effect of enalaprilat on the ...
The present study provides evidence for the presence of ACE-independent ANG II-forming pathways from ANG I or [Pro11,d-Ala12]ANG I in hamster heart and aorta. Our functional and biochemical results further suggest that multiple enzymes, including chymase, play a role in the ACE-independent ANG II formation.. In conscious hamsters, [Pro11,d-Ala12]ANG I produced dose-dependent pressor responses, which were inhibited by an AT1-receptor antagonist, but not by an ACE inhibitor, in agreement with the findings in conscious marmosets (18) and baboons (10). Because [Pro11,d-Ala12]ANG I does not directly interact with ANG II receptors and ACE does not cleave this substrate (14), the pressor responses to [Pro11,d-Ala12]ANG I are due to ACE-independent ANG II formation (10, 18). Using AT1- and AT2-receptor antagonists, we further investigated the angiotensin receptor subtypes mediating the vasoconstrictor responses to [Pro11, d-Ala12]ANG I in isolated hamster aorta. Our data clearly showed that the ...
Gli Transcription Factors Mediate the Oncogenic Transformation of Prostate Basal Cells Induced by a Kras-Androgen Receptor Axis.s profile, publications, research topics, and co-authors
The latest market report published by Credence Research, Inc. "Global Angiotensin Converting Enzyme (ACE) Inhibitors Market - Growth, Share, Opportunities, Competitive Analysis, and Forecast, 2016 - 2022," the angiotensin converting enzyme (ACE) inhibitors market was valued at USD 11,477.1 Mn in 2015, and is expected to reach USD 11,094.6 Mn by 2023, expanding at a CAGR of (0.5%) from 2016 to 2023.. Browse the full report Angiotensin Converting Enzyme (ACE) Inhibitors Market - Growth, Share, Opportunities, Competitive Analysis, and Forecast, 2016 - 2023 report at http://www.credenceresearch.com/report/angiotensin-converting-enzyme-ace-inhibitors-market. Market Insights. ACE inhibitors are class of drugs (angiotensin-converting enzyme inhibitors) that block the conversion of angiotensin I to angiotensin II, used in the treatment of hypertension and congestive heart failure and in the prevention of microvascular complications of diabetes mellitus. According to World Health Organization (WHO), ...
Whew.. But this isnt as complicated as it looks. Renin has no real effect. Angiotensinogen just makes angiotensin I. Angiotensin Is main role is to make angiotensin II. The real money here is in angiotensin II, as well as aldosterone.. Angiotensin II has the primary effect of vasoconstriction. It tightens up the vasculature, increasing blood pressure and systemic resistance. It also produces vasopressin (aka ADH, or anti-diuretic hormone) and aldosterone, which cause the kidneys to downregulate urine production - more fluid will be returned to the circulation rather than discarded into the bladder. Vasopressin also helps angiotensin II to induce further vasoconstriction.. To make a long story short, the activation of the RAAS system causes an increase in blood pressure via both vasoconstriction and a decrease in kidney output. It is always active, playing a key role in maintaining homeostasis; if you sweat out a liter of water running a marathon, or bleed out a liter from a gunshot wound, the ...
The latest market report published by Credence Research, Inc. "Global Angiotensin Converting Enzyme (ACE) Inhibitors Market - Growth, Share, Opportunities, Competitive Analysis, and Forecast, 2016 - 2022," the angiotensin converting enzyme (ACE) inhibitors market was valued at USD 11,477.1 Mn in 2015, and is expected to reach USD 11,094.6 Mn by 2023, expanding at a CAGR of (0.5%) from 2016 to 2023.. Market Insights. ACE inhibitors are class of drugs (angiotensin-converting enzyme inhibitors) that block the conversion of angiotensin I to angiotensin II, used in the treatment of hypertension and congestive heart failure and in the prevention of microvascular complications of diabetes mellitus. According to World Health Organization (WHO), globally cardiovascular disease accounts for approximately 17 million deaths a year, nearly one third of the total. Of these, complications of hypertension account for 9.4 million deaths worldwide every year ACE inhibitors market is segmented on the basis of ...
Peptide Standards are lyophilized peptides that are useful for the standardization and method development of proteomic analyses. These non-modified peptide standards are offered as partners to our line of post-translationally modified peptide standards. Each standard is Certified Mass Spec Grade and provided in convenient, lyophilized vials for easy reconstitution and usage.
Carboxypeptidase which converts angiotensin I to angiotensin 1-9, a peptide of unknown function, and angiotensin II to angiotensin 1-7, a vasodilator. Also able to hydrolyze apelin-13 and dynorphin-13 with high efficiency. May be an important regulator of heart function. May have a protective role in acute lung injury.
Angiotensin I, Bradykinin, Active Sites, Angiotensin, Angiotensin I-converting Enzyme, Binding Site, Blood, Blood Pressure, Captopril, Casein, Catalytic Domains, Food, Human, Hypertension, Ic50, Lisinopril, Plays, Pressure, Regression, Regression Analysis
This gene encodes an enzyme involved in catalyzing the conversion of angiotensin I into a physiologically active peptide angiotensin II. Angiotensin II is a potent vasopressor and aldosterone-stimulating peptide that controls blood pressure and fluid-electrolyte balance. This enzyme plays a key role in the renin-angiotensin system. Many studies have associated the presence or absence of a 287 bp Alu repeat element in this gene with the levels of circulating enzyme or cardiovascular pathophysiologies. Multiple alternatively spliced transcript variants encoding different isoforms have been identified, and two most abundant spliced variants encode the somatic form and the testicular form, respectively, that are equally active. [provided by RefSeq, May 2010 ...
breast reduction surgery costs - Drugs that block conversion of angiotensin I to angiotensin II have been used for migraine prophylaxis and a study published in 2003 showed that a drug blocking the effect of angiotensin II had a significant prophylactic effect ...
The Nogo system and the endogenous cellular role of their components in CNS neuron and glial. Signalling mechanisms of CNS neuronal growth inhibitors, particularly the Nogo-Nogo receptor axis ...
Renin is regulated by angiotensin subtype 1 (AT1) receptor, but it is unknown whether angiotensin subtype 2 (AT2) receptor contributes to this regulation. We hypothesized that AT2 receptors inhibit angiotensin II (Ang II) through inhibition of renin biosynthesis. We monitored changes in renal Ang II, renin mRNA and protein expression, and plasma renin concentration (PRC) in response to renal cortical administration of the AT1 receptor blocker valsartan or the AT2 receptor blocker PD 123319 (PD) in conscious rats administered low sodium intake (LS). Renal interstitial Ang II increased by 47-fold in response to LS and increased further in response to valsartan or PD by 67-fold and 61-fold from normal sodium diet (NS) and by 41% and 29% from LS, respectively. Renin mRNA increased 63% during LS, and either valsartan or PD increased it further by 600% and 250% from NS and 538% and 187% from LS, respectively. Similarly, renal renin content and PRC increased in response to LS and increased further in response
Angiotensin I-converting enzyme (ACE) inhibitory activity was investigated for small red bean (Phaseolus vulgaris) protein hydrolysate produced by sequential digestion of Alcalase, papain followed by in vitro gastrointestinal simulation. The hydrolysate had ACE inhibitory activity with IC50 of 67.2 ± 1.8 μg protein/mL. Peptides responsible for potent ACE inhibitory activity were isolated by a three-step purification process, including ultrafiltration, gel filtration and preparative reverse phase high performance chromatography (RP-HPLC). The fraction obtained after RP-HPLC fractionation with the highest activity yielded an IC50 of 19.3 ± 1.4 μg protein/mL. Enzymatic kinetic studies using this fraction demonstrated competitive inhibition with Ki of 11.6 ± 1.7 μg protein/mL. Mass spectrometric characterization identified for the first time the octapeptide PVNNPQIH which demonstrated an IC50 value of 206.7 ± 3.9 μM. The results expand the knowledge base of ACE inhibitory properties of small ...
Thoracic aortic aneurysms and dissections (TAAD) are a major cause of morbidity and mortality in patients. Many different risk factors have been associated TAAD, but hypertension is the largest risk factor. Subsets of TAAD patients have identifiable syndromic genetic diseases, yet a number of genetic non-syndromic patients have been identified. Infusion of angiotensin II into mouse models causes aortic disease through inflammation and fibrosis. An angiotensin type I receptor (AT1R) blocker (ARB) or an angiotensin converting enzyme (ACE) inhibitor (ACEi) can reverse aortic pathology in some mouse models. I set out to better understand the relationship between angiotensin and TAAD in our mouse models, and hypothesized that angiotensin II signaling through the AT1R contributes to thoracic aortic aneurysm formation in multiple model systems of disease, and that blocking related receptors in addition to the AT1R, such as the AT2R and Mas receptor, may have negative consequences. Previously identified genetic
... definition, any of three oligopeptides occurring in plasma, an inactive form (angiotensin I) and two varieties (angiotensin II and angiotensin III) that elevate blood pressure and stimulate the adrenal cortex to secrete aldosterone. See more.
Renin catalyzes the first step in the activation pathway of angiotensinogen--a cascade that can result in aldosterone release,vasoconstriction, and increase in blood pressure. Renin, an aspartyl protease, cleaves angiotensinogen to form angiotensin I, which is converted to angiotensin II by angiotensin I converting enzyme, an important regulator of blood pressure and electrolyte balance. Transcript variants that encode different protein isoforms and that arise from alternative splicing and the use of alternative promoters have been described, but their full-length nature has not been determined. Mutations in this gene have been shown to cause familial hyperproreninemia. [provided by RefSeq, Jul 2008 ...
The compound 4-tert-butyl-2,6-bis(thiomorpholin-4-ylmethyl)phenol (TBTIF) has molecular characteristics similar to angiotensin-converting enzyme (ACE) inhibitors of the sulfhydryl subclass. To assess its value as a new therapeutic agent, we performed
The renin-angiotensin system (RAS) regulates system blood pressure and renal function. Angiotensin-converting enzyme 2 (ACE2) is an enzymatically active homolog of ACE, being highly specific for angiotensin cleavage. ACE2 has direct effects on cardiac functions. It is expressed predominantly in vascular endothelial cells of the heart and kidney. ACE2 converts angiotensin I to angiotensin 1-9. ACE2 was also identified as a functional receptor for SARS coronavirus. ...
Angiotensin, Renin, Angiotensin Ii, Prorenin, Bradykinin, Plasma, Renin-angiotensin System, Rats, Aldosterone, Inhibition, Blood, Tissue, Angiotensin I, Human, Patients, Blood Pressure, Pressure, Diabetes Mellitus, Endothelium, Angiotensinogen
Angiotensin convertaza, cunoscuta si sub numele de kinaza II sau peptidil-dipeptidaza A, este o enzima din clasa hidrolazelor implicate in hidroliza legaturilor peptidice la nivelul C-terminal. Are localizare transmembranara si este alcatuita dintr-un singur lant polipeptidic cu doua situsuri catalitice ce contin zinc. Clivajul proteolitic elibereaza din membrana celulara in spatiul extracelular enzima functionala, circulanta6.. Majoritatea angiotensin convertazei (~90%) se gaseste legata in tesuturi si doar o mica parte circula libera in plasma. Sursa principala a enzimei este endoteliul pulmonar.. Enzima participa in cascada sistemului renina-angiotensina-aldosteron ca raspuns la hipovolemie, fiind responsabila de conversia angiotensinei I in angiotensina II, vasoconstrictor puternic care creste tensiunea arteriala. De asemenea angiotensin convertaza este responsabila si de inactivarea bradikininei (in sistemul kalikreina-kinina)3;6.. Activitatea angiotensin convertazei este crescuta in ...
ACEIs that pass through the BBB reduce AG II production also in the CNS, preventing the rise of ADH. ACEIs that dont pass through the BBB reduce only peripheral conversion of AG I to AG II. The resulting increased level of angiotensin I may cross the blood-brain barrier serving as the substrate for increased production of angiotensin II through the central renin-angiotensin system, determining hyponatriemia. As a low dose of drug blocks the peripheral ACE more than the brain one, probably also the dose of the ACEI plays a key role. Its important to underline that different authors say that AG II cant overcome the BBB, so probabily AG I cant too. But we dont exactly know if a diffusion of AGII is possible from the areas of the brain without the BBB. The importance of this mechanism is not about the hyponatremia induced by some hydrophilic ACEIs, that is an infrequent event, but is about the possible connection between the peripheral RAS and the brain RAS . Are they completely independent o ...
Alamandine | [Ala1]-Angiotensin (1-7), Angiotensin A (1-7) (Human, Rat, Mouse)4475-v 0.5 mg | 25.00 EURAla-Arg-Val-Tyr-Ile-His-Pro (M.W.
The purpose of this study is to define the dose for a Phase II study and to investigate safety and tolerability of intravenous administration of recombi
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Immobilization is a form of disuse characterized by a loss of strength and muscle mass. Among the main features are decreased IGF-1/Akt signalling and increased ubiquitin-proteasome pathway signalling, which induce greater myosin heavy chain degradation. Activation of the classical renin-angiotensin system (RAS) causes deleterious effects in skeletal muscle, including muscle wasting. In contrast, angiotensin-(1-7) [Ang-(1-7)], a peptide of the non-classical RAS, produces beneficial effects in skeletal muscle. However, the role of Ang-(1-7) in skeletal muscle disuse atrophy and independent of classical RAS activation has not been evaluated. Therefore, we assessed the functions of Ang-(1-7) and the Mas receptor in disuse muscle atrophy in vivo using unilateral cast immobilization of the hind limb in male, 12-week-old wild-type (WT) and Mas knockout (Mas KO) mice for 1 and 14 days. Additionally, we evaluated the participation of IGF-1/IGFR-1/Akt signalling and ubiquitin-proteasome pathway ...
In order to delineate further the molecular evolution of the renin-angiotensin system in vertebrates, angiotensin I (ANG I) has been isolated after incubation of plasma and kidney extracts of emu (Dromiceus novaehollandiae), axolotl (Ambystoma mexicanum), and sea lamprey (Petromyzon marinus). The identified sequences were [Asp1, Val5, Asn9] ANG I in emu, [Asp1, Val5, His9] ANG I in axolotl, and [Asn1, Val5, Thr9] ANG I in sea lamprey. These results confirmed the previous findings that tetrapods have Asp and fishes including cyclostomes have Asn at the N-terminus, and that the amino acid residue at position 9 of ANG I was highly variable but, those at other positions were well conserved among different species. Since Asp and Asn are convertible during incubation, angiotensinogen sequences were searched in the genome and/or EST database to determine the N-terminal amino acid residue from the gene. The screening detected 12 tetrapod (10 mammalian, one avian, and one amphibian) and seven teleostean ...
Skeletal muscle atrophy is a pathological condition characterized by the loss of strength and muscle mass, an increase in myosin heavy chain (MHC) degradation and increase in the expression of two muscle-specific ubiquitin ligases: atrogin-1 and MuRF-1. Angiotensin II (AngII) induces muscle atrophy. Angiotensin-(1-7) [Ang-(1-7)], through its receptor Mas, produces the opposite effects than AngII. We assessed the effects of Ang-(1-7) on the skeletal muscle atrophy induced by AngII. Our results show that Ang-(1-7), through Mas, prevents the effects induced by AngII in muscle gastrocnemius: the decrease in the fibre diameter, muscle strength and MHC levels and the increase in atrogin-1 and MuRF-1. Ang-(1-7) also induces AKT phosphorylation. In addition, our analysis in vitro using C2C12 myotubes shows that Ang-(1-7), through a mechanism dependent on Mas, prevents the decrease in the levels of MHC and the increase in the expression of the atrogin-1 and MuRF-1, both induced by AngII. Ang-(1-7) ...
Angiotensin I is converted to angiotensin II (AII) through removal of two C-terminal residues by the enzyme angiotensin-converting enzyme (ACE), primarily through ACE within the lung (but also present in endothelial cells, kidney epithelial cells, and the brain). Angiotensin II acts on the CNS to increase ADH production, and also acts on venous and arterial vessels smooth muscle to cause vasoconstriction. Angiotensin II also increases Aldosterone secretion, therefore, it acts as an endocrine, autocrine/paracrine, and intracrine hormone.. ACE is a target of ACE inhibitor drugs, which decrease the rate of Angiotensin II production. Angiotensin II increases blood pressure by stimulating the Gq protein in vascular smooth muscle cells (which in turn activates an IP3-dependent mechanism leading to a rise in intracellular calcium levels and ultimately causing contraction). In addition, angiotensin II acts at the Na/H+ exchanger in the proximal tubules of the kidney to stimulate Na reabsorption and H+ ...
Angiotensin converting enzyme 2 (ACE 2) is an exopeptidase that catalyses the conversion of angiotensin I to the nonapeptide angiotensin[1-9], or the conversion of angiotensin II to angiotensin 1-7. ACE 2 has direct effects on cardiac functiona, and is expressed predominantly in vascular endothelial cells of the heart and the kidneys. ACE 2 is the receptor for SARS virus. Renin-angiotensin system ACE inhibitors GRCh38: Ensembl release 89: ENSG00000130234 - Ensembl, May 2017 GRCm38: Ensembl release 89: ENSMUSG00000015405 - Ensembl, May 2017 "Human PubMed Reference:". "Mouse PubMed Reference:". Donoghue M, Hsieh F, Baronas E, Godbout K, Gosselin M, Stagliano N, Donovan M, Woolf B, Robison K, Jeyaseelan R, Breitbart RE, Acton S (Sep 2000). "A novel angiotensin-converting enzyme-related carboxypeptidase (ACE2) converts angiotensin I to angiotensin 1-9". Circulation Research. 87 (5): E1-9. doi:10.1161/01.res.87.5.e1. PMID 10969042. Keidar S, Kaplan M, Gamliel-Lazarovich A (Feb 2007). "ACE2 of the ...
The renin-angiotensin system (RAS) is a hormonal system that is responsible for regulating plasma sodium ion concentration and arterial blood pressure in the body. The system involves several peptides such as angiotensin I and II as well as angiotensin converting enzyme (ACE) to enable the constriction of arterial blood vessels in the lung. Angiotensin II also stimulates the production of the hormone aldosterone in the kidneys which brings sodium ions into the bloodstream in exchange for potassium ions. Malfunctions of the RAS can lead to hypertension, heart failure, diabetes and renal complications. Thus the biochemical components of this system serve as important targets for therapeutic drugs ...
Angiotensin (Ang)-(1-7), acting through the receptor Mas, has athero-protective effects; however, its role on plaque vulnerability has been poorly studied. Here, we investigated the expression of the renin-angiotensin system (RAS) components in stable and unstable human carotid plaques. In addition, we evaluated the effects of the chronic treatment with an oral formulation of Ang-(1-7) in a mouse model of shear stress-determined carotid atherosclerotic plaque. Upstream and downstream regions of internal carotid plaques were obtained from a recently published cohort of patients asymptomatic or symptomatic for ischaemic stroke. Angiotensinogen and renin genes were strongly expressed in the entire cohort, indicating an intense intraplaque modulation of the RAS. Intraplaque expression of the Mas receptor I mRNA was increased in the downstream portion of asymptomatic patients as compared to corresponding region in symptomatic patients. Conversely, AT1 receptor gene expression was not modified between ...
The renin angiotensin system (RAS) has profound effects on atherosclerosis development in animal models, which is partially complimented by evidence in the human disease. Although angiotensin II was c
In response to lowered blood pressure, the renin enzyme cleaves angiotensin-1 from angiotensin. Angiotensin-converting enzyme (ACE) then removes a dipeptide to yield the physiologically active peptide angiotensin-2, the most potent pressor substance known, which helps regulate volume and mineral balance of body fluids. The Angiotensin 2 [3-8] Peptide binds specifically to a new angiotensin binding site distinct from angiotensin 2 receptors.. ...
The existence of the intrinsic brain RAS (RASB) is well documented. According to Bunnemann et al. (1993; cited in Ref. 4), all steps, from precursor synthesis to ANG II formation, are accomplished by neuroglial elements, including the synaptic release of ANG II as a neuropeptide, and ANG II histochemistry and ANG II receptor autoradiography have shown that "angiotensinergic" neurons and their target cells constitute a network extending throughout the entire brain stem. In CVOs, RAS and RASB may interact, since brain enzymes analogous to ACE may locally generate ANG II from circulating ANG I. Indeed, ANG II and ANG I infused intravenously are similarly dipsogenic in the rat, and even in an in vitro slice preparation of the rat SFO, ANG II and ANG I are equally effective in exciting the same SFO neuron (Fig. 1C⇑), both actions being equally inhibited by losartan, a specific blocker of the AT1 receptor (10).. According to microinjections of ANG II analogs and blockers on the brain side of the ...
It is well established that renal hypoxia is associated with the development of renal injury. The purpose of this study is measure the alterations in renal blood oxygenation after angiotensin II converting enzyme inhibition. 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 ...
Angiotensin 1 converting enzyme - 67 yrs. Angiotensin 1 converting enzyme (ace) serum 126.7, what should be done? Bad? What does this mean? Life style changes. Medication? Thank you ACE levels. 51 M Notes: 67 yrs angiotensin 1 converting enzyme (ace) serum 126.7, what should be done? Bad? What does this mean? Life style changes. Medication? Thank you ANS: not enough information to help at this point. Are you 51 or 67? Need to know why it was measured, what meds, other illnesses, & what is normal in that lab. Get this information & will be happy to do 2nd opinion as I specialize in RAAS
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A genome-wide search replicates evidence of a quantitative trait locus for circulating angiotensin I-converting enzyme (ACE) unlinked to the ACE gene ...
만성 기침의 원인 분포는 지역사회, 조사 기간에 따라서 매우 다르므로 어느 병원, 어느 나라의 통계 자료를 그대로 인용할 수 없다. 기침 유발 부위의 해부학적 위치에 따른 분류에 의하여 만성 기침의 전통적인 3대 원인 질환으로서 1) 상기도 기침증후군, 2) 호산구성 기관지염이나 천식 등의 호산구성기도 질환, 3) 위식도역류병이 거론되는데, 이러한 기저 질환을 논하기 위해서는 비흡연자, 정상 흉부 방사선 사진, angiotensin converting enzyme (ACE) inhibitor와 같은 고혈압 치료약물을 복용하지 않는 경우라는 전제 조건이 필요하다. 흡연자에게는 당연히 흡연성 만성 기관지염이 흔하며, ACE inhibitor 복용자의 5-30%에서는 부작용으로 기침이 발생하는 것으로 알려져 있다. 비흡연자의 만성 기침 원인으로 30년 이상 거론된 3대 원인 질환에 대한 개념은 그 근거가 ...
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293445024 - EP 1091966 B1 2002-11-06 - N-TERMINAL SITE SELECTIVE INHIBITORS OF HUMAN ANGIOTENSIN CONVERSION ENZYME (ACE) - [origin: WO0001706A1] The invention concerns peptide derivatives useful as N-terminal site selective inhibitor of the human angiotensin conversion enzyme. Said derivatives comprise the amino acid sequence of the following formula: -Asp-Phe- psi (PO2CH2)-Ala-Xaa - wherein: psi (PO2CH2) indicates that the peptide bond (CONH) between Phe and Ala has been replaced by the phosphonic bond PO2CH2; and Xaa represents an amino acid residue. Said derivatives can be used in pharmaceutical compositions, in particular for protecting hematopoietic strain cells of patients subjected to aggressive chemotherapeutic or radiotherapy treatment.[origin: WO0001706A1] The invention concerns peptide derivatives useful as N-terminal site selective inhibitor of the human angiotensin conversion enzyme. Said derivatives comprise the amino acid sequence of the following formula: -Asp-Phe- psi (PO2CH2)-Ala-Xaa
It is now firmly established that inhibition of ACE does have a markedly beneficial effect in the treatment of heart failure. ACE inhibitor therapy, however, does not completely block angiotensin II production, and in some patients, angiotensin II levels remain elevated, in part, because of the conversion of angiotensin I to angiotensin II by chymase activity.29 Thus, continued AT2 receptor stimulation could occur. This hypothesis is indirectly supported by the relative upregulation of the AT2 receptor in human heart failure,30 31 although this finding is controversial.32 33 Currently, no therapeutic agents that specifically act on the AT2 receptor are approved for clinical trials. However, numerous AT1 receptor blockers are available that could hypothetically shunt the activity of the cardiac RAS toward stimulation of the beneficial AT2 receptor.. Two separate clinical approaches evaluate this hypothesis. First, ACE inhibitor therapy was directly compared with AT1 receptor antagonist therapy in ...
Proteomics is a rapidly emerging set of key technologies that are of major importance for proteins and drug development process, especially when mass spectrometry (MS) is being used for high-throughput characterization and identification of proteins. Since the safer and healthier angiotensin I-converting enzyme (ACE) inhibitors are extremely concerned, many research groups have combed for novel ACE inhibitors from food components by different approaches. Here, shotgun proteomics technology aided with structure-activity analysis was applied to screen ACE inhibitory peptides from hydrolyzed red deer plasma. The peptides were analysed by mass spectrometry after primary separation with Sephadex G-25 chromatography. 36 peptides were identified by searching red deer database and 165 peptide sequences derived were identified in mammalian database. Amino acid sequences of peptide and bioactivity relationship have been developed as a faster and useful way to predict and screen new inhibitors. Depending ...
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. This discovery quickly led to the characterisation of the active principle of the venom by Fereira and Greene as a family of peptides, which were named bradykinin potentiating factors as they selectively improved the biological effects of bradykinin. 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. The active peptides were isolated and teprotide became the first ACE inhibitor to be evaluated clinically. The search for an orally active compound that was sufficiently potent to be developed as an antihypertensive drug resulted in the design and development of captopril, which entered first phase clinical studies in 1977.. ACE has a key role in two ...
Renin produced by the kidney in response to glomerular hypoperfusion cata-lyzes cleavage of angiotensinogen (produced by the liver) to angiotensin (AT), which in turn is cleaved by angiotensin-converting enzyme (ACE) to angiotensin II, which acts on two receptors. The AT1 receptor mediates the vasoconstrictor effects of AT. The actions of the AT2 receptor are less well defined.. Angiotensin-converting enzyme inhibitors Mechanism of action. These drugs inhibit the conversion of angiotensin I to angiotensin II and. reduce angiotensin II mediated vasoconstriction.. Indications. The main indicators are heart failure, hypertension, diabetic nephropathy and ischaemic heart disease.. Preparations and dose. Perindopril. Tablets: 2 mg, 4 mg, 8 mg.. ■ Hypertension, initially 4 mg once daily (use 2 mg if in addition to diuretic, in the elderly, in renal impairment) subsequently adjusted according to response to maximum 8 mg daily. ■ Heart failure: initially 2 mg once daily, increased after at least 2 ...
The renin-angiotensin system plays a central role in the pathophysiology of HF. ACE inhibitors improve symptoms and reduce mortality in HF, and it is believed that these benefits can be attributed to decreased angiotensin II formation as well as to bradykinin potentiation and resultant vasodilatory and endothelial protective actions. The Evaluation of Losartan in the Elderly (ELITE) trial is a long-term, moderately sized trial. In this trial, a trend existed toward a reduction in death or hospitalization (or both) for patients with HF receiving losartan. Patients receiving losartan also had fewer adverse effects that required drug discontinuation; primarily, these patients had a lower incidence of cough. These data and another preliminary report of improved survival with losartan compared with placebo suggest a role for angiotensin-receptor blockers in HF and bring into question the mechanism by which ACE inhibitors effect clinical improvements (1). Alternate pathways of angiotensin II formation ...
The rennin-angiotensin II system (RAS) and the insulin-PI3kinase signalling pathways cross-interact with important physiological and pathophysiological consequences for cells and the whole organism. Here, the effect of 24 h pre-incubation of EA.hy926 with two different concentrations of angiotensin II, on insulin-mediated activation of the PI3kinase-AKT-eNOS signalling was investigated. Quiescent EA.hy926 cells were treated with insulin (100 nM, 30 min) following 24 h pre-treatment with or without either 0.1 or 1 µM of angiotensin II. Cell lysates were immunoblotted for phospho AKT Ser-473, phospho eNOS Ser-1177 and normalized with β-actin. Homogenates of EA.hy926 treated with insulin in the presence or absence of 1 µM angiotensin II, were also subjected to nitric oxide synthase (NOS) activity assay using titrated arginine as substrate. To exclude cytotoxicity of the 1 µM angiotensin II concentration, Trypan blue cell viability assay as well as the microscopic examination of
Dairy peptides are proposed to inhibit the activity of the angiotensin-converting enzyme (ACE). ACE is part of the renin-angiotensin system - a natural mechanism that helps regulate blood pressure in the body. In certain individuals, the renin-angiotensin system can become overactive, often due to stress, an unhealthy diet, and/or unhealthy lifestyle. Under such conditions, ACE becomes overactive and converts more angiotensin I into angiotensin II. Angiotensin II causes blood vessels to constrict, and so increases blood pressure, which has potential to lead to hypertension. But, when ACE activity is inhibited, the formation of angiotensin II is reduced. This then helps the blood vessels to relax and expand back to a normal healthy state, so blood pressure is lowered.. ...
Here are definitions of medical terms related to high blood pressure.ACE: Angiotensin-converting enzyme; an enzyme that causes inactive angiotensin I to be converted to active angiotensin II; also known as kinase IIACEI or ACE inhibitors: Other terms for angiotensin-converting enzyme inhibitorsAcute: brief; short term
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Angiotensin I-converting enzyme (ACE) expressed on the surface of endothelial cells is responsible for the last step in the synthesis of circulating angiotensin II and the inactivation of bradykinin. Mammalian ACE is also expressed in the prostate with other components of the renin-angiotensin system, and in developing spermatids, where the peptidase activity is known to be critical for normal sperm function. The importance of an ACE gene to male fertility has also been demonstrated in Drosophila melanogaster, where Ance is expressed in spermatids, and hypomorphic alleles of Ance cause a defect in spermiogenesis. Here we show that ANCE, which shares many enzymatic properties with mammalian ACE, is also a product of the male accessory gland of D. melanogaster. It is expressed in the secondary cells and is associated with the electron dense granule within the large vesicles of these cells. ACE proteolytic activity is lost from the accessory glands during mating, consistent with transfer to the ...
The background for these investigations was the discovery that formation of angiotensin II by the renin angiotensin system can take place in extravascular tissues (e.g., cardiomyocytes and neurons) and within single cells. Consequently, the question arose about whether such tissue-based systems might be differentially influenced by angiotensin I-converting enzyme (ACE) inhibitors with distinct physicochemical properties. Therefore, the aim of this study was to investigate how the membrane penetration of various ACE inhibitors depends on their lipophilia. All diacid forms of ACE inhibitors are dissociated at a pH of 7.4 and scarcely extractable into octanol (extraction coefficient ,10%). In contrast, the extraction coefficients of the parent substances showed marked differences in the following order of increasing lipophilia: enalapril=perindopril,captopril=ceranapril,ramipril,quinapril,HOE288=zofenopril,fosinopril,HOE065. For selected substances, the kinetics of diffusion through a monolayer of ...
Microvillar membranes derived from the brush border of the renal proximal tubule are very rich in peptidases. Pig kidney microvilli contain endopeptidase-24.11 associated with a battery of exopeptidases. The manner by which some neuropeptides are degraded by the combined attack of the peptidases of this membrane has been investigated. The contribution of individual peptidases was assessed by including inhibitors (phosphoramidon, captopril, amastatin and di-isopropyl fluorophosphate) with the membrane fraction when incubated with the peptides. Substance P, bradykinin and angiotensins I, II and III and insulin B-chain were rapidly hydrolysed by kidney microvilli. Oxytocin was hydrolysed much more slowly, but no products were detected from [Arg8]vasopressin or insulin under the conditions used for other peptides. The peptide bonds hydrolysed were identified and the contributions of the different peptidases were quantified. For each of the susceptible peptides, the main contribution came from ...

α2-Macroglobulin Capture Allows Detection of Mast Cell Chymase in Serum and Creates a Reservoir of Angiotensin II-Generating...α2-Macroglobulin Capture Allows Detection of Mast Cell Chymase in Serum and Creates a Reservoir of Angiotensin II-Generating...

Rapid conversion of angiotensin I to angiotensin II by neutrophil and mast cell proteinases. J. Biol. Chem. 257: 8619-8622. ... Generation of angiotensin II by serum chymase. The graph shows results of measurement of angiotensin II-generating capacity of ... Human mast cell chymase cleaves angiotensin I selectively at Phe8 to generate bioactive angiotensin II (1, 2, 3, 4). Indeed, ... 6⇓, chymase generates bioactive angiotensin II from angiotensin I when preincubated with α2M, but it has no detectable activity ...
more infohttp://www.jimmunol.org/content/182/9/5770.long

Renin Angiotensin Aldosterone System Blockade (RAASB) May Be Beneficial in Patients with Acute Kidney Injury (AKI) - The...Renin Angiotensin Aldosterone System Blockade (RAASB) May Be Beneficial in Patients with Acute Kidney Injury (AKI) - The...

Exposure to renin angiotensin aldosterone system blockade (i.e. RAASB) may have a protective effect in patients with hospital- ... Renin Angiotensin Aldosterone System Blockade (RAASB) May Be Beneficial in Patients with Acute Kidney Injury (AKI) ...
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Angiotensin II receptor - WikipediaAngiotensin II receptor - Wikipedia

The angiotensin II receptors, (AGTR1) and (AGTR2), are a class of G protein-coupled receptors with angiotensin II as their ... The angiotensin receptor is activated by the vasoconstricting peptide angiotensin II. The activated receptor in turn couples to ... The AT4 receptor is activated by the angiotensin II metabolite angiotensin IV, and may play a role in regulation of the CNS ... Angiotensin II receptor antagonist. References[edit]. *^ de Gasparo M, Catt KJ, Inagami T, Wright JW, Unger T (2000). " ...
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Renin-angiotensin system - WikipediaRenin-angiotensin system - Wikipedia

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 ...
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Angiotensin | peptide | Britannica.comAngiotensin | peptide | Britannica.com

... 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 ...
more infohttps://www.britannica.com/science/angiotensin

angiotensin : Spoonful of Medicineangiotensin : Spoonful of Medicine

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. ...
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angiotensin II | Hypertensionangiotensin II | Hypertension

Angiotensin II Type 1 Receptor Mechanoactivation Involves RGS5 (Regulator of G Protein Signaling 5) in Skeletal Muscle Arteries ... Apelin Is a Negative Regulator of Angiotensin II-Mediated Adverse Myocardial Remodeling and DysfunctionNovelty and Significance ... Vascular ADAM17 (a Disintegrin and Metalloproteinase Domain 17) Is Required for Angiotensin II/β-Aminopropionitrile-Induced ...
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Angiotensin - WikipediaAngiotensin - Wikipedia

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 ...
more infohttps://en.m.wikipedia.org/wiki/Angiotensin

Angiotensin Converting Enzyme, SerumAngiotensin Converting Enzyme, Serum

... ,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 ...
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Angiotensin Receptors | SpringerLinkAngiotensin Receptors | SpringerLink

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 ...
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angiotensin (thing) by hawkeyeMI - Everything2.comangiotensin (thing) by hawkeyeMI - Everything2.com

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 ...
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Angiotensin Receptors and Aging | HypertensionAngiotensin Receptors and Aging | Hypertension

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 ...
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Angiotensin ii | Define Angiotensin ii at Dictionary.comAngiotensin ii | Define Angiotensin ii at Dictionary.com

... 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 ...
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Angiotensin amide | Define Angiotensin amide at Dictionary.comAngiotensin amide | Define Angiotensin amide at Dictionary.com

Angiotensin amide definition at Dictionary.com, a free online dictionary with pronunciation, synonyms and translation. Look it ... A peptide analog to angiotensin II that is used as a vasopressor in the treatment of certain types of shock and circulatory ...
more infohttps://www.dictionary.com/browse/angiotensin-amide

Angiotensin II, humanAngiotensin II, human

... ; The octapeptide angiotensin II (Ang II) exerts a wide range of effects on the cardiovascular system. It ... Ang II is formed by cleavage of Ang I by the angiotensin-converting enzyme (ACE) or chymases. Human heart chymase, a ... chymotrypsin-like serine proteinase, hydrolyzes the Phe8-His9 bond to yield the octapeptide hormone angiotensin II and His-Leu ... 2010). Angiotensin II/angiotensin II type I receptor (AT1R) signaling promotes MCF-7 breast cancer cells survival via PI3- ...
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Angiotensin converting enzyme inhibitors in pregnancy.  - PubMed - NCBIAngiotensin converting enzyme inhibitors in pregnancy. - PubMed - NCBI

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 ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/9201818?dopt=Abstract

Angiotensin-Converting Enzyme Inhibitors | GreenMedInfoAngiotensin-Converting Enzyme Inhibitors | GreenMedInfo

23 Abstracts with Angiotensin-Converting Enzyme Inhibitors Research. Filter by Study Type. Animal Study. ... Pharmacological Actions : Angiotensin-Converting Enzyme Inhibitors, Antihypertensive Agents. Additional Keywords : Plant ... Pharmacological Actions : Angiotensin-Converting Enzyme Inhibitors, Antihypertensive Agents. Additional Keywords : Phytotherapy ... Additional Keywords : Angiotensin-Converting Enzyme Inhibitors, Antihypertensive Agents, Butyrate, Dysbiosis, Gastrointestinal ...
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Porcine Angiotensin Converting Enzyme from BIOPURPorcine Angiotensin Converting Enzyme from BIOPUR

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Angiotensin 2 Receptor Blocking AgentAngiotensin 2 Receptor Blocking Agent

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Angiotensin 2 Receptor Blocking AgentAngiotensin 2 Receptor Blocking Agent

... , Angiotensin Receptor Blocker, Angiotensin Blocker, Losartan, Cozaar, Irbesartan, Avapro ... Angiotensin 2 Receptor Blocking Agent. Aka: Angiotensin 2 Receptor Blocking Agent, Angiotensin Receptor Blocker, Angiotensin ... Angiotensin II, formed from angiotensin I by angiotensin-converting enzyme (ACE), stimulates the adrenal cortex to synthesize ... Irbesartan selectively and competitively blocks the binding of angiotensin II to the angiotensin I receptor. Angiotensin II ...
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Angiotensin-converting enzyme (ACE) inhibitorsAngiotensin-converting enzyme (ACE) inhibitors

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angiotensin II receptor Protein Superfamily Detailangiotensin II receptor Protein Superfamily Detail

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Angiotensin-converting Enzyme (ACE) | HowStuffWorksAngiotensin-converting Enzyme (ACE) | HowStuffWorks

Angiotensin-converting enzyme (ACE) inhibitor-diuretic combinations help treat high blood pressure. Learn more about ACE from ...
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Global Angiotensin Converting Enzyme (ACE) Inhibitors Market Is Expected To Reach USD 11,094.6 Mn By 2023 - Credence Research |...Global Angiotensin Converting Enzyme (ACE) Inhibitors Market Is Expected To Reach USD 11,094.6 Mn By 2023 - Credence Research |...

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ACE inhibitors, angiotensin receptor blockers, and atrial fibrillationACE inhibitors, angiotensin receptor blockers, and atrial fibrillation

... 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 ...
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  • It is a large molecule , produced in the liver, and only a small part of it is cleaved off to become angiotensin I . (everything2.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 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)