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.Receptors, Angiotensin: Cell surface proteins that bind ANGIOTENSINS and trigger intracellular changes influencing the behavior of cells.Receptor, Angiotensin, Type 1: An angiotensin receptor subtype that is expressed at high levels in a variety of adult tissues including the CARDIOVASCULAR SYSTEM, the KIDNEY, the ENDOCRINE SYSTEM and the NERVOUS SYSTEM. Activation of the type 1 angiotensin receptor causes VASOCONSTRICTION and sodium retention.Encyclopedias as Topic: Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)Angiotensin II Type 1 Receptor Blockers: Agents that antagonize ANGIOTENSIN II TYPE 1 RECEPTOR. Included are ANGIOTENSIN II analogs such as SARALASIN and biphenylimidazoles such as LOSARTAN. Some are used as ANTIHYPERTENSIVE AGENTS.Angiotensin Receptor Antagonists: Agents that antagonize ANGIOTENSIN RECEPTORS. Many drugs in this class specifically target the ANGIOTENSIN TYPE 1 RECEPTOR.Receptor, Angiotensin, Type 2: An angiotensin receptor subtype that is expressed at high levels in fetal tissues. Many effects of the angiotensin type 2 receptor such as VASODILATION and sodium loss are the opposite of that of the ANGIOTENSIN TYPE 1 RECEPTOR.TetrazolesAngiotensin I: A decapeptide that is cleaved from precursor angiotensinogen by RENIN. Angiotensin I has limited biological activity. It is converted to angiotensin II, a potent vasoconstrictor, after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME.Losartan: An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.Chymases: A family of neutral serine proteases with CHYMOTRYPSIN-like activity. Chymases are primarily found in the SECRETORY GRANULES of MAST CELLS and are released during mast cell degranulation.Angiotensins: Oligopeptides which are important in the regulation of blood pressure (VASOCONSTRICTION) and fluid homeostasis via the RENIN-ANGIOTENSIN SYSTEM. These include angiotensins derived naturally from precursor ANGIOTENSINOGEN, and those synthesized.Serine Endopeptidases: Any member of the group of ENDOPEPTIDASES containing at the active site a serine residue involved in catalysis.Angiotensin-Converting Enzyme Inhibitors: A class of drugs whose main indications are the treatment of hypertension and heart failure. They exert their hemodynamic effect mainly by inhibiting the renin-angiotensin system. They also modulate sympathetic nervous system activity and increase prostaglandin synthesis. They cause mainly vasodilation and mild natriuresis without affecting heart rate and contractility.Angiotensin III: A heptapeptide formed from ANGIOTENSIN II after the removal of an amino acid at the N-terminal by AMINOPEPTIDASE A. Angiotensin III has the same efficacy as ANGIOTENSIN II in promoting ALDOSTERONE secretion and modifying renal blood flow, but less vasopressor activity (about 40%).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.Aldosterone: A hormone secreted by the ADRENAL CORTEX that regulates electrolyte and water balance by increasing the renal retention of sodium and the excretion of potassium.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.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.Reflex: An involuntary movement or exercise of function in a part, excited in response to a stimulus applied to the periphery and transmitted to the brain or spinal cord.Blood Pressure: PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.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.Exons: The parts of a transcript of a split GENE remaining after the INTRONS are removed. They are spliced together to become a MESSENGER RNA or other functional RNA.Alternative Splicing: A process whereby multiple RNA transcripts are generated from a single gene. Alternative splicing involves the splicing together of other possible sets of EXONS during the processing of some, but not all, transcripts of the gene. Thus a particular exon may be connected to any one of several alternative exons to form a mature RNA. The alternative forms of mature MESSENGER RNA produce PROTEIN ISOFORMS in which one part of the isoforms is common while the other parts are different.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.Molecular Sequence Data: Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.Base Sequence: The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.RNA Splicing: The ultimate exclusion of nonsense sequences or intervening sequences (introns) before the final RNA transcript is sent to the cytoplasm.Protein Isoforms: Different forms of a protein that may be produced from different GENES, or from the same gene by ALTERNATIVE SPLICING.Peptides: Members of the class of compounds composed of AMINO ACIDS joined together by peptide bonds between adjacent amino acids into linear, branched or cyclical structures. OLIGOPEPTIDES are composed of approximately 2-12 amino acids. Polypeptides are composed of approximately 13 or more amino acids. PROTEINS are linear polypeptides that are normally synthesized on RIBOSOMES.Angiotensin II Type 2 Receptor Blockers: Agents that antagonize the ANGIOTENSIN II TYPE 2 RECEPTOR.Peptide Fragments: Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.Biphenyl CompoundsBenzimidazoles: Compounds with a BENZENE fused to IMIDAZOLES.Imidazoles: Compounds containing 1,3-diazole, a five membered aromatic ring containing two nitrogen atoms separated by one of the carbons. Chemically reduced ones include IMIDAZOLINES and IMIDAZOLIDINES. Distinguish from 1,2-diazole (PYRAZOLES).Podocytes: Highly differentiated epithelial cells of the visceral layer of BOWMAN CAPSULE of the KIDNEY. They are composed of a cell body with major CELL SURFACE EXTENSIONS and secondary fingerlike extensions called pedicels. They enwrap the KIDNEY GLOMERULUS capillaries with their cell surface extensions forming a filtration structure. The pedicels of neighboring podocytes interdigitate with each other leaving between them filtration slits that are bridged by an extracellular structure impermeable to large macromolecules called the slit diaphragm, and provide the last barrier to protein loss in the KIDNEY.Access to Information: Individual's rights to obtain and use information collected or generated by others.Periodicals as Topic: A publication issued at stated, more or less regular, intervals.Journal Impact Factor: A quantitative measure of the frequency on average with which articles in a journal have been cited in a given period of time.Cell Adhesion: Adherence of cells to surfaces or to other cells.Peer Review, Research: The evaluation by experts of the quality and pertinence of research or research proposals of other experts in the same field. Peer review is used by editors in deciding which submissions warrant publication, by granting agencies to determine which proposals should be funded, and by academic institutions in tenure decisions.Publishing: "The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing.Immunologic Factors: Biologically active substances whose activities affect or play a role in the functioning of the immune system.Cytokines: Non-antibody proteins secreted by inflammatory leukocytes and some non-leukocytic cells, that act as intercellular mediators. They differ from classical hormones in that they are produced by a number of tissue or cell types rather than by specialized glands. They generally act locally in a paracrine or autocrine rather than endocrine manner.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.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)Mineralocorticoid Receptor Antagonists: Drugs that bind to and block the activation of MINERALOCORTICOID RECEPTORS by MINERALOCORTICOIDS such as ALDOSTERONE.Receptors, Mineralocorticoid: Cytoplasmic proteins that specifically bind MINERALOCORTICOIDS and mediate their cellular effects. The receptor with its bound ligand acts in the nucleus to induce transcription of specific segments of DNA.Fadrozole: A selective aromatase inhibitor effective in the treatment of estrogen-dependent disease including breast cancer.Steroid 11-beta-Hydroxylase: A mitochondrial cytochrome P450 enzyme that catalyzes the 11-beta-hydroxylation of steroids in the presence of molecular oxygen and NADPH-FERRIHEMOPROTEIN REDUCTASE. This enzyme, encoded by CYP11B1 gene, is important in the synthesis of CORTICOSTERONE and HYDROCORTISONE. Defects in CYP11B1 cause congenital adrenal hyperplasia (ADRENAL HYPERPLASIA, CONGENITAL).Adrenal Glands: A pair of glands located at the cranial pole of each of the two KIDNEYS. Each adrenal gland is composed of two distinct endocrine tissues with separate embryonic origins, the ADRENAL CORTEX producing STEROIDS and the ADRENAL MEDULLA producing NEUROTRANSMITTERS.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.Kidney Failure, Chronic: The end-stage of CHRONIC RENAL INSUFFICIENCY. It is characterized by the severe irreversible kidney damage (as measured by the level of PROTEINURIA) and the reduction in GLOMERULAR FILTRATION RATE to less than 15 ml per min (Kidney Foundation: Kidney Disease Outcome Quality Initiative, 2002). These patients generally require HEMODIALYSIS or KIDNEY TRANSPLANTATION.

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)

*Angiotensin II receptor type 1

... or AT1 receptor is the best characterized angiotensin receptor. It has vasopressor effects and ... The angiotensin receptor is activated by the vasoconstricting peptide angiotensin II. The activated receptor in turn couples to ... "Alternatively spliced human type 1 angiotensin II receptor mRNAs are translated at different efficiencies and encode two ... Angiotensin II receptor type 1 has been shown to interact with Zinc finger and BTB domain-containing protein 16. The protein's ...

*Angiotensin II receptor

The angiotensin II receptors, (AGTR1) and (AGTR2), are a class of G protein-coupled receptors with angiotensin II as their ... angiotensin II. The AT1 and AT2 receptors share a sequence identity of ~30%, but have a similar affinity for angiotensin II, ... The angiotensin receptor is activated by the vasoconstricting peptide angiotensin II. The activated receptor in turn couples to ... The AT4 receptor is activated by the angiotensin II metabolite angiotensin IV, and may play a role in regulation of the CNS ...

*Angiotensin II receptor blocker

... s (ARBs), also known as angiotensin II receptor antagonists , AT1 receptor antagonists or ... They block the activation of AT1 receptors, preventing the binding of angiotensin II. Angiotensin II receptor blockers are used ... Kassler-Taub K, Littlejohn T, Elliott W, Ruddy T, Adler E (1998). "Comparative efficacy of two angiotensin II receptor ... Angiotensin II Type 1 Receptor Blockers at the US National Library of Medicine Medical Subject Headings (MeSH). ...

*Angiotensin II receptor type 2

... , also known as the AT2 receptor is a protein that in humans is encoded by the AGTR2 gene. ... Angiotensin II is a potent pressor hormone and a primary regulator of aldosterone secretion. It is an important effector ... Angiotensin II receptor type 2 has been shown to interact with MTUS1. Angiotensin II receptor GRCh38: Ensembl release 89: ... The angiotensin II receptors". Pharmacological Reviews. 52 (3): 415-72. PMID 10977869. D'Amore A, Black MJ, Thomas WG (December ...

*Angiotensin-converting enzyme 2

... or the conversion of angiotensin II to angiotensin 1-7. ACE 2 has direct effects on cardiac functiona, and is expressed ... "A novel angiotensin-converting enzyme-related carboxypeptidase (ACE2) converts angiotensin I to angiotensin 1-9". Circulation ... "A novel angiotensin-converting enzyme-related carboxypeptidase (ACE2) converts angiotensin I to angiotensin 1-9". Circulation ... Lazartigues E, Feng Y, Lavoie JL (2007). "The two fACEs of the tissue renin-angiotensin systems: implication in cardiovascular ...

*PRKCE

Inagaki K, Iwanaga Y, Sarai N, Onozawa Y, Takenaka H, Mochly-Rosen D, Kihara Y (Oct 2002). "Tissue angiotensin II during ... Paul K, Ball NA, Dorn GW, Walsh RA (Nov 1997). "Left ventricular stretch stimulates angiotensin II--mediated ... angiotensin II and diastolic stretch; adenosine; hypoxia and Akt-induced stem cell factor; ROS generated via pharmacologic ... Initially, PKCε was thought to protect mitochondria from MPT through its association with VDAC1, ANT, and hexokinase II; ...

*Glucocorticoid remediable aldosteronism

Angiotensin is involved in regulating aldosterone and is the core regulator. Angiotensin II acts synergistically with potassium ... by increase in the plasma concentration of angiotensin III. by increased plasma angiotensin II, ACTH, or potassium levels. The ... Aldosterone synthase normally is not ACTH sensitive, and only activated by angiotensin II. Aldosterone causes the tubules of ... Control of aldosterone release from the adrenal cortex: The role of the renin-angiotensin system: ...

*Tasosartan

... is an angiotensin II receptor antagonist. It was withdrawn from FDA review by the manufacturer after phase III ... ISBN 0-12-369417-5. Dina R, Jafari M (July 2000). "Angiotensin II-receptor antagonists: an overview". Am J Health Syst Pharm. ...

*Endothelin 1

Cazaubon S, Deshayes F, Couraud PO, Nahmias C (2006). "[Endothelin-1, angiotensin II and cancer]". Med Sci (Paris). 22 (4): 416 ... Ariza AC, Bobadilla NA, Halhali A (2007). "[Endothelin 1 and angiotensin II in preeeclampsia]". Rev. Invest. Clin. 59 (1): 48- ... 45 (2): 151-4. PMID 12855940. Doggrell SA (2006). "The endothelin system and its role in acute myocardial infarction". Expert ... 68 (2): 357-418. doi:10.1124/pr.115.011833. PMC 4815360 . PMID 26956245. This article incorporates text from the United States ...

*Angiotensinamide

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

*Salvia elegans

... attributed to its action as an angiotensin II receptor antagonist and inhibitor of the angiotensin converting enzyme. ... Lamiaceae): ACE inhibition and angiotensin II antagonism". Journal of Ethnopharmacology. 130 (2): 340-346. doi:10.1016/j.jep. ... doi:10.2980/1195-6860(2006)13[23:TDOFUB]2.0.CO;2. Hanson, Beth (2001). Gourmet Herbs. Broolyn Botanic Garden. p. 90. ISBN 978-1 ...

*Bradykinin receptor B2

Ariza AC, Bobadilla NA, Halhali A (2007). "[Endothelin 1 and angiotensin II in preeeclampsia]". Rev. Invest. Clin. 59 (1): 48- ... The B2 receptor forms a complex with angiotensin converting enzyme (ACE), and this is thought to play a role in cross-talk ... Cassano G, Susca F, Lippe C, Guanti G (1999). "Two B1 and B2 bradykinin receptor antagonists fail to inhibit the Ca2+ response ... Alternate start codons result in two isoforms of the protein. Bradykinin receptor GRCh38: Ensembl release 89: ENSG00000168398 ...

*Arnold Martin Katz

Katz AM (1990). "Angiotensin II: Hemodynamic regulator or growth factor?". J Mol Cell Cardiol. 22: 739-747. Katz AM, Katz PB ( ... Peptide separation by two-dimensional chromatography and electrophoresis. Katz AM, Chernoff AI (1959). "Structural similarities ... KATZ, AM; DREYER, WJ; ANFINSEN, CB (Nov 1959). "Peptide separation by two-dimensional chromatography and electrophoresis". The ... 180 (2): 392-402. PMID 14361747. KATZ, A. M.; KATZ, L. N.; WILLIAMS, F. L. (1 November 1955). "Registration of Left Ventricular ...

*AGTRAP

The gene product interacts with the angiotensin II type I receptor and negatively regulates angiotensin II signaling. ... "The angiotensin II type I receptor-associated protein, ATRAP, is a transmembrane protein and a modulator of angiotensin II ... Type-1 angiotensin II receptor-associated protein is a protein that in humans is encoded by the AGTRAP gene. This gene encodes ... "Entrez Gene: AGTRAP angiotensin II receptor-associated protein". Human AGTRAP genome location and AGTRAP gene details page in ...

*CMA1

... is largely responsible for converting angiotensin I to the vasoactive peptide angiotensin II. Angiotensin II has been ... Jenne DE, Tschopp J (1991). "Angiotensin II-forming heart chymase is a mast-cell-specific enzyme". Biochem. J. 276 (2): 567-8. ... Urata H, Nishimura H, Ganten D (1996). "Chymase-dependent angiotensin II forming systems in humans". Am. J. Hypertens. 9 (3): ... Caughey GH, Raymond WW, Wolters PJ (2000). "Angiotensin II generation by mast cell alpha- and beta-chymases". Biochim. Biophys ...

*Olmesartan

In studies of angiotensin II receptor antagonists such as olmesartan, patients with unilateral or bilateral renal artery ... Olmesartan medoxomil is an angiotensin II receptor antagonist which is used for the treatment of high blood pressure. It was ... "Angiotensin II receptor blocker induced fetopathy: 7 cases". Klin Padiatr. 223 (1): 10-4. doi:10.1055/s-0030-1269895. "BENICAR ... part II of II)". Int. J. Surg. Pathol. 22 (3): 202-11. doi:10.1177/1066896913502230. PMID 24021900. Rubio-Tapia, Alberto; ...

*Complications of hypertension

Tanahashi N (April 2009). "[Roles of angiotensin II receptor blockers in stroke prevention]". Nippon Rinsho (in Japanese). 67 ( ... Once blood pressure is found to be high in diabetics, there are ways to treat it: Medications like the Angiotensin-converting ... Wachtell K, Devereux RB, Lyle AP (August 2007). "The effect of angiotensin receptor blockers for preventing atrial fibrillation ... 23 (2): 86-96. doi:10.1038/jhh.2008.80. PMID 18650838. Moretti R, Torre P, Antonello RM, Manganaro D, Vilotti C, Pizzolato G ( ...

*Antagonism (chemistry)

Kalaitzidis, R; Bakris, G. L. (2009). "Effects of angiotensin II receptor blockers on diabetic nephropathy". Journal of ... For example, not only do angiotensin receptor blockers, and angiotensin-converting enzyme (ACE) inhibitors work to lower blood ... In chemistry, antagonism is a phenomenon wherein two or more agents in combination have an overall effect that is less than the ... 2-amidinopropane) dihydrochloride (AAPH)-induced oxidation: Synergistic and antagonistic effects". Journal of the American Oil ...

*Cytokine storm

... suggesting a potential benefit for angiotensin converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs), ... Marshall and co-workers also found that angiotensin II was associated with cytokine-mediated lung injury and suggested a role ... Das published a review of ACE inhibitor and angiotensin-II receptor blocker use in a number of cytokine-mediated inflammatory ... Marshall RP, Gohlke P, Chambers RC, Howell DC, Bottoms SE, Unger T, McAnulty RJ, Laurent GJ (January 2004). "Angiotensin II and ...

*Mikael Pittet

"Angiotensin II Drives the Production of Tumor-Promoting Macrophages". Immunity. 38 (2): 296-308. doi:10.1016/j.immuni.2012.10. ... "The healing myocardium sequentially mobilizes two monocyte subsets with divergent and complementary functions". J Exp Med. 204 ... 13 (2): 125-38. doi:10.1038/nmat3780. PMID 24452356. Pucci F, Rickelt S, Newton AP, Garris C, Nunes E, Evavold C, Pfirschke C, ...

*MYOZ2

Overexpression of calsarcin-1 in mice (CS1Tg) was protective against Angiotensin II-induced pathologic cardiac hypertrophy, ... by Angiotensin II, phenylephrine and endothelin-1 agonists in neonatal cardiomyocytes. ... "Calsarcin-1 protects against angiotensin-II induced cardiac hypertrophy". Circulation. 116 (22): 2587-96. doi:10.1161/ ... Two missense mutations in MYOZ2, Ser48Pro and Ile246Met, have been shown to be causal for rare forms of familial hypertrophic ...

*WASF1

Whitebread S, Mele M, Kamber B, de Gasparo M (1989). "Preliminary biochemical characterization of two angiotensin II receptor ... 1998). "In mouse brain profilin I and profilin II associate with regulators of the endocytic pathway and actin assembly". EMBO ... Suetsugu S, Miki H, Takenawa T (1999). "Identification of two human WAVE/SCAR homologues as general actin regulatory molecules ... 219 (2): 509-14. doi:10.1006/bbrc.1996.0264. PMID 8605018. Nagase T, Seki N, Ishikawa K, et al. (1997). "Prediction of the ...

*Sacubitril/valsartan

Valsartan blocks the angiotensin II receptor type 1 (AT1). This receptor is found on both vascular smooth muscle cells, and on ... Changing 100 people from an ACE inhibitor or angiotensin II receptor antagonist to sacubitril/valsartan for 2.3 years would ... Sacubitril/valsartan can be used instead of an ACE inhibitor or an angiotensin receptor blocker in people with heart failure ... August 30, 2014). "Angiotensin-Neprilysin Inhibition versus Enalapril in Heart Failure". N Engl J Med. 371: 140830040023009. ...

*LDL-receptor-related protein-associated protein

Brooke BS, Habashi JP, Judge DP, Patel N, Loeys B, Dietz HC (2008). "Angiotensin II blockade and aortic-root dilation in ... Kounnas MZ, Argraves WS, Strickland DK (Oct 1992). "The 39-kDa receptor-associated protein interacts with two members of the ... "Organ distribution in rats of two members of the low-density lipoprotein receptor gene family, gp330 and LRP/alpha 2MR, and the ... since it is able to bind calmodulin and be phosphorylated by calmodulin-dependent kinase II. LDL-receptor-related protein- ...

*Hemopexin

... , an acute phase protein, can downregulate the angiotensin (ang) II type 1 receptor (AT1-R) in vitro. Hx-dependent ... "Hemopexin activity is associated with angiotensin II responsiveness in humans". Journal of Hypertension. 31 (3): 537-41. doi: ... 3.0.CO;2-5. PMID 8647924. Miller YI, Smith A, Morgan WT, Shaklai N (October 1996). "Role of hemopexin in protection of low- ... 383 (1-2): 72-4. doi:10.1016/0014-5793(96)00225-6. PMID 8612795. Hunt RC, Hunt DM, Gaur N, Smith A (July 1996). "Hemopexin in ...

*List of DuPont Experimental Station inventions

... intensifier phosphors and screens Building 400 Hyzaar combination drug to treat hypertension Cozaar Losartan angiotensin II ... 4-d 2,4-Dichlorophenoxyacetic acid herbicides Sulfonylurea herbicides and preemergent herbicides Ludox colloidal silica Vazo ... world's first synthetic rubbers Dacron polyester Polyethylene terephthalate fibers Teflon Polytetrafluoroethylene dispersions 2 ...
All information about the latest scientific publications of the Clínica Universidad de Navarra. The inhibitory effect of leptin on angiotensin II-induced vasoconstriction is blunted in spontaneously hypertensive rats
Over the last 2 decades, it has become clear that angiotensin can be generated not only in the systemic circulation but also in multiple tissue sites, where its production can be regulated by local factors. Given the ability of angiotensin II to influence target cell proliferation, hypertrophy, and apoptosis, tissue angiotensin systems potentially play an important role in a wide variety of physiological processes. In this issue of Hypertension, De Mello and Danser1 review the evidence for the synthesis of angiotensin II in the heart and discuss its possible role in health and disease. Their review complements other recent reviews of this subject, such as that by Dostal and Baker.2 Uniquely, however, the present review discusses the potential role of intracellular angiotensin II, called intracrine angiotensin II, in intercellular signaling and calcium flux in the heart. These findings are based on De Mellos studies1 of renin, angiotensin I, and angiotensin II dialyzed into rat cardiac cells. ...
Angiotensin II receptor type 1 or AT1 receptor is the best characterized angiotensin receptor. It has vasopressor effects and regulates aldosterone secretion. It is an important effector controlling blood pressure and volume in the cardiovascular system. Angiotensin II receptor antagonists are drugs indicated for hypertension, diabetic nephropathy and congestive heart failure. The AT1 receptor mediates the major cardiovascular effects of angiotensin II. Effects include vasoconstriction, aldosterone synthesis and secretion, increased vasopressin secretion, cardiac hypertrophy, augmentation of peripheral noradrenergic activity, vascular smooth muscle cells proliferation, decreased renal blood flow, renal renin inhibition, renal tubular sodium reuptake, modulation of central sympathetic nervous system activity, cardiac contractility, central osmocontrol and extracellular matrix formation. The angiotensin receptor is activated by the vasoconstricting peptide angiotensin II. The activated receptor in ...
Nox2-containing NADPH oxidases are reported to be involved in the development of cardiac fibrosis in response to chronic angiotensin II infusion, but the cellular source(s) of Nox2 involved in fibrosis remains unclear. We investigated the role of endothelial Nox2 in angiotensin II-induced left ventricular hypertrophy (LVH). Male transgenic mice with endothelial-specific overexpression of Nox2 were compared with matched wild-type (wt) littermates after angiotensin II (1.1 mg/kg per day) or saline infusion for 14 days. Basal blood pressure and left ventricular NADPH oxidase activity were similar in wt and transgenic mice. After angiotensin II infusion, both wt and transgenic groups developed similar hypertension (170.2±11.6 vs 170.4±12.3 mm Hg; n=10) and hypertrophy (left ventricular/body weight ratio 4.8±0.2 vs 4.7±0.2 mg/g; and echocardiographic septal thickness increased by 34% wt and 37% transgenic mice; n,10). NADPH oxidase activity was higher in angiotensin II-infused transgenic compared ...
Angiotensin II exerts positive inotropic and chronotropic effects on the mammalian heart by binding to specific membrane receptors. Recently, two subtypes of angiotensin II receptors (AT1 and AT2) have been distinguished by using the nonpeptide antagonists losartan (previously known as DuP 753) and PD123177. To evaluate the tissue distribution and subtypes of angiotensin II receptors in rat heart, we performed a 125I-[Sar1,Ile8]angiotensin II in situ binding assay on tissue sections obtained from adult Sprague-Dawley rats (10 and 14 weeks old). Binding specificity was verified by competition with unlabeled [Sar1]angiotensin II. Distribution of AT1 and AT2 receptors was determined by competition with losartan and PD123177, respectively, and the density of the receptors was quantified by emulsion autoradiography. Angiotensin II receptors were widely distributed throughout the heart, with each receptor subtype accounting for approximately 50% of the specific binding. Binding density was comparable ...
The angiotensin II receptors, (AGTR1) and (AGTR2), are a class of G protein-coupled receptors with angiotensin II as their ligands. They are important in the renin-angiotensin system: they are responsible for the signal transduction of the vasoconstricting stimulus of the main effector hormone, angiotensin II. The AT1 and AT2 receptors share a sequence identity of ~30%, but have a similar affinity for angiotensin II, which is their main ligand. The AT1 receptor is the best elucidated angiotensin receptor. The AT1 subtype is found in the heart, blood vessels, kidney, adrenal cortex, lung and brain and mediates the vasoconstrictor effects. The angiotensin receptor is activated by the vasoconstricting peptide angiotensin II. The activated receptor in turn couples to Gq/11 and Gi/o and thus activates phospholipase C and increases the cytosolic Ca2+ concentrations, which in turn triggers cellular responses such as stimulation of protein kinase C. Activated receptor also inhibits adenylate cyclase and ...
Ang II infusion induces an immediate vasoconstrictive response that is typically followed by a gradual recovery despite continued infusion of the pressor agent. The buffering effect on Ang II-induced vasoconstriction is at least in part mediated by vasodilatory PGs, including PGE2.14,16-18 In a previous study, we discovered a novel role of mPGES-1-derived PGE2 in modulating Ang II-induced hypertensive response. In extension of this work, the present study demonstrated that the vasculoprotection of PGE2 is mediated by the suppression of oxidative stress.. Ang II-induced hypertension in mPGES-1−/− mice was completely prevented by Tempol treatment and was fully restored on termination of the antioxidant. Treatment with a second antioxidant, apocynin, produced a similar blood pressure-lowering effect. Apocynin is widely used as an inhibitor of NADPH oxidase19 but was recently found to inhibit vascular oxidative stress via an NADPH oxidase-independent mechanism.20 Together, the similar results ...
1. When the renin-angiotensin system of rats had been suppressed by a high salt diet or by bilateral nephrectomy, large doses of angiotensin II antiserum were required to block the pressor action of exogenous angiotensin II. Infusion of renin profoundly lowered the blocking requirement of such animals.. 2. It is postulated that renin bound to blood vessels generates angiotensin locally which is taken up by vascular receptors. Where such receptors are left unoccupied and free to bind exogenous angiotensin, high doses of blocking antisera are required.. 3. Animals with hypertension produced by renal artery constriction with contralateral nephrectomy were shown to be in positive sodium balance. Nevertheless their blocking requirement was low.. 4. It is suggested that the local generation of angiotensin may play a role in the production of renal hypertension and that this accounts for the development of hypertension even in animals immunized against angiotensin. ...
Angiotensin I is converted to angiotensin II (AII) through removal of two C-terminal residues by the enzyme angiotensin-converting enzyme (ACE), primarily through ACE within the lung (but also present in endothelial cells, kidney epithelial cells, and the brain). Angiotensin II acts on the CNS to increase ADH production, and also acts on venous and arterial vessels smooth muscle to cause vasoconstriction. Angiotensin II also increases Aldosterone secretion, therefore, it acts as an endocrine, autocrine/paracrine, and intracrine hormone.. ACE is a target of ACE inhibitor drugs, which decrease the rate of Angiotensin II production. Angiotensin II increases blood pressure by stimulating the Gq protein in vascular smooth muscle cells (which in turn activates an IP3-dependent mechanism leading to a rise in intracellular calcium levels and ultimately causing contraction). In addition, angiotensin II acts at the Na/H+ exchanger in the proximal tubules of the kidney to stimulate Na reabsorption and H+ ...
It is now firmly established that inhibition of ACE does have a markedly beneficial effect in the treatment of heart failure. ACE inhibitor therapy, however, does not completely block angiotensin II production, and in some patients, angiotensin II levels remain elevated, in part, because of the conversion of angiotensin I to angiotensin II by chymase activity.29 Thus, continued AT2 receptor stimulation could occur. This hypothesis is indirectly supported by the relative upregulation of the AT2 receptor in human heart failure,30 31 although this finding is controversial.32 33 Currently, no therapeutic agents that specifically act on the AT2 receptor are approved for clinical trials. However, numerous AT1 receptor blockers are available that could hypothetically shunt the activity of the cardiac RAS toward stimulation of the beneficial AT2 receptor.. Two separate clinical approaches evaluate this hypothesis. First, ACE inhibitor therapy was directly compared with AT1 receptor antagonist therapy in ...
In this study, we clarified for the first time the role of Nox1 in the pathogenesis of Ang II-mediated hypertension using Nox1-deficient mice. The principal findings obtained were that ROSs derived from Nox1/NADPH oxidase are crucial to the pressor response to Ang II by reducing the bioavailability of NO.. The present findings suggest that Nox1 is involved in the late phase but not in the early phase of the pressor response to Ang II. In both Nox1+/Y and Nox1−/Y, MBP was increased up to day 5 of Ang II infusion, whereas in Nox1−/Y, the pressor response was blunted after 7 days. Meanwhile, Nox1 mRNA expression was markedly upregulated from day 7 in Nox1+/Y. Vascular superoxide production is known to impair vascular relaxation through the inactivation of endothelial NO, which serves as an important component in the development and maintenance of increased blood pressure.23 It has been reported that administration of tempol, a superoxide dismutase mimetic, abolishes the pressor response to Ang ...
Ang II type 1 (AT1) receptors activate both conventional heterotrimeric G protein-dependent and unconventional G protein-independent mechanisms. We investigated how these different mechanisms activated by AT1 receptors affect growth and death of cardiac myocytes in vivo. Transgenic mice with cardiac-specific overexpression of WT AT1 receptor (AT1-WT; Tg-WT mice) or an AT1 receptor second intracellular loop mutant (AT1-i2m; Tg-i2m mice) selectively activating Gαq/Gαi-independent mechanisms were studied. Tg-i2m mice developed more severe cardiac hypertrophy and bradycardia coupled with lower cardiac function than Tg-WT mice. In contrast, Tg-WT mice exhibited more severe fibrosis and apoptosis than Tg-i2m mice. Chronic Ang II infusion induced greater cardiac hypertrophy in Tg-i2m compared with Tg-WT mice whereas acute Ang II administration caused an increase in heart rate in Tg-WT but not in Tg-i2m mice. Membrane translocation of PKCε, cytoplasmic translocation of Gαq, and nuclear localization ...
TY - JOUR. T1 - Vasopressor response to angiotensin II infusion in patients with chronic heart failure receiving β-blockers. AU - Vittorio, Timothy J.. AU - Lang, Chim C.. AU - Katz, Stuart D.. AU - Packer, Milton. AU - Mancini, Donna M.. AU - Jorde, Ulrich P.. PY - 2003/1/21. Y1 - 2003/1/21. N2 - Background - A synergistic interaction between the angiotensin II (Ang II) type 1 receptor and α1-adrenergic receptors has been described. We hypothesized that the nonselective β-antagonist carvedilol, through its α1-adrenergic blocking properties, may modulate vascular reactivity to Ang II in patients with chronic heart failure (CHF). Accordingly, we compared the vasopressor response to infused Ang II in patients treated with carvedilol and metoprolol, a selective β-antagonist. Methods and Results - All subjects were treated with carvedilol or metoprolol for at least 3 months. ACE inhibitor therapy was standardized to enalapril 40 mg/d or the maximally tolerated dose. Exogenous Ang II was ...
The rennin-angiotensin II system (RAS) and the insulin-PI3kinase signalling pathways cross-interact with important physiological and pathophysiological consequences for cells and the whole organism. Here, the effect of 24 h pre-incubation of EA.hy926 with two different concentrations of angiotensin II, on insulin-mediated activation of the PI3kinase-AKT-eNOS signalling was investigated. Quiescent EA.hy926 cells were treated with insulin (100 nM, 30 min) following 24 h pre-treatment with or without either 0.1 or 1 µM of angiotensin II. Cell lysates were immunoblotted for phospho AKT Ser-473, phospho eNOS Ser-1177 and normalized with β-actin. Homogenates of EA.hy926 treated with insulin in the presence or absence of 1 µM angiotensin II, were also subjected to nitric oxide synthase (NOS) activity assay using titrated arginine as substrate. To exclude cytotoxicity of the 1 µM angiotensin II concentration, Trypan blue cell viability assay as well as the microscopic examination of
The examination of synthetic valyl-5-angiotensin II-amide in the conscious dog revealed the following:. 1. Both the arterial and the central venous pressure responses exhibit tachyplylaxis when high doses of angiotensin II are administered, althoug not when medium or low doses are given. Cross-tachyphylaxis can be demonstrated between renin and angiotensin II but not between either of these and norepinephrine. These results suggest that tachyphylaxis to renin is due to tachyphylaxis to angiotensin.. 2. Angiotensin II and norepinephrine provoke a dose-dependent increase in central venous pressure. The threshold dose is about 10 times higher than that necessary for the effect on arterial pressure. In doses eliciting the same increase of arterial blood pressure, norepinephrine is about twice as active on the venous pressure as angiotensin II.. 3. Anesthesia and atropinization both reduce or abolish the effect of angiotensin II as well as that of norepinephrine on the venous pressure, indicating the ...
Methods and Results-Mice infused with angiotensin II showed a marked increase in interleukin-12p35 expression in cardiac macrophages. The degree of cardiac fibrosis was significantly enhanced in interleukin-12p35 knockout (p35-KO) mice compared with wild-type (WT) littermates in response to angiotensin II. Fibrotic hearts of p35-KO mice showed increased accumulation of alternatively activated (M2) macrophages and expression of M2 genes such as Arg-1 and Fizz1. Bone marrow-derived macrophages from WT or p35-KO mice did not differ in differentiation in response to angiotensin II treatment; however, in the presence of CD4+ T cells, macrophages from p35-KO mice differentiated into M2 macrophages and showed elevated expression of transforming growth factor-β. Moreover, CD4+ T-cell-treated p35-KO macrophages could stimulate cardiac fibroblasts to differentiate into α-smooth muscle actin-positive and collagen I-positive myofibroblasts in 3-dimensional nanofiber gels. Neutralizing antibodies against ...
1. This study was designed to quantify the role of angiotensin II in determining the chronic relationships between arterial pressure, renal haemodynamics and sodium excretion.. 2. In six control dogs sodium balance was achieved during chronic increases in sodium intake from 5 to 495 mmol/day with small increases in arterial pressure (7mmHg), moderate increases in glomerular filtration rate (19%) and decreases in filtration fraction. Similar increases in sodium intake in dogs whose circulating levels of angiotensin II were fixed, due to a constant intravenous infusion of 4.85 pmol of angiotensin II min−1 kg−1, caused large increases in arterial pressure (42%), glomerular filtration rate (31%), filtration fraction and calculated renal sodium reabsorption above control. In six dogs whose angiotensin II formation was blocked by SQ 14 225, sodium balance at intakes of 5-80 mmol/day occurred at reduced arterial pressure, glomerular filtration rate, filtration fraction and sodium reabsorption ...
1. Competitive or non-competitive inhibition of the myotropic and pressor response of angiotensin II is dependent on the nature of the substituent in position 8 of the antagonist peptide analogue. Substituents in other positions of the molecule, particularly position 1, contribute greatly to the potency of these antagonists.. 2. As is evidenced after adrenalectomy or after blockade with phentolamine and phenoxybenzamine, the initial pressor activity observed with all the antagonistic peptides is partially due to the release of catecholamines and partially to a direct myotropic effect.. 3. [Sar1, Thr8]angiotensin II has been found to possess the lowest agonist to antagonist ratio of all antagonists tested.. 4. [Des-Asp1, Ile8]angiotensin II selectively and specifically inhibits the release of aldosterone from adrenal cortex. Thus, unlike angiotensin II, this heptapeptide has pronounced organ specificity, suggesting that the heptapeptide (angiotensin III) is the aldosterone-releasing ...
Peptides , Angiotensins and Related Peptides , Angiotensin II, human; The octapeptide angiotensin II (Ang II) exerts a wide range of effects on the cardiovascular system. It is also implicated in the regulation of cell proliferation, fibrosis and apoptosis. Ang II is formed by cleavage of Ang I by the angiotensin-converting enzyme (ACE) or chymases. Human heart chymase, a chymotrypsin-like serine proteinase, hydrolyzes the Phe8-His9 bond to yield the octapeptide hormone angiotensin II and His-Leu.; DRVYIHPF; H-Asp-Arg-Val-Tyr-Ile-His-Pro-Phe-OH
TY - JOUR. T1 - Downregulation of vascular angiotensin II type 1 receptor by thyroid hormone. AU - Fukuyama, Kae. AU - Ichiki, Toshihiro. AU - Takeda, Kotaro. AU - Tokunou, Tomotake. AU - Iino, Naoko. AU - Masuda, Satoko. AU - Ishibashi, Minako. AU - Egashira, Kensuke. AU - Shimokawa, Hiroaki. AU - Hirano, Katsuya. AU - Kanaide, Hideo. AU - Takeshita, Akira. PY - 2003/3/1. Y1 - 2003/3/1. N2 - Thyroid hormone has a broad effect on cardiovascular system. 3,3′,5-triiodo-L-thyronine (T3), a biologically active form of thyroid hormone, increases cardiac contractility. T3 causes arterial relaxation and reduction of systemic vascular resistance, resulting in an increase in cardiac output. However, the molecular mechanisms of vascular relaxation by T3 are incompletely characterized. We studied the effect of T3 on the angiotensin (Ang) II type 1 receptor (AT1R) expression in vascular smooth muscle cells. T3 dose-dependently decreased expression levels of AT1R mRNA, with a peak at 6 hours of ...
Abstract PURPOSE OF REVIEW: The renin-angiotensin system (RAS) has undergone continuous advancement since the initial identification of renin as a pressor agent. Traditionally cons..
ABSTRACT. Angiotensin II (Ang II) is a critical component of the renin-angiotensin system that contributes to hypertension. Although platelets in blood from hypertensive subjects have an abnormal biological profile, it is unclear if circulating Ang II influences platelet aggregation or thrombus formation. One of the abnormalities presented to the platelets during hypertension is an elevated plasma concentration of serotonin (5-HT) caused by reduced 5-HT uptake secondary to loss of the 5-HT transporter (SERT) on the platelet plasma membrane. In the current study, we evaluated in vivo platelet function after 7 days of subcutaneous Ang II infusion to establish hypertension in mice and additionally assessed the biology of isolated platelets exposed to Ang II in vitro. The administration of Ang II elevated systolic blood pressure, but markers of platelet activation including P-selectin and PEJon/A staining were not changed. However, the aggregation response to collagen was reduced in isolated ...
Angiotensin II (Ang II) is a critical component of the reninangiotensin system that contributes to hypertension. Although platelets in blood from hypertensive subjects have an abnormal biological profile, it is unclear if circulating Ang II influences platelet aggregation or thrombus formation. One of the abnormalities presented to the platelets during hypertension is an elevated plasma concentration of serotonin (5-HT) caused by reduced 5-HT uptake secondary to loss of the 5-HT transporter (SERT) on the platelet plasma membrane. In the current study, we evaluated in vivo platelet function after 7 days of subcutaneous Ang II infusion to establish hypertension in mice and additionally assessed the biology of isolated platelets exposed to Ang II in vitro. The administration of Ang II elevated systolic blood pressure, but markers of platelet activation including P-selectin and PEJon/A staining were _disibledevent=font-size:10pt;line-height:1.5;font-family:Verdana;>5-HT in platelets, an event
TY - JOUR. T1 - Angiotensin II relaxes microvessels via the AT 2 receptor and Ca 2+ -activated K + (BK Ca ) channels AU - Dimitropoulou, Christiana. AU - White, Richard E.. AU - Fuchs, Leslie. AU - Zhang, Hanfang. AU - Catravas, John D.. AU - Carrier, Gerald O.. PY - 2001/1/1. Y1 - 2001/1/1. N2 - Angiotensin II (Ang II) is one of the most potent vasoconstrictor substances, yet paradoxically. Ang II may dilate certain vascular beds via an undefined mechanism. Ang II-induced vasoconstriction is mediated by the AT 1 receptor, whereas the relative expression and functional importance of the AT 2 receptor in regulating vascular resistance and blood pressure are unknown. We now report that Ang II induces relaxation of mesenteric microvessels and that this vasodilatory response was unaffected by losartan, an AT 1 receptor antagonist, but was inhibited by PD123.319. a selective antagonist of AT 2 receptors. In addition, reverse transcriptase-polymerase chain reaction studies revealed high amounts of AT ...
TY - JOUR. T1 - Impaired pulmonary conversion of angiotensin I to angiotensin II in rats exposed to chronic hypoxia. AU - Jackson, Robert. AU - Narkates, A. J.. AU - Oparil, S.. PY - 1986/1/1. Y1 - 1986/1/1. N2 - The effects of exposing rats to hypoxia at normal atmospheric pressure for periods of 21-24 days on intrapulmonary conversion of angiotensin I (ANG I) to angiotensin II (ANG II) were examined using an isolated rat lung preparation perfused at constant flow. 125I-ANG I (160 fmol) was injected alone and with graded doses (0.1, 1.0, and 100 nmol) of unlabeled ANG I into the pulmonary artery, and the effluent was collected for measurement of ANG I, ANG II, and metabolites. At low doses of injected ANG I (125I-ANG I alone or with 0.1 to 1.0 nmol unlabeled ANG I), the percent conversion of ANG I to ANG II was 67.5 ± 2.1 (SE), 65.1 ± 2.0, and 62.5 ± 1.6 in 21-day hypoxia-exposed animals and 83.8 ± 2.7, 81.4 ± 3.9, and 79.6 ± 2.3 (P , 0.01) in control rats maintained under normoxic ...
levels by elevated angiotensin II (or other mechanisms) is a major molecular mechanism in these vessels. It is important to consider that the absence of evidence for upregulation of ROS-linked tone in the arcades may be due to a more complex interaction between tolerance and the flow conditions, as discussed above.. In the arcades, angiotensin II- and PDE-mediated tone are altered, suggesting a different underlying mechanism. On the basis of our prior study (20), it is clear that nitrate therapy upregulates the calcium/calmodulin-dependent cGMP-hydrolyzing PDE 1A1. We propose the following scenario. Elevated NO increases cGMP levels. Elevated cGMP then provides a stimulus for upregulation of the PDE 1A1 as a means to hydrolyze the excess cGMP. Simultaneously, elevated NO provides a stimulus for elevated renin-angiotensin system (and other vasoconstrictor pathways). Angiotensin II activates PDE 1A1, which then hydrolyzes cGMP, decreases dilator capability, and directly constricts the vessels. ...
It has previously been demonstrated that the ability of Ang II to upregulate IGF-1R is a critical determinant of its mitogenic effects on VSMCs. Thus, IGF-1R gene-specific antisense oligonucleotides block Ang II-induced DNA synthesis.37 Furthermore, in VSMCs overexpressing IGF-1R, Ang II loses its ability to stimulate DNA synthesis, and this is related to the inability of Ang II in these conditions to further upregulate IGF-1R.37 The stimulatory effect of Ang II on IGF-1R transcription is independent of activation of the serine/threonine kinase, PKC, unlike that induced by basic fibroblastic growth factor.38 Identification of the signaling pathway involved in the Ang II activation of IGF-1R transcription is thus of major importance to understand the biological effects of Ang II. To define potential mechanisms involved in Ang II regulation of IGF-1R, we studied the effects of oxidant stress, of tyrosine kinase inhibitors, and of calcium chelators on Ang II regulation of IGF-1R expression.. Our ...
Szekeres, Mária and Nádasy, György László and Turu, Gábor and Soltész-Katona, Eszter and Benyó, Zoltán and Ruisanchez, Éva and Szabó, Eszter and Takáts, Zoltán and Bátkai, Sándor and Tóth, Zsuzsanna E. and Hunyady, László (2015) Endocannabinoid-mediated modulation of G protein-coupled receptor signaling-induced vasoconstriction and hypertension. MOLECULAR AND CELLULAR ENDOCRINOLOGY, 403C. pp. 46-56. ISSN 0303-7207 Gyires, Klára and Rónai, András Z and Zádori, Zoltán S and Tóth, Viktória E and Németh, József and Szekeres, Mária and Hunyady, László (2014) Angiotensin II-induced activation of central AT1 receptors exerts endocannabinoid-mediated gastroprotective effect in rats. Molecular and cellular endocrinology, 382 (2). pp. 971-8. ISSN 1872-8057 Gyires, Klára and Rónai, Z. András and Zádori, Zoltán Sándor and Tóth, Viktória E. and Németh, József and Szekeres, Mária and Hunyady, László (2014) Angiotensin II-induced activation of central AT1 receptors ...
Preeclamptic women produce agonistic autoantibodies to the angiotensin II type 1 receptor (AT1-AA) and exhibit increased blood pressure (mean arterial pressure), vascular sensitivity to angiotensin II (ANG II), and display a decrease in renal function. The objective of this study was to examine the renal hemodynamic changes during pregnancy in the presence of AT1-AAs with or without a slow pressor dose of ANG II. In this study, mean arterial pressure was elevated in all pregnant rats treated with ANG II with or without AT1-AA. Glomerular filtration rate was reduced from 1.90±0.16 mL/min in normal pregnant (NP) to 1.20±0.08 in ANG II+AT1-AA rats. Renal blood flow was decreased in ANG II+AT1-AA versus NP rats to 7.4±1.09 versus 15.4±1.75 mL/min. Renal vascular resistance was drastically increased between ANG II+AT1-AA versus NP rats (18.4±2.91 versus 6.4±0.77 mm Hg/mL per minute). Isoprostane excretion was increased by 3.5-fold in ANG II+AT1-AA versus NP (1160±321 versus 323±52 pg/mL). In ...
Infusion of angiotensin II continuously into the renal artery of conscious dogs led to a modest increase in arterial pressure that was associated in the steady state with increased total peripheral resistance. The dose of angiotensin II used (0.5 ng ⋅ kg−1 ⋅ min−1) was subpressor acutely (both over the 1st h and at 24 h) and reduced renal blood flow by about 15% during the 1st h of infusion. Onday 7 of the angiotensin II infusion, mean arterial pressure was still close to preinfusion values, and an increase in resting arterial pressure was observed only fromday 14 onward, with the elevation in arterial pressure being well maintained for the rest of the infusion period.. Evidence that the hypertension was due to the intrarenal actions of angiotensin II is provided by comparison with the effects of intravenous angiotensin II infusion at the same dose in the same dogs. Intravenous infusion of angiotensin II did not alter arterial pressure, and there were no significant changes in total ...
We identified an angiotensin-generating system in pancreatic islets and found that exogenously administered angiotensin II, after binding to its receptors (angiotensin II type 1 receptor [AT1R]), inhibits insulin release in a manner associated with decreased islet blood flow and (pro)insulin biosynthesis. The present study tested the hypothesis that there is a change in AT1R expression in the pancreatic islets of the obesity-induced type 2 diabetes model, the db/db mouse, which enables endogenous levels of angiotensin II to impair islet function. Islets from 10-week-old db/db and control mice were isolated and investigated. In addition, the AT1R antagonist losartan was administered orally to 4-week-old db/db mice for an 8-week period. We found that AT1R mRNA was upregulated markedly in db/db islets and double immunolabeling confirmed that the AT1R was localized to beta-cells. Losartan selectively improved glucose-induced insulin release and (pro)insulin biosynthesis in db/db islets. Oral ...
Peptides , Bradykinins , [Des-Pro2]-Bradykinin; Angiotensin I Converting Enzyme (ACE I) Inhibitor; This peptide is an inhibitor for Angiotensin I Converting Enzyme (ACE I), derived from Bradykinin. ACE I partially suppresses the renin-angiotensin-aldosterone system (RAAS), which regulates blood pressure and may mediate hypertension. ACE I converts angiotensin I to the biologically active peptide angiotensin II using a zinc- and chloride- dependent mechanism.; RPPGFSPFR; H-Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg-OH
Angiotensin II (Ang II) is one of the most potent vasoconstrictor substances, yet paradoxically. Ang II may dilate certain vascular beds via an undefined mechanism. Ang II-induced vasoconstriction is mediated by the AT1 receptor, whereas the relative expression and functional importance of the AT2 receptor in regulating vascular resistance and blood pressure are unknown. We now report that Ang II induces relaxation of mesenteric microvessels and that this vasodilatory response was unaffected by losartan, an AT1 receptor antagonist, but was inhibited by PD123.319. a selective antagonist of AT2 receptors. In addition, reverse transcriptase-polymerase chain reaction studies revealed high amounts of AT2 receptor mRNA in smooth muscle from these same microvessels. Ang II-induced relaxation was inhibited by either tetraethylammonium or iberiotoxin, suggesting involvement of the large-conductance, calcium- and voltage-activated potassium (BKCa) channel. Subsequent whole-cell and single-channel patch-clamp
UNLABELLED Angiotensin II has articularly shown to play a key role in the regulation of inflammatory processes in hypertension. AIM The present study aims to correlate the angiotensin II-induced hypertension 4th systemic inflammation. MATERIAL AND METHODS We conducted an experimental study on Wistar male rats who received Ang II via subcutaneous miniosmotic pumps for 2 weeks. Rats were exposed to a 12h light /12h dark cycle. Sham rats were used as control. Systolic load pressure measurements and a flow cytometric analysis of lymphocyte surface markers were performed. After 14 days, the animals were euthanized under anesthesia with ylazine/ketaniine. RESULTS Systolic BP progressively and significantly increased in rats 4th Ang II chronic infusion. We observed a statistical significant difference (p = 0.00001), in terms of T lymphocytes percentage between control rats plasma and Ang H treated rats lasma, in 14 days. CONCLUSIONS Angiotensin II is an important mediator of hypertension and directly
In the present study, we found that angiotensin II increases blood pressure and O2·− production in mesenteric arteries of C57Blk/6 mice and that these effects were augmented in mice lacking ecSOD. Also, endothelium-dependent relaxation was altered in the mesenteric arteries of ecSOD−/− mice when treated with angiotensin II. In contrast to the effects on resistance vessels in ecSOD−/− mice, angiotensin II paradoxically improved endothelium-dependent vasodilatation in aortic segments. This was associated with an increase in NO as detected by ESR and with a reduction in aortic O2·− production. NADPH oxidase activity was increased by angiotensin II in C57Blk/6 and ecSOD−/− mice but to a lesser extent in the latter group. Our data also show that the CCS plays a potentially important role in modulation of O2·− production in large vessels during angiotensin II-induced hypertension.. The exaggerated hypertensive response to angiotensin II in ecSOD−/− mice is in keeping with the ...
BACKGROUND AND PURPOSE Toll-like receptor 4 (TLR4) signalling contributes to inflammatory cardiovascular diseases, but its role in hypertension and the associated vascular damage is not known. We investigated whether TLR4 activation contributed to angiotensin II (AngII)-induced hypertension and the associated vascular structural, mechanical and functional alterations. EXPERIMENTAL APPROACH AngII was infused (1.44 mg · kg(-1) · day(-1), s.c.) for 2 weeks in C57BL6 mice, treated with a neutralizing anti-TLR4 antibody or IgG (1 μg · day(-1); systolic BP (SBP) and aortic cytokine levels were measured. Structural, mechanical and contractile properties of aortic and mesenteric arterial segments were measured with myography and histology. RT-PCR and Western blotting were used to analyse these tissues and cultured vascular smooth muscle cells (VSMC) from hypertensive rats (SHR). KEY RESULTS Aortic TLR4 mRNA levels were raised by AngII infusion. Anti-TLR4 antibody treatment of AngII-treated mice
... definition, any of three oligopeptides occurring in plasma, an inactive form (angiotensin I) and two varieties (angiotensin II and angiotensin III) that elevate blood pressure and stimulate the adrenal cortex to secrete aldosterone. See more.
INTRODUCTION: Recently, we could show that angiotensin II, the reactive peptide of the blood pressure-regulating renin-angiotensin-aldosterone-system, causes the formation of reactive oxygen species and DNA damage in kidneys and hearts of hypertensive mice. To further investigate on the one hand the mechanism of DNA damage caused by angiotensin II, and on the other hand possible intervention strategies against end-organ damage, the effects of substances interfering with the renin-angiotensin-aldosterone-system on angiotensin II-induced genomic damage were studied. METHODS: In C57BL/6-mice, hypertension was induced by infusion of 600 ng/kg • min angiotensin II. The animals were additionally treated with the angiotensin II type 1 receptor blocker candesartan, the mineralocorticoid receptor blocker eplerenone and the antioxidant tempol. DNA damage and the activation of transcription factors were studied by immunohistochemistry and protein expression analysis. RESULTS: Administration of ...
TY - JOUR. T1 - Increased Vascular Sensitivity to Angiotensin II in Psychosocial Hypertensive Mice. AU - Clinton Webb, R.. AU - Johnson, Joyce C.. AU - Vander, Arthur J.. AU - Henry, James P.. PY - 1983/1/1. Y1 - 1983/1/1. N2 - CBA mice develop hypertension when placed in complex population cages that facilitate social interactions and competition for territory. After 1 month, these mice have normal plasma renin levels, but blockade of converting enzyme lowers blood pressure to normal. To test the possibility that this normal-renin hypertension is caused by enhanced pressor responsiveness to angiotensin II (All), we examined the effects of All on hindquarter and renal vasculatures from 13 hypertensive and 13 normotensive mice. Both vascular beds were pump-perfused at a constant flow with plasma substitute. Optimal perfusion flows and basal pressures were similar in hindquarter (8 ml/100 g/min; 60 mm Hg) and renal vasculatures (130 ml/100 g/min; 50 mm Hg) from normotensive and hypertensive mice. ...
Angiotensin-II receptor antagonists work in a similar way to ACE inhibitors. But instead of stopping the production of angiotensin II, they block its action. This allows the blood vessels to expand, improving blood flow and reducing blood pressure. Angiotensin II is a very potent chemical that causes muscles surrounding blood vessels to contract, thereby narrowing blood vessels. This narrowing increases the pressure within the vessels and can cause high blood pressure (hypertension). Angiotensin II receptor blockers (ARBs) are medications that block the action of angiotensin II by preventing angiotensin II from binding to angiotensin II receptors on blood vessels. As a result, blood vessels enlarge (dilate) and blood pressure is reduced. Reduced blood pressure makes it easier for the heart to pump blood and can improve heart failure. In addition, the progression of kidney disease due to high blood pressure or diabetes is slowed. ARBs have effects that are similar to angiotensin converting enzyme ...
In this study we demonstrate that angiotensin II deteriorates glucose metabolism through deleterious effects on pancreatic β-cell mitochondrial function and insulin secretion. This effect involves IL-1β- and NF-κB-mediated inflammation and apoptosis and is independent of changes in blood pressure and insulin sensitivity.. In vivo infusion of angiotensin II for 4 weeks completely abolished glucose-stimulated insulin secretion. Surprisingly, after isolation and culturing, islets from angiotensin II-treated mice showed similar insulin secretion upon glucose stimulation as islets from saline-infused mice. Several possibilities can explain this finding: Angiotensin II-induced damage is reversible, and the islets had recovered between isolation and the insulin secretion assay. Alternatively, the in vivo deleterious effect of angiotensin II may be mediated via immune cells, which are lost following islet isolation. This would explain the discrepancy between the mild, direct in vitro effects of ...
To investigate whether apocynin, a NADPH oxidase inhibitor, produced cardioproteictive effects in Ang II-induced hypertensive mice, and to elucidate the underlying mechanisms. C57BL/6 mice were subcutaneously infused Ang II for 4 weeks to mimic
Telmisartan is an orally active nonpeptide angiotensin II antagonist that acts on the AT1 receptor subtype. New studies suggest that telmisartan may also have PPARγ agonistic properties that could potentially confer beneficial metabolic effects. This observation is currently being explored in clinical trials. Angiotensin II is formed from angiotensin I in a reaction catalyzed by angiotensin-converting enzyme (ACE, kininase II). Angiotensin II is the principal pressor agent of the renin-angiotensin system, with effects that include vasoconstriction, stimulation of synthesis and release of aldosterone, cardiac stimulation, and renal reabsorption of sodium. Telmisartan works by blocking the vasoconstrictor and aldosterone secretory effects of angiotensin II ...
Telmisartan is an orally active nonpeptide angiotensin II antagonist that acts on the AT1 receptor subtype. New studies suggest that telmisartan may also have PPARγ agonistic properties that could potentially confer beneficial metabolic effects. This observation is currently being explored in clinical trials. Angiotensin II is formed from angiotensin I in a reaction catalyzed by angiotensin-converting enzyme (ACE, kininase II). Angiotensin II is the principal pressor agent of the renin-angiotensin system, with effects that include vasoconstriction, stimulation of synthesis and release of aldosterone, cardiac stimulation, and renal reabsorption of sodium. Telmisartan works by blocking the vasoconstrictor and aldosterone secretory effects of angiotensin II ...
Agents that antagonize ANGIOTENSIN II TYPE 1 RECEPTOR. Included are ANGIOTENSIN II analogs such as SARALASIN and biphenylimidazoles such as LOSARTAN. Some are used as ANTIHYPERTENSIVE AGENTS ...
Angiotensin II acts through two separate receptors namely AT1 and AT2. Two AT1 receptor subtypes (AT1A and AT1B) have been described. FEBS Lett. 1992 Feb 24;298(2-3):257-60. AT1 receptors are distributed widely in tissues including the adipose tissue as well as vasculature, heart, kidney, brain, liver, adrenal gland and lung. Am J Hypertens. 2000 Jan;13(1 Pt 2):31S-38S. The classic effects of Angiotensin II namely vasoconstriction, as well as aldosterone stimulation from the adrenal gland with sodium and water reabsorption in the kidneys are mediated through the AT1 receptors. Pharmacol Rev. 1993 Jun;45(2):205-51. AT2 receptor expression which is initially widespread in the foetus, decreases post-natally and remains expressed in the adipose tissue as well as the vasculature, heart, adrenal gland, pancreas and female reproductive organs. Am J Hypertens. 2000 Jan;13(1 Pt 2):31S-38S. Angiotensin seems to act on AT2 receptors to produce effects totally opposed to those mediated by the AT1 receptor ...
The brain Renin Angiotensin System (RAS) is quickly becoming recognized as a critical mediator of blood pressure and body fluid homeostasis. In the forebrain, the median preoptic nucleus (MnPO) responds to Angiotensin II (Ang II) stimulation by increasing thirst and blood pressure. Understanding how this nuclei regulates blood pressure and body fluid homeostasis in response to Ang II has the potential to open new therapeutic avenues for treatment of hypertension. In the studies following series of studies I investigated the role of MnPO Angiotensin Type Ia receptors in the sustained hypertension induced by Chronic Intermittent Hypoxia (CIH) and thirst regulation. The first project focuses on the role of the MnPO in the sustained hypertension of CIH. Sleep apnea leads to hypertension that persists throughout the waking period. The neural mechanisms that underlie this pathophysiological increase in blood pressure are not well known. CIH is a model of the hypoxemia experienced by sleep apnea sufferers.
phdthesis{7e764889-236a-43b4-a834-40654ec9d8e3, abstract = {Angiotensin II (Ang II) is a potent vasoconstrictor that is implicated in the pathogenesis of hypertension, heart failure and atherosclerosis. In this thesis, the efficacy and safety of Ang II receptor blockers (ARB) were evaluated. The vasomotor effects of Ang II in endothelium-denuded human coronary arteries were characterized by in vitro pharmacology and the Ang II receptor mRNA levels were quantified by real-time PCR in human coronary arteries. The ARB, valsartan, and the angiotensin converting enzyme (ACE) inhibitor, enalapril, had similar effects on exercise capacity, symptoms of heart failure, quality of life, and left ventricular function and size. Moreover, it could be concluded that a shift from an ACE inhibitor to valsartan is safe.,br/,,br, ,br/,,br, The contractile effect of Ang II in human coronary arteries is mediated by Ang II type 1 (AT1) and type 2 (AT2) receptors. AT1 receptors are of major importance, since the Ang ...
Shop Type-1B angiotensin II receptor ELISA Kit, Recombinant Protein and Type-1B angiotensin II receptor Antibody at MyBioSource. Custom ELISA Kit, Recombinant Protein and Antibody are available.
Thoracic aortic aneurysms and dissections (TAAD) are a major cause of morbidity and mortality in patients. Many different risk factors have been associated TAAD, but hypertension is the largest risk factor. Subsets of TAAD patients have identifiable syndromic genetic diseases, yet a number of genetic non-syndromic patients have been identified. Infusion of angiotensin II into mouse models causes aortic disease through inflammation and fibrosis. An angiotensin type I receptor (AT1R) blocker (ARB) or an angiotensin converting enzyme (ACE) inhibitor (ACEi) can reverse aortic pathology in some mouse models. I set out to better understand the relationship between angiotensin and TAAD in our mouse models, and hypothesized that angiotensin II signaling through the AT1R contributes to thoracic aortic aneurysm formation in multiple model systems of disease, and that blocking related receptors in addition to the AT1R, such as the AT2R and Mas receptor, may have negative consequences. Previously identified genetic
Adult male mongrel dogs were placed on LS (0.05% sodium chloride) for 2 weeks. Body weight (25.4±0.4 to 23.6±0.4 kg), left ventricular systolic pressure (137.0±3.4 to 124.0±6.7 mm Hg), and mean aortic pressure (111±3.1 to 98±4.3 mm Hg) decreased. Plasma angiotensin II concentration increased (4.4±0.7 to 14.8±3.7 pg/mL). Veratrine-induced (5 µg/kg) NO-mediated vasodilation was inhibited by 44% in LS; however, the simultaneous intravenous infusion of ascorbic acid or apocynin acutely and completely reversed this inhibition. In LS heart tissues, lucigenin chemiluminescence was increased 2.3-fold to angiotensin II (10-8 mol/L), and bradykinin (10-4 mol/L) induced reduction of myocardial oxygen consumption in vitro was decreased (40±1.3% to 16±6.3%) and completely restored by coincubation with tiron, tempol or apocynin. Switching of substrate uptake from free fatty acid to glucose by the heart was observed (free fatty acid: 8.97±1.39 to 4.53±1.12 µmol/min; glucose: 1.31±0.52 to ...
Definition : Immunoassay reagents intended to perform qualitative and/or quantitative analyses on a body fluid sample (e.g., serum) to determine the level of one or both of the vasopressor hormones angiotensin I and/or angiotensin II. Angiotensin I, a decapeptide, is produced in the blood by the hydrolization of angiotensinogen (previously produced in the liver) by renin; it is rapidly converted into angiotensin II, an octapeptide, by a circulating angiotensin-converting enzyme. Angiotensin II is a powerful vasoconstrictor that also stimulates the cells of the zona glomerulosa to produce aldosterone.. Entry Terms : "Peptidyl-Dipeptidase A Determination Reagents" , "Angiotensin I/II Determination Reagents" , "Reagents, Immunoassay, Renal Metabolism, Angiotensin I/II". UMDC code : 19879 ...
The 1166 A/C polymorphism of the angiotensin II type 1 receptor gene does not correlate with the blood pressure response to angiotensin II in patients with CHF Academic Article ...
This gene encodes a transmembrane protein localized to the plasma membrane and perinuclear vesicular structures. The gene product interacts with the angiotensin II type I receptor and negatively regulates angiotensin II signaling. Alternative splicing of this gene generates multiple transcript variants encoding different isoforms. [provided by RefSeq, Jul 2008 ...
TY - JOUR. T1 - Angiotensin II reduces mitochondrial content in skeletal muscle and affects glycemic control. AU - Mitsuishi, Masanori. AU - Miyashita, Kazutoshi. AU - Muraki, Ayako. AU - Itoh, Hiroshi. PY - 2009/3. Y1 - 2009/3. N2 - OBJECTIVE-Blockade of angiotensin (Ang) II has been shown to prevent new-onset type 2 diabetes. We focused on the effects of AngII on muscle mitochondria, especially on their biogenesis, as an underlining mechanism of type 2 diabetes. RESEARCH DESIGN AND METHODS-C2C12 cells and C57bl/6 mice were used to examine roles for AngII in the regulation of muscle mitochondria and to explore whether the effect was mediated by type 1 AngII receptor (AT1R) or type 2 receptor (AT2R). RESULTS-C2C12 cells treated with 10-8-10 -6 mol/l AngII reduced the mitochondrial content associated with downregula- tion of the genes involved in mitochondrial biogenesis. The action of AngII was diminished by blockade of AT2R but not AT1R, whereas overexpression of AT2R augmented the effect. ...
Angiotensin II released serotonin from neuron terminals and accelerated synthesis of the serotonin. This increase in synthesis depended on the activation of tryptophan hydroxylase. A biphasic effect was observed: at high doses the stimulatory effect depended on conversion of angiotensin II to angiotensin III. At low doses an inhibitory effect was found, possible dependent on an angiotensin II metabolite. These actions represent a subtle regulation of the open-loop serotonin system. ...
Sigma-Aldrich offers abstracts and full-text articles by [Dan Chen, Jinjiao Liu, Bing Rui, Min Gao, Ningwei Zhao, Shuai Sun, Aijing Bi, Tingting Yang, Yingtao Guo, Zhimin Yin, Lan Luo].
What are the key age-related differences in the reflex vasoconstrictor response in skin microvessels, and how are angiotensin II and Rho-kinase activation involved? These questions and more are answered in our latest podcast on the work by Lang and Kolb. Listen as Associate Editor Debra Diz (Wake Forest University School of Medicine) interviews lead author James Lang (Des Moines University) and content expert Caitlin Thompson-Torgerson (Anne Arundel Community College) about this intriguing work which has clear thermoregulatory ramifications for older adults. Is there a potential upstream role for reactive oxygen species in upregulating Angiotensin II? How can the primary effects of aging in a healthy older adult cohort be extrapolated to disease states such as diabetes? Listen to find out.. ...
[Tyr(PO₃H₂)⁴]-Angiotensin II, Human - Calbiochem Shown to inhibit renin release in a mean arterial pressure assay with similar potency to angiotensin II amide. - Find MSDS or SDS, a COA, data sheets and more information.
The renin-angiotensin system (RAS) is a hormonal system that is responsible for regulating plasma sodium ion concentration and arterial blood pressure in the body. The system involves several peptides such as angiotensin I and II as well as angiotensin converting enzyme (ACE) to enable the constriction of arterial blood vessels in the lung. Angiotensin II also stimulates the production of the hormone aldosterone in the kidneys which brings sodium ions into the bloodstream in exchange for potassium ions. Malfunctions of the RAS can lead to hypertension, heart failure, diabetes and renal complications. Thus the biochemical components of this system serve as important targets for therapeutic drugs ...
Novartis (Basel, Switzerland) new heart failure drug, Entresto, has created a lot of buzz due to its strong efficacy and clinical demand. This first-in-class small molecule drug was fast-tracked due to impressive clinical trial results. Entresto is a combination drug: Valsartan and Sacubitril. They work together to lower blood pressure, which lowers the strain on the heart and lessens the accumulation of fluid in tissues such as the lungs-a key symptom of heart failure. Valsartan is an angiotensin II receptor inhibitor; it stops angiotensin II. Why is stopping angiotensin II important?. Angiotensin II is a small hormone. When it attaches to the angiotensin receptor, it causes a cascade of reactions to occur. That cascade ultimately causes blood vessels to constrict, which causes blood pressure to increase. Think about it like this-it takes more pressure to move a fluid through a narrow tube than through a wide one. Angiotensin II also promotes the release of a second hormone, aldosterone, which ...
293445024 - EP 1091966 B1 2002-11-06 - N-TERMINAL SITE SELECTIVE INHIBITORS OF HUMAN ANGIOTENSIN CONVERSION ENZYME (ACE) - [origin: WO0001706A1] The invention concerns peptide derivatives useful as N-terminal site selective inhibitor of the human angiotensin conversion enzyme. Said derivatives comprise the amino acid sequence of the following formula: -Asp-Phe- psi (PO2CH2)-Ala-Xaa - wherein: psi (PO2CH2) indicates that the peptide bond (CONH) between Phe and Ala has been replaced by the phosphonic bond PO2CH2; and Xaa represents an amino acid residue. Said derivatives can be used in pharmaceutical compositions, in particular for protecting hematopoietic strain cells of patients subjected to aggressive chemotherapeutic or radiotherapy treatment.[origin: WO0001706A1] The invention concerns peptide derivatives useful as N-terminal site selective inhibitor of the human angiotensin conversion enzyme. Said derivatives comprise the amino acid sequence of the following formula: -Asp-Phe- psi (PO2CH2)-Ala-Xaa
Whew.. But this isnt as complicated as it looks. Renin has no real effect. Angiotensinogen just makes angiotensin I. Angiotensin Is main role is to make angiotensin II. The real money here is in angiotensin II, as well as aldosterone.. Angiotensin II has the primary effect of vasoconstriction. It tightens up the vasculature, increasing blood pressure and systemic resistance. It also produces vasopressin (aka ADH, or anti-diuretic hormone) and aldosterone, which cause the kidneys to downregulate urine production - more fluid will be returned to the circulation rather than discarded into the bladder. Vasopressin also helps angiotensin II to induce further vasoconstriction.. To make a long story short, the activation of the RAAS system causes an increase in blood pressure via both vasoconstriction and a decrease in kidney output. It is always active, playing a key role in maintaining homeostasis; if you sweat out a liter of water running a marathon, or bleed out a liter from a gunshot wound, the ...
This gene encodes an enzyme involved in catalyzing the conversion of angiotensin I into a physiologically active peptide angiotensin II. Angiotensin II is a potent vasopressor and aldosterone-stimulating peptide that controls blood pressure and fluid-electrolyte balance. This enzyme plays a key role in the renin-angiotensin system. Many studies have associated the presence or absence of a 287 bp Alu repeat element in this gene with the levels of circulating enzyme or cardiovascular pathophysiologies. Multiple alternatively spliced transcript variants encoding different isoforms have been identified, and two most abundant spliced variants encode the somatic form and the testicular form, respectively, that are equally active. [provided by RefSeq, May 2010 ...
Renin produced by the kidney in response to glomerular hypoperfusion cata-lyzes cleavage of angiotensinogen (produced by the liver) to angiotensin (AT), which in turn is cleaved by angiotensin-converting enzyme (ACE) to angiotensin II, which acts on two receptors. The AT1 receptor mediates the vasoconstrictor effects of AT. The actions of the AT2 receptor are less well defined.. Angiotensin-converting enzyme inhibitors Mechanism of action. These drugs inhibit the conversion of angiotensin I to angiotensin II and. reduce angiotensin II mediated vasoconstriction.. Indications. The main indicators are heart failure, hypertension, diabetic nephropathy and ischaemic heart disease.. Preparations and dose. Perindopril. Tablets: 2 mg, 4 mg, 8 mg.. ■ Hypertension, initially 4 mg once daily (use 2 mg if in addition to diuretic, in the elderly, in renal impairment) subsequently adjusted according to response to maximum 8 mg daily. ■ Heart failure: initially 2 mg once daily, increased after at least 2 ...
Elevated dietary salt intake has previously been demonstrated to have dramatic effects on microvascular structure and function. The purpose of this study was to determine whether a high-salt diet modulates physiological angiogenesis in skeletal muscle. Male Sprague-Dawley rats were placed on a control diet (0.4% NaCl by weight) or a high-salt diet (4.0% NaCl) before implantation of a chronic electrical stimulator. After seven consecutive days of unilateral hindlimb muscle stimulation, animals on control diets demonstrated a significant increase in microvessel density in the tibialis anterior muscle of the stimulated hindlimb relative to the contralateral control leg. High salt-fed rats demonstrated a complete inhibition of this angiogenic response, as well as a significant reduction in plasma ANG II levels compared with those of control animals. To investigate the role of ANG II suppression on the inhibitory effect of high-salt diets, a group of rats that were fed high salt were chronically ...
BioAssay record AID 37544 submitted by ChEMBL: Affinity for Angiotensin II receptor, type 1 by measuring its ability to antagonise the contractile effect of AngII in rabbit isolated thoracic aorta.
In response to lowered blood pressure, the renin enzyme cleaves angiotensin-1 from angiotensin. Angiotensin-converting enzyme (ACE) then removes a dipeptide to yield the physiologically active peptide angiotensin-2, the most potent pressor substance known, which helps regulate volume and mineral balance of body fluids. The Angiotensin 2 [3-8] Peptide binds specifically to a new angiotensin binding site distinct from angiotensin 2 receptors.. ...
The Renin-Angiotensin System (RAS) is well known for its function as a regulator of blood pressure and fluid and electrolyte balance with its major effective peptide Angiotensin II. Beside the systemic RAS, a lot of other tissues such as the heart, lungs, liver and the blood vessels have been shown to produce Ang II. The RAS was first known to act only in the periphery. Later RAS and its components were found in the brain and appeared to be autonomous. The development of selective receptor antagonists led to the discovery of the angiotensin receptors. Among these, the AT1 and AT2 receptor subtypes seem to play an important role in ischemic processes. The numerous studies of angiotensin receptors in the last two decades showed that the AT1 receptor was found to be abundant in the mature brain while the AT2 receptor was highly expressed before and during the neonatal period and its expression decreased speedily afterwards. Therefore the AT1 receptor has been studied profusely while much less was ...
In the domestic fowl, angiotensin (ANG) II causes a unique vasodepressor response in vivo and vascular relaxation of aortic rings in vitro that appear to be mediated by ANG II receptors. In initial studies using radioligand binding techniques, we identified specific vascular ANG II receptors in the fowl aorta. In the present study, we have characterized fowl vascular ANG II receptors in terms of binding specificity and their modulation by divalent cations and guanine nucleotide, to understand how the fowl receptor might differ from mammalian vascular ANG II receptors that mediate vasoconstriction. Competitive displacement of [125I] ANG II binding by ANG agonist and antagonist analogs revealed a unique pattern of receptor specificity, with the potency rank order: [Asn1, Val5]ANG II greater than [Asp1, Ile5]ANG II greater than [Asp1, Val5, Ser9] ANG I = [Asp1, Val5]ANG II much greater than [Val5]ANG III greater than [sarcosine(Sar)1, Ile5]ANG II greater than [Sar1, Ile8]ANG II much greater than ...
BioAssay record AID 37515 submitted by ChEMBL: In vivo inhibitory concentration against Angiotensin II receptor, type 1 of rabbit aorta membrane.
Looking for angiotensin? Find out information about angiotensin. A decapeptide hormone that influences blood vessel constriction and aldosterone secretion by the adrenal cortex. Also known as hypertensin Explanation of angiotensin
Renal dopamine D1 and angiotensin II AT1 receptors by regulating proximal tubular sodium transporters maintain sodium homeostasis and blood pressure. Recently w...
We investigated in mice whether atherosclerosis exacerbates the development of post-ischemic heart failure and alters the beneficial effects of long-term angiotensin II type 1 receptor blockade in this model. ApoE-deficient (ApoE(-/-)) and C57BL/6J (
ATRAP (angiotensin II type 1 receptor-associated protein) is a molecule which directly interacts with AT1R and inhibits AT1R signaling. The aim of this study was to examine the effects of continuous angiotensin II (ANG II) infusion on the intrarenal expression and distribution of ATRAP, and to determine the role of AT1R signaling in mediating these effects. C57BL/6 male mice were subjected to vehicle or ANG II infusions at doses of 200, 1000, or 2500 ng/kg/min for 14 days. ANG II infusion caused significant suppression of ATRAP expression in the kidney, but did not affect ATRAP expression in the testis or liver. Although only the highest ANG II dose (2500 ng/kg/min) provoked renal pathological responses, such as an increase in the mRNA expression of angiotensinogen and α−subunit of the epithelial sodium channel, ANG II-induced decreases in ATRAP were observed even at the lowest dose (200 ng/kg/min), particularly in the outer medulla of the kidney, based on immunohistochemical staining and ...
Angiotensin convertaza, cunoscuta si sub numele de kinaza II sau peptidil-dipeptidaza A, este o enzima din clasa hidrolazelor implicate in hidroliza legaturilor peptidice la nivelul C-terminal. Are localizare transmembranara si este alcatuita dintr-un singur lant polipeptidic cu doua situsuri catalitice ce contin zinc. Clivajul proteolitic elibereaza din membrana celulara in spatiul extracelular enzima functionala, circulanta6.. Majoritatea angiotensin convertazei (~90%) se gaseste legata in tesuturi si doar o mica parte circula libera in plasma. Sursa principala a enzimei este endoteliul pulmonar.. Enzima participa in cascada sistemului renina-angiotensina-aldosteron ca raspuns la hipovolemie, fiind responsabila de conversia angiotensinei I in angiotensina II, vasoconstrictor puternic care creste tensiunea arteriala. De asemenea angiotensin convertaza este responsabila si de inactivarea bradikininei (in sistemul kalikreina-kinina)3;6.. Activitatea angiotensin convertazei este crescuta in ...
OBJECTIVE: The current study was undertaken to localize and identify angiotensin II (Ang II) receptor subtypes in the microcirculation of striated muscle.. METHODS: Cremaster muscles from 7- to 8-week-old Sprague-Dawley rats were excised, placed in a dissection solution maintained at 4 degrees C, and 3 branch orders of arterioles and venules, as well as capillaries and a muscle specimen, were microdissected under a stereomicroscope. Reverse transcription polymerase chain reaction (RT-PCR) methods were developed for purification and amplification of extremely small amounts of RNA (,5 ng/microL) from whole tissue samples. RNA was isolated from each sample, reverse transcribed, and the cDNA products were amplified by polymerase chain reactions (PCR) specifically primed with either AT(1a), AT(1b), or AT(2) receptor primers. The products were electrophoretically size-fractionated on an agarose gel, stained with ethidium bromide to visualize DNA bands, and analyzed to determine the presence or absence ...
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The selective antagonism of receptors with simple competitive antagonists offers a method of determining whether receptor populations are heterogeneous, by comparison with a model that assumes receptor homogeneity. This approach is based on the assumption that the Schild regressions result in a seemingly linear regression with a slope of unity and an intercept of KB for competitive antagonists (Kenakin, 1992). In this study, we evaluated the effects of losartan and PD123319 on Ang II-induced contractions.. PD123319 did not produce any significant effect. Following incubation with losartan, Ang II-induced curves shifted rightward of the control in a concentration-dependent manner. Interestingly, this effect was followed by a decrease in Emax,resulting in a Schild plot slope of less than 1. Several mechanisms have been postulated to explain this effect: 1) tachyphylaxis to the agonist, 2) equilibrium conditions between antagonist and antagonist-receptors have not been attained, (3) the interaction ...
Angiotensin II signal transduction in vascular smooth muscle cells: role of tyrosine kinases.: Originally known to be a vasoconstrictor and thought to play a cr
The renin-angiotensin system (RAS) plays a fundamental role in cardiovascular pathophysiology. In particular, angiotensin II (AII) has been identified as a culprit in endothelial and vascular damage, elevated blood pressure, and cardiac failure. Pharmacological inhibition of this system is available through two mechanisms; the reduction of AII formation by inhibition of angiotensin-converting enzyme (ACE), and by direct blockade of the type 1 angiotensin II receptor by angiotensin II receptor blockers (ARBs ...
It is well established that renal hypoxia is associated with the development of renal injury. The purpose of this study is measure the alterations in renal blood oxygenation after angiotensin II converting enzyme inhibition. The understanding of kidney adaptive mechanisms to renin angiotensin system effects in healthy subjects will be useful for the early detection of renal disease and for the development of new therapies to decrease the progression of the disease and its consequences ...
It is well established that renal hypoxia is associated with the development of renal injury. The purpose of this study is measure the alterations in renal blood oxygenation after angiotensin II converting enzyme inhibition. The understanding of kidney adaptive mechanisms to renin angiotensin system effects in healthy subjects will be useful for the early detection of renal disease and for the development of new therapies to decrease the progression of the disease and its consequences ...
This page includes the following topics and synonyms: Angiotensin 2 Receptor Blocking Agent, Angiotensin Receptor Blocker, Angiotensin Blocker, Losartan, Cozaar, Irbesartan, Avapro, Candesartan, Atacand, Eprosartan, Teveten, Telmisartan, Micardis, Valsartan, Diovan, Olmesartan, Benicar, Entresto, Exforge, Azor.
Angiotensin II (AII) is an octapeptide, produced in the blood as a result of two different enzymatic hydrolyses, which occur in the renal hypertensor system. Among many others pharmacological...
Side Effects for GIAPREZA (angiotensin ii injection) are also known as adverse reactions. Below is a summary of known side effects for Giapreza.
The angiotensin receptors are seven-membrane G-protein-coupled receptors. They mediate the cardiovascular and other effects of angiotensin II which is a bioactive peptide of the renin-angiotensin system.. ...
Product name: Avalide. Active component: Irbesartan Hydrochlorothiazide. Used to: Generic Avalide is a combination medication used to treat high blood pressure. One component belongs to a class of blood pressure medications that prevents the hormone angiotensin II from constricting the blood vessels, thereby allowing blood to flow more freely and keeping blood pressure down. The other component is a diuretic that increases the output of urine, removing excess fluid from the body and thus lowering blood pressure.. Known As: Avalide / Irovel. Manufacturer: Sun Pharma. To order: Go to store. Payment method: Visa / MasterCard / AmEx / Wiretransfer. Delivery Time: 5-7 business days by Courier Service or 10-21 business days by Standard International Airmail. Bonus options: Special Internet Prices (up to 40% off average US price) Best quality drugs NO PRIOR PRESCRIPTION NEEDED! 100% Anonimity and Discreet shipping Fast FREE shipping (4 to 7 days) Loyalty program Friendly customer support 4 Free ...
Product name: Avalide. Active ingredient: Irbesartan Hydrochlorothiazide. Is used for: Generic Avalide is a combination medication used to treat high blood pressure. One component belongs to a class of blood pressure medications that prevents the hormone angiotensin II from constricting the blood vessels, thereby allowing blood to flow more freely and keeping blood pressure down. The other component is a diuretic that increases the output of urine, removing excess fluid from the body and thus lowering blood pressure.. Similar Titles: Avalide / Irovel. Manufacturer: Sun Pharma. Purchase: Click here. Payment method: Visa / MasterCard / Western Union / MoneyGram. Delivery Time: 5-7 business days by Courier Service or 10-21 business days by Standard International Airmail. Discount program: FREE pills! FREE shipping! Discounts! (up to 10%) & more.... ...
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Angiotensin 1 converting enzyme - 67 yrs. Angiotensin 1 converting enzyme (ace) serum 126.7, what should be done? Bad? What does this mean? Life style changes. Medication? Thank you ACE levels. 51 M Notes: 67 yrs angiotensin 1 converting enzyme (ace) serum 126.7, what should be done? Bad? What does this mean? Life style changes. Medication? Thank you ANS: not enough information to help at this point. Are you 51 or 67? Need to know why it was measured, what meds, other illnesses, & what is normal in that lab. Get this information & will be happy to do 2nd opinion as I specialize in RAAS
... ! Cozaar is an effective medication which helps to fight with the symptoms of high blood pressure and to reduce the risk of stroke in people with hypertension. It is used in the treatment of kidney problems in people with type 2 diabetes. Cozaar acts by preventing the hormone angiotensin II from constricting the blood vessels, which tends to raise blood pressure.
an antihypertensive drug that blocks the formation of angiotensin II in the kidney, leading to relaxation of the arteries; promotes the excretion of salt and water by inhibiting the activity of the angiotensin converting enzyme; also used to treat congestive heart failure. ...
The presence of intracellular receptors for ANG II and ANG-(1-7) within the kidney necessitates the delivery and/or intracellular generation of the requisite ligands. Binding of ANG II to the AT1 receptor on the cell surface induces rapid internalization of the ligand-receptor complex (46, 59, 99). Chronic AT1 receptor blockade or AT1 receptor deletion significantly reduces renal content of ANG II, suggesting that receptor-mediated uptake of ANG II contributes directly to intracellular peptide levels and/or stimulates intracellular synthesis (10, 13, 57, 58, 63, 78). Our preliminary studies find that ANG II administration restores the depleted levels of ANG II in the kidney of tissue ACE knockout mice to that of the wild-type mice (64). Similar to other peptidergic GPCR systems, the internalized AT1 receptor complex is sorted into either endosomal or lysosomal compartments (7, 46, 100). In the kidney, endosomal sorting of ANG II may protect the peptide from immediate metabolism and provide a ...
ACE inhibitors prevent the conversion of angiotensin I to angiotensin II by angiotensin converting enzyme (ACE) in the lungs, in turn reducing effects of angiotensin II. These effects include:. ...
Angiotensin is part of the renin-angiotensin-aldosterone system. It does not generally exist simply as angiotensin, but rather as angiotensinogen, befor...
A large number of studies have investigated the specific peripheral mechanisms activated and/or inhibited after stimulation of central HA receptors that contribute to changes in blood pressure and heart rate. Figure 2⇓ is a schematic representation of cardiovascular regulatory systems affected by CNS HA neuron stimulation. The vasoconstrictor activity of the sympathetic nervous system as well as the vasoconstrictor hormones vasopressin and angiotensin II are implicated in contributing to cardiovascular responses mediated by CNS HA systems.. The role of central HA in activation of the sympathetic nervous system has been evaluated by measuring plasma concentrations of catecholamines after CNS administration of exogenous HA and after stimulation of endogenous HA systems. Infusion of HA into the lateral cerebral ventricles as well as stimulation of the HA cell bodies in the TMN increase plasma concentrations of norepinephrine. In addition, cardiac responses evoked by central HA are attenuated by ...
Previous studies have demonstrated that angiotensin II receptors are present in several brain regions,1 39 and angiotensin II binding sites have been identified on cerebral blood vessels.19 40 41 In this study saralasin attenuated a hypoxia-mediated increase in CBF, suggesting that activation of angiotensin II receptors was in part responsible for the increase in CBF. In contrast, neither saralasin nor captopril attenuated increases in blood flow to the caudate nucleus and the thalamus during hypoxia. Previous 125I binding studies have reported that the caudate nucleus is nearly without angiotensin II binding sites, and except for the subthalamic nucleus, the thalamus showed only moderate labeling of angiotensin II binding sites.1 Thus, the lower density of angiotensin II receptors in these areas may account for the lack of influence by the angiotensin II receptor antagonist saralasin and the ACE inhibitor captopril during hypoxia.. The specificity and selectivity of saralasin has been ...
Angiotensin II effects on cyclic AMP production and steroid output were studied in a sensitive preparation of isolated rat adrenal glomerulosa cells. With increasing concentrations of angiotensin II logarithmic dose-response curves for aldosterone and cyclic AMP production were similar. The minimum effective dose (0.2nm) for stimulation of aldosterone production also significantly (P,0.001) increased cyclic AMP output. For both aldosterone and cyclic AMP production, the peptide hormone concentration eliciting maximal response (0.2μm) and the ED50 (median effective dose) values (1nm) were the same; this is consistent with cyclic AMP acting as an intracellular mediator for angiotensin II-stimulated aldosterone production by glomerulosa cells. The angiotensin II antagonist [Sar1,Ala8]angiotensin II inhibited angiotensin II-stimulated corticosterone and aldosterone production in these cells. An equimolar concentration of antagonist halved the response to 20nm-angiotensin II, and complete inhibition ...
TY - JOUR. T1 - Modeling sex differences in the renin angiotensin system and the efficacy of antihypertensive therapies. AU - Leete, Jessica. AU - Gurley, Susan. AU - Layton, Anita T.. PY - 2018/4/6. Y1 - 2018/4/6. N2 - The renin angiotensin system is a major regulator of blood pressure and a target for many anti-hypertensive therapies; yet the efficacy of these treatments varies between the sexes. We use published data for systemic RAS hormones to build separate models for four groups of rats: male normotensive, male hypertensive, female normotensive, and female hypertensive rats. We found that plasma renin activity, angiotensinogen production rate, angiotensin converting enzyme activity, and neutral endopeptidase activity differ significantly among the four groups of rats. Model results indicate that angiotensin converting enzyme inhibitors and angiotensin receptor blockers induce similar percentage decreases in angiotensin I and II between groups, but substantially different absolute ...
Looking for online definition of Angiotensin I-Converting Enzyme in the Medical Dictionary? Angiotensin I-Converting Enzyme explanation free. What is Angiotensin I-Converting Enzyme? Meaning of Angiotensin I-Converting Enzyme medical term. What does Angiotensin I-Converting Enzyme mean?
The biologic actions of the cardiac peptide hormone atrial natriuretic peptide (ANP) of vasorelaxation, diuresis and natriuresis, suppression of aldosterone, vasopressin release, and thirst are the opposite of those of the renin angiotensin system. This close relationship is further strengthened by the complementary localization of their receptors in the brain, adrenal gland, vasculature, and kidney. In many physiologic situations including postural changes, volume expansion, water immersion, high altitude, and lower body negative pressure, the plasma levels of ANP and angiotensin II change inversely. In congestive heart failure, renin and aldosterone levels may initially be suppressed by high levels of ANP. Similarly the low renin levels associated with increasing age and with elderly hypertensive patients, may be the result of the elevation of plasma ANP that occurs with aging. ANP may thus be the endogenous antagonist of the renin angiotensin aldosterone system. These two opposing systems ...
Progressive deterioration of renal function occurs during normal aging. Previous studies on the aging kidney have demonstrated glomerular hemodynamic changes, specifically, glomerular capillary hypertension, as maladaptations that lead to proteinuria and glomerular sclerosis over time. Aging rats treated with angiotensin-converting enzyme inhibition have relatively less proteinuria and sclerosis, suggesting that age-related changes in renal function may be associated with alterations in the intrarenal renin-angiotensin system, which thus may play a major role in the pathogenesis of these maladaptations. To investigate this possibility, renal and systemic renin-angiotensin systems were examined at an early phase of the aging process (3 months) and at a later phase (12 months) in male Sprague-Dawley rats. Although plasma renin and serum angiotensin-converting enzyme concentrations did not differ significantly, the intrarenal system showed down-regulation of renin mRNA and angiotensin-converting ...
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How is Human Aortic Vascular Smooth Muscle Cell (cardiology) abbreviated? h-SMC stands for Human Aortic Vascular Smooth Muscle Cell (cardiology). h-SMC is defined as Human Aortic Vascular Smooth Muscle Cell (cardiology) very rarely.
The effects of retinoids on adrenal aldosterone synthase gene (CYP11B2) expression and aldosterone secretion are still unknown. We therefore examined the effects of nuclear retinoid X receptor (RXR) pan-agonist PA024 on CYP11B2 expression, aldosterone secretion and blood pressure, to elucidate its potential as a novel anti-hypertensive drug. We demonstrated that PA024 significantly suppressed angiotensin II (Ang II)-induced CYP11B2 mRNA expression, promoter activity and aldosterone secretion in human adrenocortical H295R cells. Human CYP11B2 promoter functional analyses using its deletion and point mutants indicated that the suppression of CYP11B2 promoter activity by PA024 was in the region from -1521 (full length) to -106 including the NBRE-1 and the Ad5 elements, and the Ad5 element may be mainly involved in the PA024-mediated suppression. PA024 also significantly suppressed the Ang II-induced mRNA expression of transcription factors NURR1 and NGFIB that bind to and activate the Ad5 element. ...

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

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

Aldosterone synthase inhibition: cardiorenal protection in animal disease models and translation of hormonal effects to human...Aldosterone synthase inhibition: cardiorenal protection in animal disease models and translation of hormonal effects to human...

For the Ang-II-infusion model, an initial loading dose of 300 ng/kg angiotensin II (Ang II) was followed by 100 ng/kg/min ... Montezano AC, Callera GE, Yogi A, He Y, Tostes RC, He G, Schiffrin EL, Touyz RM: Aldosterone and angiotensin II synergistically ... Min LJ, Mogi M, Li JM, Iwanami J, Iwai M, Horiuchi M: Aldosterone and angiotensin II synergistically induce mitogenic response ... After 1 h of Ang II or ACTH infusion, a blood sample was collected for determining the post-Ang II or ACTH baseline (i.e., ...
more infohttps://translational-medicine.biomedcentral.com/articles/10.1186/s12967-014-0340-9

RENIN ANGIOTENSIN ALDOSTERONE SYSTEM INHIBITORS					RENIN ANGIOTENSIN ALDOSTERONE SYSTEM INHIBITORS

Angiotensinogen di ubah menjadi angiotensin 1 dengan katalisis renin. Selanjutnya angiotensin… ... Angiotensin adalah hormone petida yang berasal dari protein angiotensinogen. ... Selanjutnya angiotensin I akan di ubah menjadi angiotensin II dengan di katalisasi oleh enzim ACE ( angiotensin-converting ... Obat ini beraksi menghambat reseptor angiotensin II. Aksinya sebenarnya mirip dengan ACE inhibitor, bedanya obat ini menghambat ...
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Angiotensin II receptor - WikipediaAngiotensin II receptor - Wikipedia

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

Angiotensin II receptor - WikipediaAngiotensin II receptor - Wikipedia

The angiotensin II receptors, (AGTR1) and (AGTR2), are a class of G protein-coupled receptors with angiotensin II as their ... angiotensin II. The AT1 and AT2 receptors share a sequence identity of ~30%, but have a similar affinity for angiotensin II, ... The angiotensin receptor is activated by the vasoconstricting peptide angiotensin II. The activated receptor in turn couples to ... The AT4 receptor is activated by the angiotensin II metabolite angiotensin IV, and may play a role in regulation of the CNS ...
more infohttps://en.wikipedia.org/wiki/Angiotensin_II_receptor

Angiotensin II - DrugBankAngiotensin II - DrugBank

Angiotensin II has been investigated for the treatment, basic science, and diagnostic of Hypertension, Renin Angiotensin System ... The novelty of the medication lies in the fact that it is the first and only use of synthetic human angiotensin II to help ... As of December 21, 2017 the FDA approved La Jolla Pharmaceuticals Giapreza (angiotensin II) Injection for Intravenouse ... Angiotensin II is under investigation for the treatment of Sepsis, Septic Shock, Diabetes Mellitus, and Acute Renal Failure. ...
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Angiotensin II, humanAngiotensin II, human

... ; The octapeptide angiotensin II (Ang II) exerts a wide range of effects on the cardiovascular system. It ... Ang II is formed by cleavage of Ang I by the angiotensin-converting enzyme (ACE) or chymases. Human heart chymase, a ... hydrolyzes the Phe8-His9 bond to yield the octapeptide hormone angiotensin II and His-Leu.; DRVYIHPF; H-Asp-Arg-Val-Tyr-Ile-His ... 2010). Angiotensin II/angiotensin II type I receptor (AT1R) signaling promotes MCF-7 breast cancer cells survival via PI3- ...
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Angiotensin ii | Define Angiotensin ii at Dictionary.comAngiotensin ii | Define Angiotensin ii at Dictionary.com

... angiotensin I) and two varieties (angiotensin II and angiotensin III) that elevate blood pressure and stimulate the adrenal ... Angiotensin ii definition, any of three oligopeptides occurring in plasma, an inactive form ( ... angiotensin ii in Medicine Expand. angiotensin II n. An octapeptide that is a potent vasopressor and a powerful stimulus for ... Angiotensin II is formed from inactive angiotensin I by the action of angiotensin-converting enzyme (or ACE). See also ACE ...
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angiotensin II receptor Protein Superfamily Detailangiotensin II receptor Protein Superfamily Detail

Term: angiotensin II receptor. ID: PIRSF038557 Mouse Protein Superfamily Annotations. Select one or more mouse PIRSF members to ...
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ExRx.net : Angiotensin II Receptor Blockers (ARB)ExRx.net : Angiotensin II Receptor Blockers (ARB)

1996). Effects of angiotensin II receptor blockade during exercise: comparison of losartan and saralasin. J Cardiovasc ... Saralasin, a partial agonist angiotensin II receptor, does not appear to affect mean arterial pressure (MAP) and systemic ... Lowers blood pressure by blocking the vasoconstrictor effects of the hormone angiotensin II ...
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Angiotensin II and Coronary Sympathetic Vasodilation | CirculationAngiotensin II and Coronary Sympathetic Vasodilation | Circulation

Angiotensin II and Coronary Sympathetic Vasodilation. Kenneth M. Kessler, Rhonda M. Kessler ... There is no question that angiotensin II can play its enhancing effects on the sympathetic nervous system at various levels and ... Saino A, Pomidossi G, Perondi R, Valentini R, Rimini A, Di Francesco L, Mancia G. Intracoronary angiotensin II potentiates ... The suggestion is that higher local concentrations of either angiotensin II or perindoprilat are achieved when a vessel is ...
more infohttp://circ.ahajournals.org/content/97/18/1873

Angiotensin II receptor blockers (ARBs) | HealthLink BCAngiotensin II receptor blockers (ARBs) | HealthLink BC

All medicines can cause side effects. Many people dont have side effects. And minor side effects sometimes go away after a while. But sometimes side effects can be a problem or can be serious. If youre having problems with side effects, talk to your doctor. He or she may be able to lower your dose or change to a different medicine. You will likely have regular blood tests to monitor how the medicine is working in your body and to see if this medicine is causing problems.. Always be sure you get specific information on the medicine youre taking. For a full list of side effects, check the information that came with the medicine youre using. If you have questions, talk to your pharmacist or doctor. ...
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Angiotensin II, Oxidant Signaling, and Hypertension | HypertensionAngiotensin II, Oxidant Signaling, and Hypertension | Hypertension

... is critical in angiotensin II (Ang II)-mediated regulation of blood pressure and hypertension.4,5 Using an established viral ... Angiotensin II, Oxidant Signaling, and Hypertension. Down to a T?. Robin L. Davisson, Matthew C. Zimmerman ... Superoxide mediates angiotensin II-induced influx of extra cellular calcium in neural cells. Hypertension. 2005; 45: 717-723. ... Hypertension caused by angiotensin II infusion involves increased superoxide production in the central nervous system. Circ Res ...
more infohttp://hyper.ahajournals.org/content/55/2/228

Angiotensin 2 Receptor Blocking AgentAngiotensin 2 Receptor Blocking Agent

Angiotensin Receptor Blocker, Angiotensin Blocker, Losartan, Cozaar, Irbesartan, Avapro, Candesartan, Atacand, Eprosartan, ... ARBs do not effect Angiotensin II type 2 receptors. *Results in less effect on fibrosis and blood flow ... Angiotensin 2 Receptor Blocking Agent. search Angiotensin 2 Receptor Blocking Agent, Angiotensin Receptor Blocker, Angiotensin ... Bradykinin related reaction that recurs with ARBs in 2% of patients who had Angioedema on ACE Inhibitor ...
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Angiotensin II modulates CD40 exp... preview & related info | MendeleyAngiotensin II modulates CD40 exp... preview & related info | Mendeley

AngII (angiotensin II), which induces oxidative stress and inflammation, is ... ... AngII (angiotensin II), which induces oxidative stress and inflammation, is also implicated in the progression of ... Angiotensin II modulates CD40 expression in vascular smooth muscle cells. *Souza H ... cyclo-oxygenase-2) expression. We conclude that AngII stimulation of vascular cells leads to a ROS-dependent increase in CD40/ ...
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Drugs:Angiotensin-II blockers Further side-effects - Healthy.netDrugs:Angiotensin-II blockers Further side-effects - Healthy.net

Tagged asallergic reactionsangioedemaangiotensin IIangiotensin-receptor blockersARBsbirth defectsbreast milkcoughdiarrhoea ... Drugs:Angiotensin-II blockers Further side-effects. What Doctors Dont Tell You1 min read ...
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Pharmacological properties of angiotensin II receptor antagonists.  - PubMed - NCBIPharmacological properties of angiotensin II receptor antagonists. - PubMed - NCBI

... of the important actions of angiotensin II, and avoid the nonspecificity of the angiotensin I converting enzyme inhibitors. ... Pharmacological properties of angiotensin II receptor antagonists.. Timmermans PB1.. Author information. 1. Tularik Inc, South ... The availability of selective, potent, orally active and long acting nonpeptide angiotensin II type 1 (AT1) receptor ... antagonists has provided the opportunity to obtain the benefits of selectively blocking the renin-angiotensin-aldosterone ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/10579749?dopt=Abstract

Angiotensin II, human, FAM-labeledAngiotensin II, human, FAM-labeled

... ; This is a fluorescent (FAM)-labeled Angiotensin II peptide, Abs/Em=494/518 nm. FAM ( ... This is a fluorescent (FAM)-labeled Angiotensin II peptide, Abs/Em=494/518 nm. FAM (carboxyfluorescein) exhibits better ...
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Angiotensin 2 Receptor Blocking AgentAngiotensin 2 Receptor Blocking Agent

Angiotensin Receptor Blocker, Angiotensin Blocker, Losartan, Cozaar, Irbesartan, Avapro, Candesartan, Atacand, Eprosartan, ... Irbesartan selectively and competitively blocks the binding of angiotensin II to the angiotensin I receptor. Angiotensin II ... Angiotensin II, formed from angiotensin I by angiotensin-converting enzyme (ACE), stimulates the adrenal cortex to synthesize ... This prevents angiotensin II-induced vasoconstriction and interferes with angiotensin II-mediated aldosterone secretion, ...
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Angiotensin II Type 1 Receptor peptide (ab176148)Angiotensin II Type 1 Receptor peptide (ab176148)

Buy our Angiotensin II Type 1 Receptor peptide. Ab176148 is a blocking peptide for ab124505 and has been validated in BL. Abcam ... Angiotensin II Type 1 Receptor peptide. See all Angiotensin II Type 1 Receptor proteins and peptides. ... Receptor for angiotensin II. Mediates its action by association with G proteins that activate a phosphatidylinositol-calcium ... Blocking - Blocking peptide for Anti-Angiotensin II Type 1 Receptor antibody (ab124505) ...
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Renal injury from angiotensin II-mediated hypertension. | HypertensionRenal injury from angiotensin II-mediated hypertension. | Hypertension

Angiotensin II (Ang II)-mediated hypertension induces vascular smooth muscle cell hypertrophy and hyperplasia in systemic blood ... Renal injury from angiotensin II-mediated hypertension.. R J Johnson, C E Alpers, A Yoshimura, D Lombardi, P Pritzl, J Floege, ... Renal injury from angiotensin II-mediated hypertension.. R J Johnson, C E Alpers, A Yoshimura, D Lombardi, P Pritzl, J Floege ... Renal injury from angiotensin II-mediated hypertension.. R J Johnson, C E Alpers, A Yoshimura, D Lombardi, P Pritzl, J Floege ...
more infohttp://hyper.ahajournals.org/content/19/5/464

Angiotensin II ELISA Kits: Novus BiologicalsAngiotensin II ELISA Kits: Novus Biologicals

Browse our Angiotensin II ELISA Kits all backed by our Guarantee+. ... Angiotensin II ELISA Kits available through Novus Biologicals. ...
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DOPAMINE D2 RECEPTOR STIMULATION INHIBITS ANGIOTENSIN II-INDUCED ...: Ingenta ConnectDOPAMINE D2 RECEPTOR STIMULATION INHIBITS ANGIOTENSIN II-INDUCED ...: Ingenta Connect

Angiotensin II and ET-1, both at 10 nmol/L, induced myocyte hypertrophy, as demonstrated by increased protein content and ... DOPAMINE D2 RECEPTOR STIMULATION INHIBITS ANGIOTENSIN II-INDUCED HYPERTROPHY IN CULTURED NEONATAL RAT VENTRICULAR MYOCYTES ... Therefore, the effects of the D2 receptor agonist bromocriptine and the D2 receptor antagonist haloperidol on angiotensin (Ang ... II- or endothelin (ET)-1-induced hypertrophy of cultured neonatal rat ventricular myocytes were investigated in the present ...
more infohttps://www.ingentaconnect.com/content/bsc/cep/2009/00000036/00000003/art00011

Angiotensin II regulation of renal vascular ENaC proteins.Angiotensin II regulation of renal vascular ENaC proteins.

In renal epithelial tissue, ENaC expression is regulated by angiotensin II (Ang II). However, whether Ang II regulates vascular ... homeostatic role of angiotensin ii.. 3578396 - The interaction between serotonin and angiotensin ii in the chronically ... Angiotensin II / administration & dosage*. Animals. Blood Pressure / drug effects. Disease Models, Animal. Epithelial Sodium ... 8853336 - Brain angiotensin ii tonically modulates sympathetic baroreflex in rabbit ventrolateral.... 1999906 - ...
more infohttp://www.biomedsearch.com/nih/Angiotensin-II-Regulation-Renal-Vascular/19325536.html

Angiotensin II receptor blocker - WikipediaAngiotensin II receptor blocker - Wikipedia

Angiotensin II receptor blockers (ARBs), also known as angiotensin II receptor antagonists , AT1 receptor antagonists or ... They block the activation of AT1 receptors, preventing the binding of angiotensin II. Angiotensin II receptor blockers are used ... Kassler-Taub K, Littlejohn T, Elliott W, Ruddy T, Adler E (1998). "Comparative efficacy of two angiotensin II receptor ... Angiotensin II Type 1 Receptor Blockers at the US National Library of Medicine Medical Subject Headings (MeSH). ...
more infohttps://en.wikipedia.org/wiki/Angiotensin_II_receptor_blocker
  • The availability of selective, potent, orally active and long acting nonpeptide angiotensin II type 1 (AT1) receptor antagonists has provided the opportunity to obtain the benefits of selectively blocking the renin-angiotensin-aldosterone system at the level of the AT1 receptor that mediates most, if not all, of the important actions of angiotensin II, and avoid the nonspecificity of the angiotensin I converting enzyme inhibitors. (nih.gov)
  • 22-24 However, recent studies suggest that the AT 1B R predominantly mediates Ang II-induced contraction in mouse abdominal aorta, femoral artery, and mesenteric resistance vessels. (ahajournals.org)
  • First, monoclonal antibodies directed against osteopontin have been found completely to block the stimulatory effects of Ang II on cultured rat cardiac fibroblasts. (ahajournals.org)
  • The novelty of the medication lies in the fact that it is the first and only use of synthetic human angiotensin II to help maintain body blood pressure. (drugbank.ca)
  • Preclinical and clinical studies have shown that Ang II inhibition is pivotal to the treatment of heart failure and ischemic heart disease. (ahajournals.org)
  • 27-29 Exons 1 and 2 constitute the 5′-untranslated region (UTR) sequence, whereas exon 3 harbors the uninterrupted open reading frame (ORF) for the rAT 1A R and the entire 3′-UTR, which contains 2 polyadenylation sequences. (ahajournals.org)
  • Exons 1 and 2 encode for 5' untranslated mRNA sequence and exon 3 harbors the entire uninterrupted open reading frame. (thefullwiki.org)
  • Such renin release allows for the production of the alpha-2-globulin angiotensinogen predominantly in the liver and to some extent, the kidneys and other organs. (drugbank.ca)
  • The suggestion is that higher local concentrations of either angiotensin II or perindoprilat are achieved when a vessel is noradrenergically preconstricted by infused norepinephrine or lower body negative pressure. (ahajournals.org)
  • 18,19 In addition, Ang II has been shown to increase osteopontin mRNA expression in fresh samples of human myocardium. (ahajournals.org)
  • The immunomodulator FTY720 interferes with effector functions of human monocyte-derived dendritic cells," European Journal of Immunology , vol. 35, no. 2, pp. 533-545, 2005. (hindawi.com)
  • 1995). "Molecular characterization and chromosome localization of a human angiotensin II AT2 receptor gene highly expressed in fetal tissues. (thefullwiki.org)