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
Receptors, Angiotensin
Angiotensin II Type 1 Receptor Blockers
Receptor, Angiotensin, Type 2
Angiotensin Receptor Antagonists
Angiotensin I
Losartan
Angiotensin III
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.
Saralasin
1-Sarcosine-8-Isoleucine Angiotensin II
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.
Imidazoles
Renin
Angiotensins
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.
Aldosterone
Hypertension
Rats, Sprague-Dawley
Kidney
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.
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.
Pyridines
Enalapril
Rats, Inbred SHR
Cells, Cultured
Rats, Inbred WKY
Vasoconstriction
Dose-Response Relationship, Drug
Teprotide
Hypertension, Renal
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.
Valine
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.
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.
Rats, Wistar
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.
Chymases
Angiotensin Amide
Benzoates
Myocardium
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.
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.
Lisinopril
Diet, Sodium-Restricted
Adrenal Glands
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.
Subfornical Organ
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.
Hypertrophy
Hemodynamics
Fibrosis
Sodium
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.
Disease Models, Animal
Vascular Resistance
Arginine Vasopressin
Rats, Inbred Strains
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.
Kidney Tubules, Proximal
Zona Glomerulosa
Aorta, Thoracic
Phenylephrine
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.
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.
Glutamyl Aminopeptidase
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.
Ramipril
Enzyme Inhibitors
Rabbits
Kidney Glomerulus
Mesenteric Arteries
Kidney Cortex
Atrial Natriuretic Factor
Endothelin-1
A 21-amino acid peptide produced in a variety of tissues including endothelial and vascular smooth-muscle cells, neurons and astrocytes in the central nervous system, and endometrial cells. It acts as a modulator of vasomotor tone, cell proliferation, and hormone production. (N Eng J Med 1995;333(6):356-63)
Aldosterone 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.
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.
Endothelium, Vascular
Adrenal Cortex
The outer layer of the adrenal gland. It is derived from MESODERM and comprised of three zones (outer ZONA GLOMERULOSA, middle ZONA FASCICULATA, and inner ZONA RETICULARIS) with each producing various steroids preferentially, such as ALDOSTERONE; HYDROCORTISONE; DEHYDROEPIANDROSTERONE; and ANDROSTENEDIONE. Adrenal cortex function is regulated by pituitary ADRENOCORTICOTROPIN.
Superoxides
Highly reactive compounds produced when oxygen is reduced by a single electron. In biological systems, they may be generated during the normal catalytic function of a number of enzymes and during the oxidation of hemoglobin to METHEMOGLOBIN. In living organisms, SUPEROXIDE DISMUTASE protects the cell from the deleterious effects of superoxides.
NG-Nitroarginine Methyl Ester
Sodium, Dietary
Dogs
Oxidative Stress
Kidney Medulla
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)
Spironolactone
A potassium sparing diuretic that acts by antagonism of aldosterone in the distal renal tubules. It is used mainly in the treatment of refractory edema in patients with congestive heart failure, nephrotic syndrome, or hepatic cirrhosis. Its effects on the endocrine system are utilized in the treatments of hirsutism and acne but they can lead to adverse effects. (From Martindale, The Extra Pharmacopoeia, 30th ed, p827)
Endothelins
21-Amino-acid peptides produced by vascular endothelial cells and functioning as potent vasoconstrictors. The endothelin family consists of three members, ENDOTHELIN-1; ENDOTHELIN-2; and ENDOTHELIN-3. All three peptides contain 21 amino acids, but vary in amino acid composition. The three peptides produce vasoconstrictor and pressor responses in various parts of the body. However, the quantitative profiles of the pharmacological activities are considerably different among the three isopeptides.
Arterioles
Enzyme Activation
Reactive Oxygen Species
Molecules or ions formed by the incomplete one-electron reduction of oxygen. These reactive oxygen intermediates include SINGLET OXYGEN; SUPEROXIDES; PEROXIDES; HYDROXYL RADICAL; and HYPOCHLOROUS ACID. They contribute to the microbicidal activity of PHAGOCYTES, regulation of signal transduction and gene expression, and the oxidative damage to NUCLEIC ACIDS; PROTEINS; and LIPIDS.
Protein Kinase C
An serine-threonine protein kinase that requires the presence of physiological concentrations of CALCIUM and membrane PHOSPHOLIPIDS. The additional presence of DIACYLGLYCEROLS markedly increases its sensitivity to both calcium and phospholipids. The sensitivity of the enzyme can also be increased by PHORBOL ESTERS and it is believed that protein kinase C is the receptor protein of tumor-promoting phorbol esters.
Vasodilation
Phosphorylation
Cilazapril
Furosemide
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.
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.
Infusion Pumps
Fluid propulsion systems driven mechanically, electrically, or osmotically that are used to inject (or infuse) over time agents into a patient or experimental animal; used routinely in hospitals to maintain a patent intravenous line, to administer antineoplastic agents and other drugs in thromboembolism, heart disease, diabetes mellitus (INSULIN INFUSION SYSTEMS is also available), and other disorders.
Mineralocorticoid Receptor Antagonists
Analysis of Variance
Glomerular Filtration Rate
Blood Vessels
Receptor, Bradykinin B2
A constitutively expressed subtype of bradykinin receptor that may play a role in the acute phase of the inflammatory and pain response. It has high specificity for intact forms of BRADYKININ and KALLIDIN. The receptor is coupled to G-PROTEIN, GQ-G11 ALPHA FAMILY and G-PROTEIN, GI-GO ALPHA FAMILY signaling proteins.
Diuresis
Gene Expression Regulation
Ventricular Remodeling
Drinking Behavior
Pressoreceptors
Perindopril
Diabetic Nephropathies
KIDNEY injuries associated with diabetes mellitus and affecting KIDNEY GLOMERULUS; ARTERIOLES; KIDNEY TUBULES; and the interstitium. Clinical signs include persistent PROTEINURIA, from microalbuminuria progressing to ALBUMINURIA of greater than 300 mg/24 h, leading to reduced GLOMERULAR FILTRATION RATE and END-STAGE RENAL DISEASE.
Tetrahydroisoquinolines
Heart Failure
A heterogeneous condition in which the heart is unable to pump out sufficient blood to meet the metabolic need of the body. Heart failure can be caused by structural defects, functional abnormalities (VENTRICULAR DYSFUNCTION), or a sudden overload beyond its capacity. Chronic heart failure is more common than acute heart failure which results from sudden insult to cardiac function, such as MYOCARDIAL INFARCTION.
Glomerular Mesangium
Gene Expression
Up-Regulation
Desoxycorticosterone
Peptide Fragments
Potassium
An element in the alkali group of metals with an atomic symbol K, atomic number 19, and atomic weight 39.10. It is the chief cation in the intracellular fluid of muscle and other cells. Potassium ion is a strong electrolyte that plays a significant role in the regulation of fluid volume and maintenance of the WATER-ELECTROLYTE BALANCE.
Hypertrophy, Left Ventricular
Amlodipine
Body Weight
Blotting, Western
Myocytes, Smooth Muscle
Nitric Oxide Synthase
Infusions, Parenteral
Immunohistochemistry
Inositol Phosphates
Myocytes, Cardiac
Indomethacin
Calcium Channel Blockers
Reverse Transcriptase Polymerase Chain Reaction
Adrenocorticotropic Hormone
An anterior pituitary hormone that stimulates the ADRENAL CORTEX and its production of CORTICOSTEROIDS. ACTH is a 39-amino acid polypeptide of which the N-terminal 24-amino acid segment is identical in all species and contains the adrenocorticotrophic activity. Upon further tissue-specific processing, ACTH can yield ALPHA-MSH and corticotrophin-like intermediate lobe peptide (CLIP).
Kidney Tubules
Long convoluted tubules in the nephrons. They collect filtrate from blood passing through the KIDNEY GLOMERULUS and process this filtrate into URINE. Each renal tubule consists of a BOWMAN CAPSULE; PROXIMAL KIDNEY TUBULE; LOOP OF HENLE; DISTAL KIDNEY TUBULE; and KIDNEY COLLECTING DUCT leading to the central cavity of the kidney (KIDNEY PELVIS) that connects to the URETER.
Heart Ventricles
Nicotinic Acids
Receptors, Endothelin
Mitogen-Activated Protein Kinases
A superfamily of PROTEIN-SERINE-THREONINE KINASES that are activated by diverse stimuli via protein kinase cascades. They are the final components of the cascades, activated by phosphorylation by MITOGEN-ACTIVATED PROTEIN KINASE KINASES, which in turn are activated by mitogen-activated protein kinase kinase kinases (MAP KINASE KINASE KINASES).
Cardiovascular System
Nitric Oxide Synthase Type III
Tachyphylaxis
Transforming Growth Factor beta
A factor synthesized in a wide variety of tissues. It acts synergistically with TGF-alpha in inducing phenotypic transformation and can also act as a negative autocrine growth factor. TGF-beta has a potential role in embryonal development, cellular differentiation, hormone secretion, and immune function. TGF-beta is found mostly as homodimer forms of separate gene products TGF-beta1, TGF-beta2 or TGF-beta3. Heterodimers composed of TGF-beta1 and 2 (TGF-beta1.2) or of TGF-beta2 and 3 (TGF-beta2.3) have been isolated. The TGF-beta proteins are synthesized as precursor proteins.
Baroreflex
A response by the BARORECEPTORS to increased BLOOD PRESSURE. Increased pressure stretches BLOOD VESSELS which activates the baroreceptors in the vessel walls. The net response of the CENTRAL NERVOUS SYSTEM is a reduction of central sympathetic outflow. This reduces blood pressure both by decreasing peripheral VASCULAR RESISTANCE and by lowering CARDIAC OUTPUT. Because the baroreceptors are tonically active, the baroreflex can compensate rapidly for both increases and decreases in blood pressure.
Infusions, Intravenous
Drug Interactions
Prostaglandins
Radioligand Assay
Receptors, Mineralocorticoid
Nitroprusside
Water-Electrolyte Balance
Mitogen-Activated Protein Kinase 3
Stimulation, Chemical
The increase in a measurable parameter of a PHYSIOLOGICAL PROCESS, including cellular, microbial, and plant; immunological, cardiovascular, respiratory, reproductive, urinary, digestive, neural, musculoskeletal, ocular, and skin physiological processes; or METABOLIC PROCESS, including enzymatic and other pharmacological processes, by a drug or other chemical.
Collagen
Cattle
Medulla Oblongata
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.
Rats, Inbred Dahl
Receptor, Endothelin A
Reference Values
Quantification of baroreceptor influence on arterial pressure changes seen in primary angiotension-induced hypertension in dogs. (1/7785)
We studied the role of the sino-aortic baroreceptors in the gradual development of hypertension induced by prolonged administration of small amounts of angiotensin II (A II) in intact dogs and dogs with denervated sino-aortic baroreceptors. Short-term 1-hour infusions of A II(1.0-100 ng/kg per min) showed that conscious denervated dogs had twice the pressor sensitivity of intact dogs. Long-term infusions of A II at 5.0 ng/kg per min (2-3 weeks) with continuous 24-hour recordings of arterial pressure showed that intact dogs required 28 hours to reach the same level of pressure attained by denervated dogs during the 1st hour of infusion. At the 28th hour the pressure in both groups was 70% of the maximum value attained by the 7th day of infusion. Both intact and denervated dogs reached nearly the same plateau level of pressure, the magnitude being directly related both the the A II infusion rate and the daily sodium intake. Cardiac output in intact dogs initially decreased after the onset of A II infusion, but by the 5th day of infusion it was 38% above control, whereas blood volume was unchanged. Heart rate returned to normal after a reduction during the 1st day of infusion in intact dogs. Plasma renin activity could not be detected after 24 hours of A II infusion in either intact or denervated dogs. The data indicate that about 35% of the hypertensive effect of A II results from its acute pressor action, and an additional 35% of the gradual increase in arterial pressure is in large measure a result of baroreceptor resetting. We conclude that the final 30% increase in pressure seems to result from increased cardiac output, the cause of which may be decreased vascular compliance. since the blood volume remains unaltered. (+info)Acute and chronic dose-response relationships for angiotensin, aldosterone, and arterial pressure at varying levels of sodium intake. (2/7785)
We examined the acute and chronic dose-response relationships between intravenously infused angiotensin II (A II) and the resulting changes in arterial pressure and plasma aldosterone concentration at varying levels of sodium intake. Sequential analysis of plasma aldosterone at each A II infusion rate resulted in an acute dose-related increase in plasma aldosterone which was markedly attenuated after the first 24 hours of infusion, the final level being directly related to the dose of A II and inversely related to sodium intake. A II infused at 5,15, and 23 ng/kg per min was associated with an initial increase (2nd to 8th hour) in plasma aldosterone to 2,6, and 9 times control values, respectively, in dogs receiving 40 mEq Na+/day. But, after the 1st day, aldosterone averaged only 1, 1.7, and 3 times control values for the next 2 weeks at the same rates of A II infusion. Dogs receiving 120 mEq Na+/day during A II infusion exhibited only a transient increase in plasma aldosterone during the 1st day. Sustained hypertension developed over a period of a week at all doses of A II at normal and high sodium intake, but did not occur at any dose of A II in sodium-depleted dogs. Increasing sodium intake from 40 to 120 mEq/day resulted in higher levels of hypertension, 125% compared to 140% of ocntrol values for dogs infused with A II, 5.0 ng/kg per min. We conclude that primary angiotensin-induced hypertension need not be associated with increased levels of plasma aldosterone, which appears to remain elevated only with amounts of A II greater than those required to sustain a significant degree of hypertension. (+info)Relaxin is a potent renal vasodilator in conscious rats. (3/7785)
The kidneys and other nonreproductive organs vasodilate during early gestation; however, the "pregnancy hormones" responsible for the profound vasodilation of the renal circulation during pregnancy are unknown. We hypothesized that the ovarian hormone relaxin (RLX) contributes. Therefore, we tested whether the administration of RLX elicits renal vasodilation and hyperfiltration in conscious adult, intact female rats. After several days of treatment with either purified porcine RLX or recombinant human RLX 2 (rhRLX), effective renal plasma flow (ERPF) and glomerular filtration rate (GFR) increased by 20%-40%. Comparable renal vasodilation and hyperfiltration was also observed in ovariectomized rats, suggesting that estrogen and progesterone are unnecessary for the renal response to rhRLX. The nitric oxide synthase inhibitor Nomega-nitro-L-arginine methyl ester completely abrogated the increase in ERPF and GFR elicited by chronic administration of purified porcine RLX. In contrast, the renal vasoconstrictory response to angiotensin II was attenuated by the RLX treatment. Short-term infusion of purified porcine RLX to conscious rats over several hours failed to increase ERPF and GFR. Plasma osmolality was consistently reduced by the chronic administration of both RLX preparations. In conclusion, the renal and osmoregulatory effects of chronic RLX administration to conscious rats resemble the physiological changes of pregnancy in several respects: (a) marked increases in ERPF and GFR with a mediatory role for nitric oxide; (b) attenuation of the renal circulatory response to angiotensin II; and (c) reduction in plasma osmolality. (+info)Angiotensin II type 1 receptor-mediated inhibition of K+ channel subunit kv2.2 in brain stem and hypothalamic neurons. (4/7785)
Angiotensin II (Ang II) has powerful modulatory actions on cardiovascular function that are mediated by specific receptors located on neurons within the hypothalamus and brain stem. Incubation of neuronal cocultures of rat hypothalamus and brain stem with Ang II elicits an Ang II type 1 (AT1) receptor-mediated inhibition of total outward K+ current that contributes to an increase in neuronal firing rate. However, the exact K+ conductance(s) that is inhibited by Ang II are not established. Pharmacological manipulation of total neuronal outward K+ current revealed a component of K+ current sensitive to quinine, tetraethylammonium, and 4-aminopyridine, with IC50 values of 21.7 micromol/L, 1.49 mmol/L, and 890 micromol/L, respectively, and insensitive to alpha-dendrotoxin (100 to 500 nmol/L), charybdotoxin (100 to 500 nmol/L), and mast cell degranulating peptide (1 micromol/L). Collectively, these data suggest the presence of Kv2.2 and Kv3.1b. Biophysical examination of the quinine-sensitive neuronal K+ current demonstrated a macroscopic conductance with similar biophysical properties to those of Kv2.2 and Kv3.1b. Ang II (100 nmol/L), in the presence of the AT2 receptor blocker PD123,319, elicited an inhibition of neuronal K+ current that was abolished by quinine (50 micromol/L). Reverse transcriptase-polymerase chain reaction analysis confirmed the presence of Kv2.2 and Kv3.1b mRNA in these neurons. However, Western blot analyses demonstrated that only Kv2.2 protein was present. Coexpression of Kv2.2 and the AT1 receptor in Xenopus oocytes demonstrated an Ang II-induced inhibition of Kv2.2 current. Therefore, these data suggest that inhibition of Kv2.2 contributes to the AT1 receptor-mediated reduction of neuronal K+ current and subsequently to the modulation of cardiovascular function. (+info)Recent progress in angiotensin II type 2 receptor research in the cardiovascular system. (5/7785)
Angiotensin II (Ang II) plays an important role in regulating cardiovascular hemodynamics and structure. Multiple lines of evidence have suggested the existence of Ang II receptor subtypes, and at least 2 distinct receptor subtypes have been defined on the basis of their differential pharmacological and biochemical properties and designated as type 1 (AT1) and type 2 (AT2) receptors. To date, most of the known effects of Ang II in adult tissues are attributable to the AT1 receptor. Recent cloning of the AT2 receptor contributes to reveal its physiological functions, but many functions of the AT2 receptor are still an enigma. AT1 and AT2 receptors belong to the 7-transmembrane, G protein-coupled receptor family. However, accumulating evidence demonstrates that the function and signaling mechanisms of these receptor subtypes are quite different, and these receptors may exert opposite effects in terms of cell growth and blood pressure regulation. We will review the role of the AT2 receptor in the cardiovascular system and the molecular and cellular mechanisms of AT2 receptor action. (+info)Intracellular sodium modulates the expression of angiotensin II subtype 2 receptor in PC12W cells. (6/7785)
Although the angiotensin II subtype 2 receptor (AT2-R) is expressed abundantly in the adrenal medulla, its physiological significance has not yet been determined. To obtain fundamental knowledge of the regulation of AT2-R expression in the adrenal medulla, we investigated the effects of modulating several ion channels on AT2-R expression in PC12W cells. Experiments were performed after 24 hours of serum depletion under subconfluent conditions. After 48 hours of treatment with various agonists or antagonists, the receptor density and mRNA level of AT2-Rs were quantified by 125I-[Sar1, Ile8]angiotensin II binding and Northern blot analysis. Ouabain (10 to 100 nmol/L) and insulin (10 to 100 nmol/L) dose-dependently increased receptor density and mRNA level. Analysis of the binding characteristics revealed that the ouabain-dependent increase in AT2-R levels was due to an increase in binding capacity without a change in the Kd value. These increases were blocked by lowering the Na+ concentration in the medium. A low concentration of the sodium ionophore monensin (10 nmol/L), the K+-channel blocker quinidine (10 micromol/L), and the ATP-sensitive K+-channel blockers tolbutamide (100 micromol/L) and glybenclamide (10 micromol/L) also significantly increased receptor density, but the ATP-sensitive K+-channel agonist cromakalim (100 micromol/L) decreased receptor density significantly (P<0.01). Nifedipine (10 micromol/L) decreased basal receptor density and completely blocked the increase in receptor density caused by these agents. The increase in receptor density caused by an increase in intracellular Na+ was accompanied by an increase in mRNA level, whereas the ATP-sensitive K+-channel blockers did not change mRNA level. Nifedipine slightly decreased mRNA level. These results suggest that AT2-R expression is sensitively regulated by intracellular cation levels. The change in intracellular Na+ level transcriptionally regulates AT2-R expression, whereas the K+-channel blocker-dependent upregulation appears to be at least in part posttranslational. (+info)Kidney aminopeptidase A and hypertension, part II: effects of angiotensin II. (7/7785)
Aminopeptidase A (APA) is the principal enzyme that metabolizes angiotensin II (Ang II) to angiotensin III. Previously, we showed that kidney APA was elevated in spontaneously hypertensive rats and was reduced after angiotensin-converting enzyme inhibition. In the present study, we sought to determine whether kidney APA expression was altered after chronically elevated Ang II, either exogenously delivered via osmotic minipumps or endogenously produced in two-kidney, one clip (2K1C) hypertensive rats. Ang II (200 ng. kg-1. min-1) was infused subcutaneously for 1 or 2 weeks by osmotic minipumps, and 2K1C rats were tested 4 weeks after unilateral renal artery clipping. Blood pressure was not significantly elevated in the Ang II-infused animals but was significantly increased at 3 and 4 weeks in the 2K1C animals. APA was significantly elevated approximately 2-fold in kidney cortical membranes from Ang II-infused animals but was decreased 45% in the clipped kidney and 18% in the nonclipped kidneys from 2K1C animals. Isolated glomeruli from Ang II-infused animals and the nonclipped kidneys from 2K1C animals had markedly higher APA activity and immunoreactivity. Likewise, histochemical and immunohistochemical studies indicated that APA levels were increased in glomeruli from angiotensin-infused animals and in both nonclipped and clipped kidneys from 2K1C animals. In contrast, tubular APA was decreased in tubular elements from 2K1C animals, most markedly in the clipped kidneys. Thus, despite the increase in glomerular APA expression in kidneys from 2K1C animals, the decrease in tubular APA expression is more extensive and accounts for the measured reduction in total APA in cortical homogenates. Because clipped kidneys are not exposed to high blood pressure, these results suggest that glomerular APA expression is positively regulated and tubular APA negatively regulated by Ang II. These results further suggest that changes in kidney APA expression could influence the progression of angiotensin-dependent hypertension. (+info)Insulin-like growth factor-1 induces Mdm2 and down-regulates p53, attenuating the myocyte renin-angiotensin system and stretch-mediated apoptosis. (8/7785)
Insulin-like growth factor (IGF)-1 inhibits apoptosis, but its mechanism is unknown. Myocyte stretching activates p53 and p53-dependent genes, leading to the formation of angiotensin II (Ang II) and apoptosis. Therefore, this in vitro system was used to determine whether IGF-1 interfered with p53 function and the local renin-angiotensin system (RAS), decreasing stretch-induced cell death. A single dose of 200 ng/ml IGF-1 at the time of stretching decreased myocyte apoptosis 43% and 61% at 6 and 20 hours. Ang II concentration was reduced 52% at 20 hours. Additionally, p53 DNA binding to angiotensinogen (Aogen), AT1 receptor, and Bax was markedly down-regulated by IGF-1 via the induction of Mdm2 and the formation of Mdm2-p53 complexes. Concurrently, the quantity of p53, Aogen, renin, AT1 receptor, and Bax was reduced in stretched myocytes exposed to IGF-1. Conversely, Bcl-2 and the Bcl-2-to-Bax protein ratio increased. The effects of IGF-1 on cell death, Ang II synthesis, and Bax protein were the consequence of Mdm2-induced down-regulation of p53 function. In conclusion, the anti-apoptotic impact of IGF-1 on stretched myocytes was mediated by its capacity to depress p53 transcriptional activity, which limited Ang II formation and attenuated the susceptibility of myocytes to trigger their endogenous cell death pathway. (+info)Regulation of proximal tubule transport by angiotensin II<...
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ACE226
- ACE2, a close homologue of ACE, functions as a negative regulator of the angiotensin system and was identified as a key receptor for SARS (severe acute respiratory syndrome) coronavirus infections. (nih.gov)
- The mechanism of entry of SARS-COV-2 into the human host cell is through the ACE2 receptor. (viamedica.pl)
- In coronavirus infection disease (Covid-19), SARS-CoV-2 binds ACE2 which is highly expressed by the epithelial cells of blood vessel, intestine and lung. (ejmamr.com)
- The expression of ACE2 is augmented by angiotensin converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), ibuprofen, statins, thiazolidinedione and by cigarette smoking. (ejmamr.com)
- Polymorphism of ACE2 has been associated with different cardio-metabolic disorders, thus implication of ACE2 and angiotensin receptor type 2 (ATR2) receptors in Covid-19-induced pneumonia should be considerably regarded with ACE2 polymorphisms. (ejmamr.com)
- Covid-19 leads to significant lung injury through down-regulation of ACE2, which is attenuated by administration of angiotensin-receptor blockers (ARBs). (ejmamr.com)
- Therefore, ACE2 receptors are protective against SARS-CoV-2 pathogenesis. (ejmamr.com)
- Therefore, ACE2 is regarded as an important entry-point for SARS-CoV-2 and up-regulation of ACE2 by ACEIs, ARBs and during development of cytokine storm is regarded as a protective compensatory mechanism to overcome hyperinflammatory-induced ALI and ARDS. (ejmamr.com)
- Pathological activation of ADAM17 (A disintegrin and metalloproteinase -17) may potentiate inflammation and diminish ACE2-mediated tissue protection through proteolytic shedding, contributing to SARS-CoV-2 pathogenesis . (bvsalud.org)
- We aim to examine plasma soluble ACE2 and angiotensin profiles in relation to outcomes by enrolling consecutive patients admitted for COVID-19 with baseline blood collection at admission and repeated sampling at 7 days. (bvsalud.org)
- Moreover, patients having an upward trajectory of soluble ACE2 were characterized by an imbalance in the Ang 1-7/Ang II ratio. (bvsalud.org)
- The observed dysregulation of ACE2 and angiotensin peptides with disease progression suggest a potential role of ADAM17 inhibition and enhancing the beneficial Ang 1-7/Mas axis to improve outcomes against SARS-CoV-2 infection. (bvsalud.org)
- Aligned ACE2 protein sequences from human, rhesus macaque, African green monkey, cat, dog, American mink, mouse, and chicken cells in study of susceptibility to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) of cell lines and substrates used to diagnose and isolate influenza and other viruses. (cdc.gov)
- The now familiar spiked virus enters human cells via the also pervasive angiotensin-converting enzyme 2, or ACE2, receptor. (prohealth.com)
- The virus' binding to the receptor for ACE2 has been shown to decrease ACE2 levels and increase levels of the powerful blood vessel constrictor angiotensin II, because less angiotensin II gets degraded and fewer vasodilators get produced, which worsens the patient's prognosis. (prohealth.com)
- Histopathology and localization of SARS-CoV-2 and its host cell entry receptor ACE2 in tissues from naturally infected US- farm ed mink (Neovison vison). (cdc.gov)
- We characterized the pathological findings in 72 mink from US farm s with SARS-CoV-2 outbreaks, localized SARS-CoV-2 and its host cellular receptor angiotensin-converting enzyme 2 (ACE2) in mink respiratory tissues, and evaluated the utility of various test methods and specimens for SARS-CoV-2 detection in necropsy tissues. (cdc.gov)
- The SARS-CoV-2 receptor ACE2 was extensively detected by IHC within turbinate epithelium, with decreased detection in lower respiratory tract epithelium and alveolar macrophages. (cdc.gov)
- They identified a new association with a rare genetic variant at the Xp22.2 locus (rs190509934) that downregulates the expression of angiotensin-converting enzyme 2 (ACE2). (cdc.gov)
- If the vaccinated subject is subsequently exposed to the SARS-CoV-2 coronavirus, its T-cell protection and neutralising antibodies are expected to inhibit the viral spike protein from binding to the usual human cell surface of the ACE2 (angiotensin converting enzyme 2), thus possibly attenuating or stopping the SARS-CoV-2 infection that triggers COVID-19. (pharma-industry-review.com)
- The virus uses a special protein (angiotensin-converting enzyme 2, or ACE2) to sneak into cells and reproduce. (healthgrades.com)
- Interestingly, Study 2 found in one of their datasets that the Caucasian samples actually had higher ACE2 expression compared to the Asian samples, but this trend disappeared after other independent variables were accounted for. (theamericansun.com)
- Interestingly, while two of the studies found no relationship and Study 2 found a positive correlation between smoking and ACE2 expression, there are rat-model studies published in 2015 (5) and 2017 (6) that actually found the opposite. (theamericansun.com)
- In the case of SARS-CoV-2, angiotensin-converting enzyme 2 (ACE2) has been identified as a necessary receptor, but not all ACE2-expressing cells are equally infected, suggesting that other extracellular factors are involved in host cell invasion by SARS-CoV-2. (mit.edu)
- Here, we present evidence that extracellular vimentin might act as a critical component of the SARS-CoV-2 spike protein-ACE2 complex in mediating SARS-CoV-2 cell entry. (mit.edu)
- We demonstrate direct binding between vimentin and SARS-CoV-2 pseudovirus coated with the SARS-CoV-2 spike protein and show that antibodies against vimentin block in vitro SARS-CoV-2 pseudovirus infection of ACE2-expressing cells. (mit.edu)
ARBs12
- Angiotensin II Receptor Blockers (ARBs) are drugs that are used to treat high blood pressure and heart failure. (medmovie.com)
- BACKGROUND: Randomised controlled trials have shown a reduced risk of heart failure (HF) hospitalisation among users of ACE inhibitors (ACEIs) or angiotensin II type 1 receptor antagonists (angiotensin receptor blockers [ARBs]), but these results have limited generalisability. (greenmedinfo.com)
- During the pandemic, a hypothesis has been proposed that angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs) could be risk factors for the development of severe SARS-COV-2 infection. (viamedica.pl)
- OBJECTIVE: To evaluate the effects of treatments based on angiotensin II receptor blockers (ARBs) on the risk of myocardial infarction (MI), cardiovascular and all-cause death, as compared with conventional treatment or placebo. (uniroma1.it)
- Angiotensin II receptor blockers ( ARBs ), also known as angiotensin receptor blockers , are a class of medication primarily used to treat high blood pressure , heart failure , coronary heart disease , and kidney disease . (mdwiki.org)
- Those people taking angiotensin receptor blockers (ARBs) were 35-40% less likely to develop AD than those using other antihypertensives. (mdwiki.org)
- Indeed, as a consequence of AT 1 blockade, ARBs increase angiotensin II levels several-fold above baseline by uncoupling a negative-feedback loop. (mdwiki.org)
- The general approach to therapy of ischemic nephropathy involves control of hypertension, preferably with angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs). (medscape.com)
- It has been suggested that angiotensin converting enzyme inhibitors (ACE-1 inhibitors), such as enalapril and ramipril, and angiotensin receptor antagonists (colloquially called angiotensin receptor blockers or ARBs), such as candesartan and valsartan, may be of value in preventing and treating the effects of the coronavirus SARS-CoV-2 (also known as 2019-nCoV), the cause of the infection called COVID-19. (cebm.net)
- The two others are not recruiting: "Recombinant human angiotensin-converting enzyme 2 (rhACE2) as a treatment for patients with COVID-19" (registered on 21 February but listed on clinicaltrials.gov as withdrawn) and "Clinical study for the effects of ACEIs/ARBs on the infection of novel coronavirus pneumonia (CoVID-19)" (registered on 2 March). (cebm.net)
- Also known as ARBs, these are heart medications that block the angiotensin II hormone and widen or dilate blood vessels to improve blood flow. (cdc.gov)
- 3 These disparities exist despite similar proportions of blacks, whites, and Hispanics meeting recommendations for glycolated hemoglobin and blood pressure control and similar proportions with rennin-angiotensin system blockade via use of angiotensin-converting enzyme (ACE) inhibitors or angiotensin II type 1 receptor blockers (ARBs). (jabfm.org)
Inhibitors17
- Rather than lowering levels of angiotensin II (as ACE inhibitors do), angiotensin II receptor blockers prevent this chemical from having any effects on the heart and blood vessels. (medmovie.com)
- ACE Inhibitors/Angiotensin II type 1 receptor antagonists do not reduce hospitalisations in older patients with heart failure. (greenmedinfo.com)
- Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers can reduce proteinuria. (medscape.com)
- This shift of pressure natriuresis provides the basis for the chronic blood pressure-lowering effects in hypertensive patients of the angiotensin-converting enzyme inhibitors and angiotensin II receptor antagonists. (brainkart.com)
- May induce a more complete inhibition of the renin-angiotensin system than ACE inhibitors, does not affect the response to bradykinin, and is less likely to be associated with cough and angioedema. (medscape.com)
- Overexpression of the alpha-2,6-sialyltransferase in MDCK cells increases influenza virus sensitivity to neuraminidase inhibitors. (cdc.gov)
- ACE-1 inhibitors inhibit the conversion of angiotensin I to angiotensin II and of angiotensin(1-9) to angiotensin(1-7). (cebm.net)
- Inhibitors of ACE-2 have been developed, but none has been marketed. (cebm.net)
- Some ACE inhibitors have been found to slow the process that leads to kidney damage in many people with type 2 diabetes. (cdc.gov)
- For hypertension not controlled by diuretics, calcium channel blockers or angiotensin-converting enzyme inhibitors are generally useful. (medscape.com)
- To block VASOCONSTRICTION and HYPERTENSION effect of angiotensin II, patients are often treated with ACE INHIBITORS or with ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS. (bvsalud.org)
- Two of the drugs being trialed, lopinavir and ritonavir, being trialed are protease inhibitors. (theamericansun.com)
- Reeder, Guy S. Angiotensin converting enzyme inhibitors and receptor blockers in acute myocardial infarction: Clinical trials. (bvs.br)
- http://www.uptodate.com/contents/angiotensin-converting-enzyme-inhibitors-and-receptor-blockers-in-acute-myocardial-infarction-clinical-trials?source=search_result&search=ANGIOTENSIN+CONVERTING+ENZYME+INHIBITORS+AND+RECEPTOR+BLOCKERS+IN+ACUTE+MYOCARDIAL+INFARCTION%3A+CLINICAL+TRIALS&selectedTitle=1~150 Acesso em: 8 dez 2014. (bvs.br)
- Strippoli Giovanni FM, Bonifati Carmen, Craig Maria E, Navaneethan Sankar D, Craig Jonathan C. Angiotensin converting enzyme inhibitors and angiotensin II receptor antagonists for preventing the progression of diabetic kidney disease. (bvs.br)
- Some blood pressure medications are considered safe to use during pregnancy , but angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers and renin inhibitors are generally avoided during pregnancy . (psichologyanswers.com)
- 2. Patients treated with angiotensin converting enzyme inhibitors (ACE-I) or angiotensin receptor blockers (ARB) on the day of surgery. (who.int)
Converting Enzyme20
- Angiotensin-converting enzyme (ACE) plays a central role in generating angiotensin II from angiotensin I, and capillary blood vessels in the lung are one of the major sites of ACE expression and angiotensin II production in the human body. (nih.gov)
- These study results suggest that both systemic angiotensin II and myeloid leukocyte-bound angiotensin converting enzyme (ACE)-1 promote protection against pathogens via distinct mechanisms. (infectiousdiseaseadvisor.com)
- For instance, the local availability and functional consequence of angiotensin II (Ang II), the bioactive substance of the system, may depend on the Angiotensin converting enzyme (ACE) concentration or on the Ang II receptor density [ 4 ]. (alliedacademies.org)
- 72 Chinese primary IgAN patients who had undergone renal biopsy in Zhongshan Hospital between January 2009 and June 2009, had not received glucocorticoid, immunosuppressants, angiotensin converting enzyme inhibitor or angiotensin IIreceptor blocker, and gave informed consent were included in the study. (alliedacademies.org)
- We conclude that acute hypoxia is associated with a reversible decrease in pulmonary angiotensin converting enzyme availability. (uab.edu)
- 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). (wikidoc.org)
- Dysregulation of ACE (Angiotensin-Converting Enzyme)-2 and Renin-Angiotensin Peptides in SARS-CoV-2 Mediated Mortality and End-Organ Injuries. (bvsalud.org)
- ACE ( angiotensin -converting enzyme )-2 as the target for SARS-CoV-2 also negatively regulates the renin-angiotensin system . (bvsalud.org)
- SARS-CoV-1 and SARS-CoV-2, which share about 80% structural identity, do this by harnessing the action of the angiotensin converting enzyme, ACE-2, which is expressed in the membranes of many cells in the body, including lung alveolar epithelial cells. (cebm.net)
- Captopril is a specific competitive inhibitor of angiotensin I-converting enzyme (ACE), the enzyme responsible for the conversion of angiotensin I to angiotensin II. (nih.gov)
- Angiotensin I is then converted by angiotensin converting enzyme (ACE) to angiotensin II, a potent endogenous vasoconstrictor substance. (nih.gov)
- Moreover, this increase in left ventricular mass index occurs in children who have ADPKD with borderline hypertension (75th to 95th percentile) and is prevented with angiotensin-converting enzyme inhibitor (ACEI) monotherapy. (lww.com)
- Competitive inhibitor of angiotensin-converting enzyme. (medscape.com)
- It is produced from angiotensin I after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME . (bvsalud.org)
- Angiotensin-converting enzyme DD genotype in patients with primary pulmonary hypertension: increased frequency and association with preserved haemodynamics. (cdc.gov)
- Impact of angiotensin-converting enzyme, angiotensinogen, endothelial NO synthase, and bradykinin receptor B2 gene polymorphisms on myocardium in patients with hypertension and in athletes]. (cdc.gov)
- Neutral endopeptidase and angiotensin I converting enzyme insertion/deletion gene polymorphism in humans. (cdc.gov)
- The influence of I/D polymorphism of the angiotensin I converting enzyme (ACE) gene and 4G/5G polymorphism of plasminogen activator inhibitor (PAI-1) gene promoter on the haemostatic system in patients with essential hypertension and dyslipidemia]. (cdc.gov)
- Effects of angiotensin-converting enzyme gene polymorphism and serum vitamin D levels on ambulatory blood pressure measurement and left ventricular mass in Turkish hypertensive population. (cdc.gov)
- Angiotensin-converting enzyme 2 is a protein on the surface of various cells that interacts with peptide hormones angiotensin I and II. (theamericansun.com)
Hypertension24
- Tumor necrosis factor-α produced in the kidney contributes to angiotensin II-dependent hypertension. (duke.edu)
- Because Th1 cells generate interferon-γ and tumor necrosis factor-α (TNF-α), we hypothesized that interferon-γ and TNF-α propagate renal damage during hypertension induced by activation of the renin-angiotensin system. (duke.edu)
- As angiotensin II-infused TNF knockout mice had exaggerated endothelial nitric oxide synthase expression in the kidney and enhanced nitric oxide bioavailability, we examined the actions of TNF-α generated from renal parenchymal cells in hypertension by transplanting wild-type or TNF knockout kidneys into wild-type recipients before the induction of hypertension. (duke.edu)
- The angiotensin II subtype 1 receptor (AT1R) has been linked to the development and progression of renovascular hypertension. (elsevier.com)
- Hypertension , 51 (2 PART 2), 466-473. (elsevier.com)
- and releases arachidonic acid from tissue phospholipids which mediate or modulate one or more cardiovascular effects of angiotensin Bay 65-1942 HCl II and has been implicated in hypertension. (immune-source.com)
- These data suggest that angiotensin II-induced hypertension and associated cardiovascular pathophysiological changes are mediated by cPLA2? (immune-source.com)
- is crucial for the development of Ang II-induced hypertension and associated cardiovascular dysfunction and hypertrophy cardiac fibrosis inflammation oxidative stress and activation of ERK1/2 and cSrc in mice. (immune-source.com)
- Therefore it appears that metabolites of AA with Bay 65-1942 HCl pro-hypertensive effects contribute to the development of hypertension caused by Ang II in these mice. (immune-source.com)
- Hypertension , 64 (2), 227-228. (elsevier.com)
- Savoia, C & Volpe, M 2014, ' Impact of the direct angiotensin II type 2 receptor stimulation on renal function: Toward a sex-specific therapeutic approach for hypertension ', Hypertension , vol. 64, no. 2, pp. 227-228. (elsevier.com)
- Seidelin, PH & Struthers, AD 1991, ' Angiotensin II augments the stroke volume response to isoprenaline in man ', Journal of Hypertension , vol. 9, no. 11, pp. 1041-1047. (dundee.ac.uk)
- Angiotensin II receptor blockers are used primarily for the treatment of hypertension where the person is intolerant of ACE inhibitor therapy primarily because of persistent cough . (mdwiki.org)
- Hypertension;79(2): 365-378, 2022 02. (bvsalud.org)
- Its beneficial effects in hypertension and heart failure appear to result primarily from suppression of the renin-angiotensin-aldosterone system. (nih.gov)
- by the risk of hypertension, you may be prescribed to avoid herbs that can lower your blood pressure any medication if you're type 2 diabetes and undiabetes. (jewishledger.com)
- Renal injury from angiotensin II-mediated hypertension. (semanticscholar.org)
- In addition to hypertension, the resultant angiotensin in ADPKD is a pivotal factor in cyst proliferation and expansion, increased sympathetic and endothelin activity, oxidant injury, and fibrosis. (lww.com)
- hypertension treatment antidepressant is diagnosed with angiotensin II receptor blockers. (centrumlucina.cz)
- Renin-angiotensin gene polymorphism in children with uremia and essential hypertension. (cdc.gov)
- Journal of human hypertension 2004 Feb 18 (2): 119-25. (cdc.gov)
- Polymorphism in angiotensin II receptor genes and hypertension. (cdc.gov)
- Angiotensin II type 1 receptor A1166C gene polymorphism and essential hypertension in San Luis. (cdc.gov)
- Heran Balraj S, Wong Michelle MY, Heran Inderjit K, Wright James M. Blood pressure lowering efficacy of angiotensin receptor blockers for primary hypertension. (bvs.br)
Receptors9
- Angiotensin II acts on a number of different angiotensin receptors. (infectiousdiseaseadvisor.com)
- Peripheral action of angiotensin was cardioaccelerator via direct stimulation of beta-receptors of the atria in isolated atrial preparations. (who.int)
- Increased levels of circulating angiotensin II result in unopposed stimulation of the AT 2 receptors, which are, in addition, upregulated. (mdwiki.org)
- they have differential affinity for angiotensin receptors , although their exact role is still unclear. (wikidoc.org)
- Role of angiotensin II AT1 receptors. (jci.org)
- Angiotensin II is an agonist at both angiotensin AT 1 and angiotensin AT 2 receptors. (cebm.net)
- Angiotensin(1-7) is an antagonist at angiotensin AT 1 receptors and an agonist at MAS-1 receptors. (cebm.net)
- Angiotensin receptor antagonists block the actions of angiotensin II and angiotensin(1-7) at angiotensin AT 1 receptors. (cebm.net)
- It selectively and competitively blocks the vasoconstricting and aldosterone-secreting effects of angiotensin II by selectively antagonising its binding to AT1 receptors. (com.bd)
Renal16
- Transplant recipients lacking TNF solely in the kidney had blunted hypertensive responses to angiotensin II and augmented renal endothelial nitric oxide synthase expression, confirming a role for kidney-derived TNF-α to promote angiotensin II-induced blood pressure elevation by limiting renal nitric oxide generation. (duke.edu)
- Intrarenal angiotensin II plays an important role in renal fibrosis in primary IgA nephropathy. (alliedacademies.org)
- Intrarenal Ang II plays an important role in renal fibrosis in IgAN, particularly at the tubulointerstitial level. (alliedacademies.org)
- Intervention in the renin-angiotensin-aldosterone system (RAAS) has convincingly shown to delay progression of renal disease in patients with diabetes mellitus with elevated urinary albumin excretion (UAE) in several large trials. (biomedcentral.com)
- Our objective was to assess circulating, renal, cardiac, and vascular Ang II in a canine model of rapid ventricular pacing-induced heart failure that evolves from early left ventricular dysfunction to overt congestive heart failure. (elsevier.com)
- Overt congestive heart failure was characterized by further impaired cardiac function and cardiac enlargement, reduced renal perfusion pressure, urinary sodium retention, and increased plasma renin activity and plasma Ang II. (elsevier.com)
- In early left ventricular dysfunction dogs, renal cortical, renal medullary, ventricular, and aortic Ang II were unchanged, and atrial Ang II was decreased. (elsevier.com)
- The greatest increase in tissue Ang II occurred in the renal medulla. (elsevier.com)
- We conclude that early increases in local renal, myocardial, and vascular Ang II do not occur in this model of early left ventricular dysfunction and may even be suppressed. (elsevier.com)
- In contrast, increased myocardial and particularly renal Ang II in association with increased circulating Ang II are hallmarks of overt experimental congestive heart failure. (elsevier.com)
- Dual blockade of renin-angiotensin system increases risks of hypotension, hyperkalemia, and renal impairment. (medscape.com)
- Analysis of renal structural and functional features in two rat strains with a different susceptibility to glomerular sclerosis. (semanticscholar.org)
- Renal Volume, Renin-Angiotensin-Aldosterone System, Hyperten. (lww.com)
- Renal cyst enlargement in ADPKD in adults is associated with stimulation of both the circulating and intrarenal renin-angiotensin-aldosterone system. (lww.com)
- The effect of renin-angiotensin-aldosterone system inhibition with dual blockade, ACEI and angiotensin receptor antagonists, on renal volume and kidney function is under study in the Halt Progression of Polycystic Kidney Disease (HALT PKD) trial. (lww.com)
- 2 Similarly, the incidence of reported end-stage renal disease in people with diabetes is more than 4 times as high in African Americans and 4 to 6 times as high in Mexican Americans than in the general population of diabetes patients. (jabfm.org)
Vasoconstriction5
- Angiotensin II, a key effector peptide of the system, causes vasoconstriction and exerts multiple biological functions. (nih.gov)
- AngII not only activates the angiotensin type 1 receptor (AT 1 R) to mediate vasoconstriction but also angiotensin type 2 receptor (AT 2 R) to cause vasodilation. (bioone.org)
- Angiotensin II, the production of which has been reported to increase after burn, is thought to be one of the primary mediators of postburn mesenteric vasoconstriction. (utmb.edu)
- Angiotensin is a peptide hormone that causes vasoconstriction and an increase in blood pressure . (wikidoc.org)
- Angiotensin II acts on the CNS to increase vasopressin production, and also acts on venous and arterial smooth muscle to cause vasoconstriction. (wikidoc.org)
Levels of angiotensin1
- Conversely, when sodium intake is reduced below normal, increased levels of angiotensin II cause sodium and water retention and oppose reductions in arterial blood pressure that would otherwise occur. (brainkart.com)
Inhibitor6
- Aliskiren/valsartan formulated 150 mg-160 mg (a partial dose of each of 2 RAAS inhibitor drugs) was considered a partial dose (submaximum). (ajmc.com)
- Moreover administration of inhibitor of AA metabolism ETYA blocked Ang II-induced increase in SBP in cPLA2? (immune-source.com)
- Objective: To investigate the role of angiotensin II as a mediator of burn- and sepsis-induced gut ischemia and reperfusion injury and to determine whether treatment with the angiotensin II inhibitor DuP753 can attenuate mucosal injury and bacterial translocation in a burn/endotoxemia porcine model. (utmb.edu)
- ACE is a target of ACE inhibitor drugs, which decrease the rate of angiotensin II production. (wikidoc.org)
- Colucci, Wilson S. Angiotensin II receptor blocker and neprilysin inhibitor therapy in heart failure due to systolic dysfunction. (bvs.br)
- http://www.uptodate.com/contents/angiotensin-ii-receptor-blocker-and-neprilysin-inhibitor-therapy-in-heart-failure-due-to-systolic-dysfunction?source=search_result&search=ANGIOTENSIN+II+RECEPTOR+BLOCKERS+IN+HEART+FAILURE+DUE+TO+SYSTOLIC+DYSFUNCTION%3A+THERAPEUTIC+USE&selectedTitle=2~150 Acesso em: 8 dez 2014. (bvs.br)
Abstract2
- abstract = "Many studies in experimental animal models suggest that there is an interaction between angiotensin II and the sympathetic nervous system. (dundee.ac.uk)
- ABSTRACT The aim of this study in 2006-08 was to determine the prevalence and risk factors of CVD in an Iranian population of patients with type 2 diabetes mellitus. (who.int)
Angiotensinogen6
- Angiotensinogen is made by the liver and forms angiotensin I in the blood. (infectiousdiseaseadvisor.com)
- The expression of intrarenal renin, angiotensinogen (AGT), Ang II, Ang IIreceptor was examined by immunohistochemistry staining (IHCS). (alliedacademies.org)
- Angiotensinogen is an α-2-globulin produced constitutively and released into the circulation mainly by the liver. (wikidoc.org)
- Plasma angiotensinogen levels are increased by plasma corticosteroid , estrogen , thyroid hormone , and angiotensin II levels. (wikidoc.org)
- Angiotensin I ( CAS # 11128-99-7), also called proangiotensin , is formed by the action of renin on angiotensinogen . (wikidoc.org)
- Angiotensinogen is converted to angiotensin I by renin. (cebm.net)
Aldosterone secretion5
- Angiotensin II also increases aldosterone secretion, therefore, it acts as an endocrine , autocrine / paracrine , and intracrine hormone. (wikidoc.org)
- Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion. (medscape.com)
- Angiotensin II also stimulates aldosterone secretion from the adrenal cortex, thereby contributing to sodium and fluid retention. (nih.gov)
- Inhibition of ACE results in decreased plasma angiotensin II and increased plasma renin activity (PRA), the latter resulting from loss of negative feedback on rennin release caused by reduction in angiotensin II.The reduction of angiotensin II leads to decreased aldosterone secretion, and, as a result, small increases in serum potassium may occur along with sodium and fluid loss. (nih.gov)
- Reduces angiotensin II levels, decreasing aldosterone secretion. (medscape.com)
Hypertensive6
- Spironolactone and chlorthalidone in uncontrolled elderly hypertensive patients treated with calcium antagonists and angiotensin II receptor-blocker: effects on endothelial function, inflammation, and oxidative stress. (druglib.com)
- The purpose of the present study was to evaluate the differences between spironolactone and chlorthalidone in hypertensive elderly patients treated with calcium antagonists and angiotensin II receptor blockers. (druglib.com)
- activation most likely through the release of arachidonic acid and generation of eicosanoids with predominant pro-hypertensive effects and activation of one or more signaling molecules including ERK1/2 and cSrc. (immune-source.com)
- selectively catalyzes release of AA from tissue lipids12 and Ang II is known to Bay 65-1942 HCl activate cPLA2 to release AA cPLA2 appears to mediate the hypertensive effect of Ang II via AA release. (immune-source.com)
- Irbesartan and losartan have trial data showing benefit in hypertensive patients with type 2 diabetes , [ citation needed ] and may delay the progression of diabetic nephropathy . (mdwiki.org)
- Association of aldosterone synthase gene -344T/C polymorphism with plasma aldosterone and angiotensin II concentration in hypertensive patients]. (cdc.gov)
Although angiotensin II2
- Although angiotensin II is one of the most powerful sodium- and water-retaining hormones in the body, neither a decrease nor an increase in circulating angiotensin II has a large effect on extracellular fluid volume or blood volume. (brainkart.com)
- Although angiotensin II (Ang II) has been implicated in the pathophysiology of congestive heart failure, its temporal and regional changes during the development and progression of the disease are poorly defined. (elsevier.com)
Inhibition3
- van Ginkel, S.L.. / The effect of exercise and ACE inhibition on angiotensin II . (vu.nl)
- Captopril prevents the conversion of angiotensin I to angiotensin II by inhibition of ACE, a peptidyldipeptide carboxy hydrolase. (nih.gov)
- This inhibition has been demonstrated in both healthy human subjects and in animals by showing that the elevation of blood pressure caused by exogenously administered angiotensin I was attenuated or abolished by captopril. (nih.gov)
Medication1
- can blood pressure medication change your personality of the two number in the pressure is the normal blood pressure, the pressure readings are too low. (centrumlucina.cz)
Treatment with angiotensin1
- Results showed that treatment with angiotensin II was associated with increased bacterial clearance from the blood and the peritoneal cavity, as well as a modified host immune response, following CLP. (infectiousdiseaseadvisor.com)
Peptides2
- Oxytocinase (EC 3.4.11.3), a pregnancy-related oxytocin-inactivating α-aminoacyl hydrolase, also has the ability to degrade vasopressin, angiotensin II and some synthetic peptides. (nus.edu.sg)
- Two such peptides, S-benzyl-L-cysteine-p-nitroanilide (BCN) and L-leucine-p-nitroanilide (LN) with proven substrate specificity, have been widely used to study oxytocinase activity in vitro. (nus.edu.sg)
Patients20
- The trial provided substantial evidence of the effectiveness of angiotensin II in raising blood pressure over placebo in patients with distributive shock, while keeping catecholamine levels constant. (medscape.com)
- Data from the literature show lights and shadows about the use of angiotensin II (Ang II), for instance as an alternative vasopressor in patients with vasodilatory shock that requires high doses of catecholamines. (biomedcentral.com)
- Secondly, Ang II could be administered to specific patients. (biomedcentral.com)
- In this perspective, could we hypothesize that an early infusion of Ang II has a positive effect on these patients? (biomedcentral.com)
- Thirdly, the safety profile of Ang II has never been tested in patients with vasodilatory shock and concurrent myocardial dysfunction. (biomedcentral.com)
- If put into practice in human patients, are there any patient-specific risk factors or considerations clinicians should be aware of if angiotensin II treatment were to be administered to a patient undergoing septic shock? (infectiousdiseaseadvisor.com)
- It is too soon to say which patients might benefit from the immune effects of angiotensin II in sepsis. (infectiousdiseaseadvisor.com)
- Further studies that can identify patients who may benefit from angiotensin II are still needed. (infectiousdiseaseadvisor.com)
- To investigate the relationship of intrarenal angiotensin II (Ang II) expression with clinicpathological injury index and intrarenal expression and regulation of RAS (renin-angiotensin system) components in IgAN (immunoglobulin A nephropathy) patients. (alliedacademies.org)
- In this month's EM Quick Hits podcast: Anand Swaminathan on the approach to cardiogenic shock, Hania Bielawska on the myths of radiation dose in pregnant patients, Hans Rosenberg & Michael Gottlieb on PoCUS in airway management, Menaka Pai on VIPIT following AstraZeneca COVID-19 vaccination, Brit Long & Michael Gottlieb on Angiotensin II for emergency clinicians, Michael Schull on tips on the safety of short-term steroid use. (player.fm)
- Individual patients show a large variability in albuminuria response to angiotensin receptor blockers (ARB). (biomedcentral.com)
- Data from patients with type 2 diabetes and microalbuminuria (n = 49) treated with irbesartan 300 mg/day were used for discovery. (biomedcentral.com)
- Therefore, the aims of this study were to first discover and validate a serum metabolite classifier that predicts response in albuminuria to angiotensin II receptor blocker (ARB) therapy in patients with diabetes mellitus and micro- or macroalbuminuria, and secondly, to integrate the identified metabolites in a molecular process model capturing disease pathophysiology at the interface of drug mechanism of action to decipher the underlying molecular processes driving albuminuria response to ARB. (biomedcentral.com)
- In contrast, when angiotensin levels cannot be decreased in response to increased sodium intake (high angiotensin II curve), as occurs in some hyper-tensive patients who have impaired ability to decrease renin secretion, the pressure natriuresis curve is not nearly as steep. (brainkart.com)
- METHODS: In this multicentre, placebo-controlled, double-blind, randomised, phase 2 clinical trial, we enrolled patients (aged 22-89 years) with postherpetic neuralgia of at least 6 months' duration from 29 centres across six countries. (ox.ac.uk)
- Coinfection with SARS-CoV-2 and other respiratory pathogens in patients with COVID-19 in Guangzhou, China. (cdc.gov)
- The epidemiology and clinical characteristics of co-infection of SARS-CoV-2 and influenza viruses in patients during COVID-19 outbreak. (cdc.gov)
- The high prevalence of CVD in Iranian patients with type 2 diabetes underscores the importance of better detection and treatment of metabolic risk factors of CVD in these patients. (who.int)
- RÉSUMÉ La présente étude visait à déterminer la prévalence et les facteurs de risque des maladies cardio-vasculaires dans une population iranienne de patients atteints de diabète de type 2 entre 2006 et 2008. (who.int)
- Les antécédents et les examens cliniques de 752 patients consultant dans un centre de recherche sur l'endocrinologie et le métabolisme ont été consignés et des analyses en laboratoire ont été réalisées. (who.int)
Protein6
- The protein expression of PLA2 but not PLC?2 PLD1 or PLD2 was also absent in cPLA2? (immune-source.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). (wikidoc.org)
- Hoffmann M , Kleine-Weber H , Pöhlmann S . A multibasic cleavage site in the spike protein of SARS-CoV-2 is essential for infection of human lung cells. (cdc.gov)
- A BLAST search restricted to mammalian protein sequence, a transmembrane domain, and 2-heptad repeats. (cdc.gov)
- The spike protein is a large type I transmembrane protein containing two subunits, S1 and S2. (bioss.com.cn)
- The California based biotech plans to use a well-known replicating cell line (human erythroleukemia, K562) to integrate the spike protein of SARS-CoV-2 or its S1 domain onto the cell membrane simulating that the viral protein is introduced on a decoy cell surface to evoke T cell and B cell immunity to COVID-19. (pharma-industry-review.com)
Increases7
- Angiotensin II also increases the ability of white blood cells to kill bacteria through phagocytosis. (infectiousdiseaseadvisor.com)
- Excessive Angiotensin II Does Not Cause Large Increases in Extracellular Fluid Volume Because Increased Arterial Pressure Counterbalances Angiotensin-Mediated Sodium Retention. (brainkart.com)
- The reason for this is that with large increases in angiotensin II levels, as occurs with a renin-secreting tumor of the kidney, the high angiotensin II levels initially cause sodium and water retention by the kidneys and a small increase in extracellular fluid volume. (brainkart.com)
- This also initi-ates a rise in arterial pressure that quickly increases kidney output of sodium and water, thereby overcom-ing the sodium- and water-retaining effects of the angiotensin II and re-establishing a balance between intake and output of sodium at a higher blood pres-sure. (brainkart.com)
- Conclusions: Angiotensin II appears to play a pivotal role in the bum- and endotoxin-induced intestinal ischemia and reperfusion injury, with subsequent increases in permeability and bacterial translocation. (utmb.edu)
- benazepril increases effects of synthetic human angiotensin II by unspecified interaction mechanism. (medscape.com)
- quinapril increases effects of synthetic human angiotensin II by unspecified interaction mechanism. (medscape.com)
Receptor type1
- [6] They work by blocking the angiotensin II receptor type 1 (AT 1 ) thereby preventing the effects of angiotensin II . (mdwiki.org)
Plasma angiotensin1
- Virgin, pregnant (at different days of gestation) and post-partum Sprague-Dawley rats were used to determine uterine artery hemodynamics using micro ultrasound and plasma angiotensin II levels by ELISA. (bioone.org)
Human angiotensin3
- azilsartan decreases effects of synthetic human angiotensin II by pharmacodynamic antagonism. (medscape.com)
- synthetic human angiotensin II and finerenone both increase serum potassium. (medscape.com)
- olmesartan decreases effects of synthetic human angiotensin II by pharmacodynamic antagonism. (medscape.com)
Selective angiotensin2
- Further analysis showed that the effects of angiotensin II treatment on bacteremia burden following CLP were negated by selective angiotensin type 1 receptor (AT1R) deletion in myeloid-lineage leukocytes. (infectiousdiseaseadvisor.com)
- EMA401, an orally administered highly selective angiotensin II type 2 receptor antagonist, as a novel treatment for postherpetic neuralgia: a randomised, double-blind, placebo-controlled phase 2 clinical trial. (ox.ac.uk)
Losartan3
- These treatments included intraperitoneal angiotensin II alone, intraperitoneal angiotensin II plus losartan, subcutaneous angiotensin II, or vehicle. (infectiousdiseaseadvisor.com)
- Similar results were observed when angiotensin II was co-administered with losartan, suggesting that the effects of angiotensin II on bacteremia burden are mediated via AT1R. (infectiousdiseaseadvisor.com)
- Losartan is an angiotensin II receptor antagonist. (com.bd)
Renin-Angiotensin15
- The renin-angiotensin system (RAS) plays a key role in maintaining blood pressure homeostasis, as well as fluid and salt balance. (nih.gov)
- Multiple short-term effects of lead on the renin-angiotensin system. (cdc.gov)
- Biological Function Essential counter-regulatory carboxypeptidase of the renin-angiotensin hormone system that is a critical regulator of blood volume, systemic vascular resistance, and thus cardiovascular homeostasis (PubMed:27217402). (qedbio.com)
- A number of studies have shown that activation of intrarenal renin-angiotensin system (RAS) plays an important role in development and progression of chronic kidney disease (CKD). (alliedacademies.org)
- Thus, changes in activity of the renin-angiotensin system act as a powerful amplifier of the pressure natriuresis mechanism for maintaining stable blood pressures and body fluid volumes. (brainkart.com)
- Angiotensin II (Ang II) is the key peptide hormone in the renin-angiotensin-aldosterone system (RAAS). (elsevier.com)
- Mit der Einführung des ACE-Hemmers Captopril begann 1981 die Erfolgsgeschichte der therapeutischen Intervention in das Renin-Angiotensin-System (RAS) bei kardiovaskulären und renalen Erkrankungen. (arzneimitteltherapie.de)
- Journal of the Renin-Angiotensin-Aldosterone System , 2 (4), 205-210. (monash.edu)
- Renin-angiotensin system (RAS) is a signaling pathway for regulation of blood pressure, blood volume, natriuresis, and other vascular functions. (ejmamr.com)
- It is part of the renin-angiotensin system , which regulates blood pressure. (wikidoc.org)
- A simplified version of the pharmacology of the renin-angiotensin system is shown in the diagram below. (cebm.net)
- Therapeutisch werden standardmäßig Medikamente zur Senkung des Blutzuckerspiegels (Inhibitoren des Renin-Angiotensin-Aldosteron-Systems (RAAS), Metformin, Inhibitoren des Natrium-Glucose-Transporters-2 (SGLT2) und des Blutdrucks (Erstlinien Therapie mit Inhibitoren des RAAS, sekundäre Therapie mit Statinen sowie Nikotinentwöhnung und salzarme Ernährung) eingesetzt. (uni-muenchen.de)
- Journal of the renin-angiotensin-aldosterone system : JRAAS 2002 Jun 3 (2): 109-15. (cdc.gov)
- Journal of the renin-angiotensin-aldosterone system : JRAAS 2003 Mar 4 (1): 27-30. (cdc.gov)
- Impact of genetic polymorphisms of the renin-angiotensin system and of non-genetic factors on kidney transplant function--a single-center experience. (cdc.gov)
Type7
- Importantly, angiotensin II is Food and Drug Administration (FDA)-approved to treat hypotension of the type that often accompanies sepsis. (infectiousdiseaseadvisor.com)
- The angiotensin II type 2 receptor (AT2R) is a new target for neuropathic pain. (ox.ac.uk)
- E 2 decreases expression of the angiotensin II type 1 receptor (AT 1 R), a receptor with known relevance to water and salt intakes, in multiple areas of the brain where ERα and ERβ are differentially expressed. (uky.edu)
- As a result of more about 106% of those with latest medicine for diabetes type 2 a high risk of developing it needs to achieve the health condition. (giveherbal.com)
- type 2 it drugs in diabetes medicines Patanjali pipeline and are completely superior to detect it management. (giveherbal.com)
- We report a patient with type 2 diabetes mellitus and chronic lymphocytic leukemia who had been infected for 42 weeks with SARS-CoV-2. (cdc.gov)
- In this context, teeth proved to be important elements in this type of identification, due to the high probability that there are not two people having the same exact dental features, as well as the relatively high degree of physical and chemical resistance of dental structures 15 . (bvsalud.org)
Vasoconstrictor2
- Converts angiotensin I to angiotensin 1-9, a nine-amino acid peptide with anti-hypertrophic effects in cardiomyocytes, and angiotensin II to angiotensin 1-7, which then acts as a beneficial vasodilator and anti-proliferation agent, counterbalancing the actions of the vasoconstrictor angiotensin II (PubMed:10969042, PubMed:10924499, PubMed:11815627, PubMed:19021774, PubMed:14504186). (qedbio.com)
- Para inhibir el efecto vasoconstrictor e hipertensivo de la angiotensina II, a menudo se trata a los pacientes con INHIBIDORES DE LA ECA o con BLOQUEANTES DEL RECEPTOR DE TIPO 1 DE LA ANGIOTENSINA II. (bvsalud.org)
Effects19
- Based on the agreements emanating from the special protocol assessment to assess blood pressure effects, the data from this single study supported approval of angiotensin II by the Food and Drug Administration for marketing in the USA. (medscape.com)
- The effects of lead (7439921) on the relationship between plasma renin and angiotensin II were studied. (cdc.gov)
- The effects of lead, 0.5 milligrams per minute, administered by continuous infusion for 3 hours, on these parameters and on arterial angiotensin II were measured. (cdc.gov)
- Interestingly, no difference in adverse effects was remarkable between the two groups. (biomedcentral.com)
- Matthew D. Taylor, MD, provides insight into the potential effects of angiotensin II on bacterial clearance and the systemic inflammatory response in clinical sepsis. (infectiousdiseaseadvisor.com)
- To assess the effects of angiotensin II on the immune response to CLP, the researchers randomly assigned 4 cohorts of mice to 4 different treatments. (infectiousdiseaseadvisor.com)
- There are theoretical reasons as to why angiotensin II might be preferable to norepinephrine - the current first-line drug - that include but are not limited to its associated immune effects. (infectiousdiseaseadvisor.com)
- Because angiotensin II has several important effects in increas-ing tubular reabsorption of sodium, a reduced level of angiotensin II decreases tubular reabsorption of sodium and water, thus increasing the kidneys' excretion of sodium and water. (brainkart.com)
- The use of drugs to block the effects of angiotensin II has proved to be important clinically for improv-ing the kidneys' ability to excrete salt and water. (brainkart.com)
- Many of the Ang II effects on glomerulosa cells involve a precisely coordinated regulation of signaling cascades and gene expression. (elsevier.com)
- The development of genome-wide gene arrays has allowed the definition of transcriptome-wide effects of Ang II in adrenocortical cells. (elsevier.com)
- Analysis of the Ang II gene targets reveals broad effects on cellular gene expression, particularly the rapid induction of numerous transcription factors that may regulate long-term steroid metabolism and cell growth/proliferation. (elsevier.com)
- The effects of angiotensin II were studied on isolated atrial preparations of nonreserpinised and reserpinised rabbits, before and after treating the preparations by propranolol. (who.int)
- The angiotensin II receptor blockers have differing potencies in relation to blood pressure control, with statistically differing effects at the maximal doses. (mdwiki.org)
- However, recent data suggest AT 2 receptor stimulation may be less beneficial than previously proposed, and may even be harmful under certain circumstances through mediation of growth promotion, fibrosis , and hypertrophy , as well as eliciting proatherogenic and proinflammatory effects. (mdwiki.org)
- Nonpeptide angiotensin II receptor antagonist that blocks the vasoconstricting and aldosterone-secreting effects of angiotensin II. (medscape.com)
- The mechanistic basis for the disparate effects of angiotensin II on coronary collateral growth. (omeka.net)
- Together, the results reveal selective effects of ER subtypes on ingestive behaviors, advancing our understanding of E 2 's inhibitory role in the controls of fluid intake by female rats. (uky.edu)
- During septic shock, fluid therapy is aimed at increasing cardiac output and improving tissue oxygenation, but it poses two problems: it has inconsistent and transient efficacy, and it has many well-documented deleterious effects. (bvsalud.org)
Decreases1
- Estradiol (E 2 ) decreases both water and saline intakes by female rats. (uky.edu)
Intrarenal2
- Surprisingly, little information is available about the RAS expression and regulation in the human kidney and particularly in kidney diseases and data on the intrarenal RAS expression and regulation were mostly obtained in animals [ 1 , 2 ]. (alliedacademies.org)
- Hypercalcemia stimulates expression of intrarenal phospholipase A2 and prostaglandin H synthase-2 in rats. (jci.org)
STIMULATES1
- Angiotensin also stimulates the release of aldosterone from the adrenal cortex to promote sodium retention by the kidneys. (wikidoc.org)
Kidney5
- In overt congestive heart failure dogs, Ang II was increased in the kidney and heart compared with normal dogs and in all tissues compared with early left ventricular dysfunction dogs. (elsevier.com)
- In addition, angiotensin II acts at the Na + /H + exchanger in the proximal tubules of the kidney to stimulate Na reabsorption and H + excretion which is coupled to bicarbonate reabsorption. (wikidoc.org)
- Genetic identification of two major modifier loci of polycystic kidney disease progression in pcy mice. (jci.org)
- 2015. The two kidney to one kidney transition and transplant glomerulopathy: a podocyte perspective. . (umich.edu)
- 2012. Angiotensin II-dependent persistent podocyte loss from destabilized glomeruli causes progression of end stage kidney disease. . (umich.edu)
Vasopressin4
- Moreover, during the first 48 hours from the randomization, doses of the vasopressors (norepinephrine (NE) and vasopressin) were significantly reduced in the Ang II group but not in the placebo group. (biomedcentral.com)
- 3. The pressor responses to intraventricular perfusions of angiotensin II were normal in Long-Evans rats, virtually absent in rats homozygous for hereditary hypothalamic diabetes insipidus, irrespective of whether they were injected with vasopressin tannate or not, and intermediate in rats heterozygous for hypothalamic diabetes insipidus. (portlandpress.com)
- 4. The results suggest that the pressor response to intraventricular angiotensin II is related to the release of vasopressin. (portlandpress.com)
- Judged by the Ki values of the octapeptides which negatively reflect their inactivation or hydrolysis by oxytocinases, it is concluded that the enzyme component which inactivates angiotensin II is predominant in all the samples tested followed by the oxytocin and vasopressin-inactivating components. (nus.edu.sg)
Endothelial1
- This study aimed to investigate the inhibitory effect of blueberry anthocyanin (BBA) on Angiotensin II (Ang II)-induced apoptosis of human umbilical vein endothelial cells (HUVECs), and its regulation mechanisms involving Bax and Caspase 3. (medscimonit.com)
Decapeptide2
Arterial2
- The use of angiotensin II to raise the mean arterial pressure (MAP) could provide additional therapy and the opportunity to evaluate a catecholaminesparing effect by decreasing the dose of concomitant catecholamines while maintaining a target MAP. (medscape.com)
- Thus, the inabil-ity to suppress angiotensin II formation when there is excess sodium reduces the slope of pressure natriure-sis and makes arterial pressure very salt sensitive. (brainkart.com)
Coronavirus7
- Microbial infection) Acts as a receptor for human coronaviruses SARS-CoV and SARS-CoV-2, as well as human coronavirus NL63/HCoV-NL63. (qedbio.com)
- Isoform 2]: (Microbial infection) Non-functional as a receptor for human coronavirus SARS-CoV-2. (qedbio.com)
- severe acute respiratory syndrome coronavirus 2 from patient with coronavirus disease, United States. (cdc.gov)
- US CDC Real-time reverse transcription PCR panel for detection of severe acute respiratory syndrome coronavirus 2. (cdc.gov)
- Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes respiratory disease in mink similar to human COVID-19. (cdc.gov)
- Compared to adults, children with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) have predominantly mild or asymptomatic infections, but the underlying immunological differences remain unclear. (nature.com)
- In most cases, SARS-CoV-2, the novel coronavirus that causes COVID-19, enters the body via the airway. (healthgrades.com)
Pathogenesis2
Elevated during SARS-CoV-2 in1
- Plasma Ang I, Ang 1-7 ( angiotensin 1-7) levels, and the Ang 1-7/Ang II ( angiotensin II ) ratio were elevated during SARS-CoV-2 infection related to downregulation of ACE activity at baseline. (bvsalud.org)
ACEI3
- The objective of the study was to conduct a meta-analysis of the association between ACEI or ARB use and SARS-COV-2 infection severity or mortality. (viamedica.pl)
- We searched PubMed, EMBASE, Google scholar and the Cochrane Database of Systematic Reviews for observational studies published between December 2019 and August 4, 2020 Studies were included if they contained data on ACEI or ARB use and SARS-COV-2 infection severity or mortality. (viamedica.pl)
- At present, the evidence available does not support the hypothesis of increased SARS-COV-2 risk with ACEI or ARB drugs. (viamedica.pl)
Systemic1
- Angiotensin II was found to be associated with an increase in the myeloid innate immune response during severe systemic infection, suggesting angiotensin II may improve immune responses in the setting of clinical sepsis. (infectiousdiseaseadvisor.com)
Stimulation1
- We have now sought evidence for such an interaction using angiotensin II and beta-adrenoceptor stimulation with isoprenaline. (dundee.ac.uk)
Hypotension1
- NICE is unable to make a recommendation on angiotensin II for treating vasosuppressor-resistant hypotension caused by septic or distributive shock. (bvsalud.org)
Rats3
- A basal secretion rate of 16 ± 3 × 10 -15 mol of immunoreactive angiotensin 11/min was calculated for intact rats. (portlandpress.com)
- Lever-pressing behavior caused by intraseptal Angiotensin II in water-satiated rats. (bvsalud.org)
- 2. Rats were treated with bosentan or vehicle (5% gum arabic) for 7 days by gavage. (shengsci.com)
Drugs3
- Unfortunately, these two classes of drugs may lead to increased serum creatinine levels and hyperkalemia, limiting their utility. (medscape.com)
- Telmisartan belongs to the class of drugs called Angiotensin II receptor antagonists that works by blocking the angiotensin II receptor, relaxing the blood vessels and lowering the blood pressure. (apollopharmacy.in)
- Telmisartan belongs to the class of drugs called Angiotensin II receptor antagonists. (apollopharmacy.in)
Blood pressure10
- When blood pressure changes, Angiotensin II is produced and released into the bloodstream. (centerwatch.com)
- Interferon deficiency had no impact on blood pressure elevation or urinary albumin excretion during chronic angiotensin II infusion. (duke.edu)
- Note that when the angiotensin control of natriuresis is fully functional, the pressure natriuresis curve is steep (normal curve), indicating that only minor changes in blood pressure are needed to increase sodium excretion when sodium intake is raised. (brainkart.com)
- II formation appropriately in response to excess sodium, the same rise in sodium intake causes blood pressure to rise as much as 50 mm Hg. (brainkart.com)
- 90mmHg systolic blood pressure [2] ) at the juxtaglomerular cells , or decreased delivery of Na+ and Cl- to the macula densa . (wikidoc.org)
- selection was based on blood pressure and reported sodium intake levels as described below to ensure a wide range of values for these two related measures. (cdc.gov)
- Olkem Beta 50 Tablet 10's is a combination of two high blood pressure-lowering medicines: Telmisartan and Metoprolol. (apollopharmacy.in)
- It works by blocking the angiotensin II receptor, thereby relaxing the blood vessels and lowering the blood pressure. (apollopharmacy.in)
- 2015. NMDA Receptor Plasticity in the Hypothalamic Paraventricular Nucleus Contributes to the Elevated Blood Pressure Produced by Angiotensin II. . (cornell.edu)
- supplements to take for high blood pressure taurine to reduce blood pressure, including various foods, vitamins, potassium, which can lead to angiotensin II. (gordanaj.com)
Cardiovascular1
- Angiotensin II also increased cardiac infiltration of F4/80+ macrophages and CD3+ T lymphocytes cardiovascular oxidative stress expression of endoplasmic reticulum stress markers p58and CHOP in cPLA2? (immune-source.com)
Physiological2
- The effect of comparable levels of hypoxemia on the conversion of continuous intravenous infusions of pharmacological doses (1000 times physiological) of angiotensin I was greater: from 55 ± 14 to 33 ± 13% (P (uab.edu)
- This study provides evidence that a physiological dose of angiotensin II can synergistically augment the stroke volume effect of beta-agonism in man. (dundee.ac.uk)
Vascular1
- Normal pregnancy is associated with decreased uterine vascular contraction and increased blood flow even though angiotensin II (AngII) levels are increased. (bioone.org)
Infusion4
- This conclusion is based on our finding that infusion of Ang II increased SBP measured by tail cuff as well as radio telemetry in cPLA2? (immune-source.com)
- mice.16 31 32 In the present study Ang II infusion increased the urinary output of PGEM TXB2 20 in cPLA2? (immune-source.com)
- Isoprenaline significantly reduced total peripheral resistance and this reduction was not affected by concomitant infusion of angiotensin II. (dundee.ac.uk)
- Two techniques that are currently being investigated are neurostimulation and the spinal infusion pump. (moreliaclinic.com)
Activates2
- Angiotensin II activates cPLA2? (immune-source.com)
- After the S1 subunit of the spike binds to the ACE-2 enzyme on the cell membrane surface, TMPRSS2 activates the spike and cleaves ACE-2. (cebm.net)
Myocardial1
- The issue of whether angiotensin II receptor antagonists slightly increase the risk of myocardial infarction (MI or heart attack) is currently being investigated. (mdwiki.org)
Infection9
- Kim D , Quinn J , Pinsky B , Shah NH , Brown I . Rates of co-infection between SARS-CoV-2 and other respiratory pathogens. (cdc.gov)
- Host and viral determinants for efficient SARS-CoV-2 infection of the human lung. (cdc.gov)
- Here, we describe clinical features, virology, longitudinal cellular, and cytokine immune profile, SARS-CoV-2-specific serology and salivary antibody responses in a family of two parents with PCR-confirmed symptomatic SARS-CoV-2 infection and their three children, who tested repeatedly SARS-CoV-2 PCR negative. (nature.com)
- These data indicate that children can mount an immune response to SARS-CoV-2 without virological confirmation of infection, raising the possibility that immunity in children can prevent the establishment of SARS-CoV-2 infection. (nature.com)
- This finding pointed to the importance of interferons (IFNs), during the initial infection, for clearing SARS-CoV-2 and concerns about using glucocorticoids, which could inhibit IFN signaling in COVID-19 treatment. (cdc.gov)
- The proactive approach to international collaboration and sharing of resources have enabled the discovery of previously unknown pathophysiological mechanisms of SARS-CoV-2 infection and revealed the complex genetic architecture of COVID-19. (cdc.gov)
- While we have made an impressive sprint to uncover the genetic anchors for response to COVID-19 infection just two years into the pandemic, the next major challenge is to use these biologic findings to inform treatment and prevention. (cdc.gov)
- Most important of these in terms of SARS-2 is the lungs, as they are the primary site of infection, and along with the oral cavity, that is where infection will begin. (theamericansun.com)
- Our results suggest new therapeutic strategies for preventing and slowing SARS-CoV-2 infection, focusing on targeting cell host surface vimentin. (mit.edu)