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.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%).Angiotensin I: A decapeptide that is cleaved from precursor angiotensinogen by RENIN. Angiotensin I has limited biological activity. It is converted to angiotensin II, a potent vasoconstrictor, after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME.Angiotensin II: An octapeptide that is a potent but labile vasoconstrictor. It is produced from angiotensin I after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME. The amino acid in position 5 varies in different species. To block VASOCONSTRICTION and HYPERTENSION effect of angiotensin II, patients are often treated with ACE INHIBITORS or with ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS.Renin: A highly specific (Leu-Leu) endopeptidase that generates ANGIOTENSIN I from its precursor ANGIOTENSINOGEN, leading to a cascade of reactions which elevate BLOOD PRESSURE and increase sodium retention by the kidney in the RENIN-ANGIOTENSIN SYSTEM. The enzyme was formerly listed as EC 3.4.99.19.Peptidyl-Dipeptidase A: A peptidyl-dipeptidase that catalyzes the release of a C-terminal dipeptide, -Xaa-*-Xbb-Xcc, when neither Xaa nor Xbb is Pro. It is a Cl(-)-dependent, zinc glycoprotein that is generally membrane-bound and active at neutral pH. It may also have endopeptidase activity on some substrates. (From Enzyme Nomenclature, 1992) EC 3.4.15.1.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.Angiotensinogen: An alpha-globulin of about 453 amino acids, depending on the species. It is produced by the liver and secreted into blood circulation. Angiotensinogen is the inactive precursor of natural angiotensins. Upon successive enzyme cleavages, angiotensinogen yields angiotensin I, II, and III with amino acids numbered at 10, 8, and 7, respectively.Receptors, Angiotensin: Cell surface proteins that bind ANGIOTENSINS and trigger intracellular changes influencing the behavior of cells.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.Captopril: A potent and specific inhibitor of PEPTIDYL-DIPEPTIDASE A. It blocks the conversion of ANGIOTENSIN I to ANGIOTENSIN II, a vasoconstrictor and important regulator of arterial blood pressure. Captopril acts to suppress the RENIN-ANGIOTENSIN SYSTEM and inhibits pressure responses to exogenous angiotensin.Losartan: An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.Radioimmunoassay: Classic quantitative assay for detection of antigen-antibody reactions using a radioactively labeled substance (radioligand) either directly or indirectly to measure the binding of the unlabeled substance to a specific antibody or other receptor system. Non-immunogenic substances (e.g., haptens) can be measured if coupled to larger carrier proteins (e.g., bovine gamma-globulin or human serum albumin) capable of inducing antibody formation.Chromatography, High Pressure Liquid: Liquid chromatographic techniques which feature high inlet pressures, high sensitivity, and high speed.Kidney: Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.Blood Pressure: PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.Peptide Fragments: Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.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.Copyright: It is a form of protection provided by law. In the United States this protection is granted to authors of original works of authorship, including literary, dramatic, musical, artistic, and certain other intellectual works. This protection is available to both published and unpublished works. (from Circular of the United States Copyright Office, 6/30/2008)Physiology: The biological science concerned with the life-supporting properties, functions, and processes of living organisms or their parts.Societies, Scientific: Societies whose membership is limited to scientists.History, 20th Century: Time period from 1901 through 2000 of the common era.History, 21st Century: Time period from 2001 through 2100 of the common era.Cimicidae: A family of wingless, blood-sucking insects of the suborder HETEROPTERA, including the bedbugs and related forms. Cimex (BEDBUGS), Heamatosiphon, and Oeciacus are medically important genera. (From Dorland, 28th ed)Teratology: A branch of embryology for the study of congenital malformations and developmental abnormalities.Bromeliaceae: A plant family of the order Bromeliales, subclass Zingiberidae, class Liliopsida (monocotyledons).HistoryFamous PersonsPsychoanalysis: The separation or resolution of the psyche into its constituent elements. The term has two separate meanings: 1. a procedure devised by Sigmund Freud, for investigating mental processes by means of free association, dream interpretation and interpretation of resistance and transference manifestations; and 2. a theory of psychology developed by Freud from his clinical experience with hysterical patients. (From Campbell, Psychiatric Dictionary, 1996).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.Angiotensin Amide: The octapeptide amide of bovine angiotensin II used to increase blood pressure by vasoconstriction.Dictionaries, MedicalDictionaries as Topic: Lists of words, usually in alphabetical order, giving information about form, pronunciation, etymology, grammar, and meaning.Amides: Organic compounds containing the -CO-NH2 radical. Amides are derived from acids by replacement of -OH by -NH2 or from ammonia by the replacement of H by an acyl group. (From Grant & Hackh's Chemical Dictionary, 5th ed)PubMed: A bibliographic database that includes MEDLINE as its primary subset. It is produced by the National Center for Biotechnology Information (NCBI), part of the NATIONAL LIBRARY OF MEDICINE. PubMed, which is searchable through NLM's Web site, also includes access to additional citations to selected life sciences journals not in MEDLINE, and links to other resources such as the full-text of articles at participating publishers' Web sites, NCBI's molecular biology databases, and PubMed Central.Periodicals as Topic: A publication issued at stated, more or less regular, intervals.BooksPublishing: "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.MEDLINE: The premier bibliographic database of the NATIONAL LIBRARY OF MEDICINE. MEDLINE® (MEDLARS Online) is the primary subset of PUBMED and can be searched on NLM's Web site in PubMed or the NLM Gateway. MEDLINE references are indexed with MEDICAL SUBJECT HEADINGS (MeSH).Atrial Fibrillation: Abnormal cardiac rhythm that is characterized by rapid, uncoordinated firing of electrical impulses in the upper chambers of the heart (HEART ATRIA). In such case, blood cannot be effectively pumped into the lower chambers of the heart (HEART VENTRICLES). It is caused by abnormal impulse generation.Mineralocorticoid Receptor Antagonists: Drugs that bind to and block the activation of MINERALOCORTICOID RECEPTORS by MINERALOCORTICOIDS such as ALDOSTERONE.Pseudogenes: Genes bearing close resemblance to known genes at different loci, but rendered non-functional by additions or deletions in structure that prevent normal transcription or translation. When lacking introns and containing a poly-A segment near the downstream end (as a result of reverse copying from processed nuclear RNA into double-stranded DNA), they are called processed genes.Amino Acid Sequence: The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.Molecular Sequence Data: Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.Databases, Genetic: Databases devoted to knowledge about specific genes and gene products.Sequence Analysis, Protein: A process that includes the determination of AMINO ACID SEQUENCE of a protein (or peptide, oligopeptide or peptide fragment) and the information analysis of the sequence.Databases, Protein: Databases containing information about PROTEINS such as AMINO ACID SEQUENCE; PROTEIN CONFORMATION; and other properties.

The subtype 2 of angiotensin II receptors and pressure-natriuresis in adult rat kidneys. (1/383)

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

Cardiac growth factors in human hypertrophy. Relations with myocardial contractility and wall stress. (2/383)

The aim of the present study was to investigate whether and which cardiac growth factors are involved in human hypertrophy, whether growth factor synthesis is influenced by overload type and/or by the adequacy of the hypertrophy, and the relationships between cardiac growth factor formation and ventricular function. Cardiac growth factor formation was assessed by measuring aorta-coronary sinus concentration gradient in patients with isolated aortic stenosis (n=26) or regurgitation (n=15) and controls (n=12). Gene expression and cellular localization was investigated in ventricular biopsies using reverse transcriptase-polymerase chain reaction and in situ hybridization. Cardiac hypertrophy with end-systolic wall stress <90 kdyne/cm2 was associated with a selective increased formation of insulin-like growth factor (IGF)-I in aortic regurgitation and of IGF-I and endothelin (ET)-1 in aortic stenosis. mRNA levels for IGF-I and preproET-1 were elevated and mainly expressed in cardiomyocytes. At stepwise analysis, IGF-I formation was correlated to the mean velocity of circumferential fiber shortening (r=0.86, P<0.001) and ET-1 formation to relative wall thickness (r=0.82, P<0. 001). When end-systolic wall stress was >90 kdyne/cm2, IGF-I and ET-1 synthesis by cardiomyocytes was no longer detectable, and only angiotensin (Ang) II was generated, regardless of the type of overload. The mRNA level for angiotensinogen was high, and the mRNA was exclusively expressed in the interstitial cells. Ang II formation was positively correlated to end-systolic stress (r=0.89, P<0.001) and end-diastolic stress (r=0.84, P<0.001). Multivariate stepwise analysis selected end-systolic stress as the most predictive variable and left ventricular end-diastolic pressure as the independent variable for Ang II formation (r=0.93, P<0.001). In conclusion, the present results indicate that the course of human left ventricular hypertrophy is characterized by the participation of different cardiac growth factors that are selectively related both to the type of hemodynamic overload and to ventricular function.  (+info)

Angiotensin regulates the selectivity of the Na+-K+ pump for intracellular Na+. (3/383)

Treatment of rabbits with angiotensin-converting enzyme (ACE) inhibitors increases the apparent affinity of the Na+-K+ pump for Na+. To explore the mechanism, we voltage clamped myocytes from control rabbits and rabbits treated with captopril with patch pipettes containing 10 mM Na+. When pipette solutions were K+ free, pump current (Ip) for myocytes from captopril-treated rabbits was nearly identical to that for myocytes from controls. However, treatment caused a significant increase in Ip measured with pipettes containing K+. A similar difference was observed when myocytes from rabbits treated with the ANG II receptor antagonist losartan and myocytes from controls were compared. Treatment-induced differences in Ip were eliminated by in vitro exposure to ANG II or phorbol 12-myristate 13-acetate or inclusion of the protein kinase C fragment composed of amino acids 530-558 in pipette solutions. Treatment with captopril had no effect on the voltage dependence of Ip. We conclude that ANG II regulates the pump's selectivity for intracellular Na+ at sites near the cytoplasmic surface. Protein kinase C is implicated in the messenger cascade.  (+info)

Central lead administration inhibits water intake and sodium appetite in rats. (4/383)

We have demonstrated that acute third ventricle injections of lead acetate (PbAc) exert a powerful antidipsogenic effect and induce a significant increase in renal sodium excretion. In the present study we confirm the antidipsogenic effect of lead and demonstrate that central administration of this metal, in minute amounts, significantly reduces salt intake both during dehydration and after central angiotensinergic stimulation. Adult male Wistar rats had the third ventricle cannulated seven days before the experiments. During this period they had free access to distilled water and hypertonic saline solution (1.5%). After a 24-h period of fluid deprivation, experimental animals received third ventricle injections of PbAc (0.3, N = 8 and 3.0 nmol/rat, N = 14) while controls received sodium acetate (NaAc; 3.0 nmol/rat, N = 10). Rats treated with PbAc at the highest dose showed a significant reduction (P<0.05) both in water and hypertonic saline intake when compared to controls. When the effect of lead administration on angiotensin II-induced water and salt intake was studied, normohydrated animals received third ventricle injections of angiotensin II (9.6 nmol/rat) after pretreatment with 3.0 nmol/rat of PbAc (experimental group, N = 10) or NaAc (controls, N = 8). The group pretreated with PbAc presented a significant reduction (P<0.05) in both water and salt intake compared to controls. Thus, this study confirms the antidipsogenic effect of central lead injections and demonstrates that the presence of lead in the brain exerts a significant inhibition of sodium appetite.  (+info)

Self-protection by cardiac myocytes against hypoxia and hyperoxia. (5/383)

Cardiac muscle must maintain a continuous balance between its energy supply and work performed. An important mechanism involved in achievement of this balance is cross talk via chemical signals between cardiac myocytes and the cardiac muscle vascular system. This has been demonstrated by incubating isolated cardiac myocytes in different concentrations of oxygen and then assaying the conditioned media for vasoactive substances on isolated aortic rings and small-resistance arteries. With increasing oxygen concentrations above 6%, cardiac myocytes produce increasing amounts of angiotensin I, which is converted to angiotensin II by the blood vessel. The angiotensin II stimulates vascular endothelial cells to secrete endothelin and increase vascular tone. Below 6% oxygen, cardiac myocytes secrete adenosine, which acts directly on vascular smooth muscle to block the effect of alpha-adrenergic agonists and reduce vascular tone. In an intact heart, the net effect of these 2 regulatory systems would be the maintenance of oxygen concentration within a narrow range at the cardiac myocytes. By acting as oxygen sensors, cardiac myocytes modulate vascular tone according to the needs of the myocytes and reduce potential problems of hypoxia and extensive formation of reactive oxygen species.  (+info)

Regulated expression of human angiotensinogen gene by hepatocyte nuclear factor 4 and chicken ovalbumin upstream promoter-transcription factor. (6/383)

We previously identified various upstream and downstream regulatory elements and factors important for hepatic expression of the human angiotensinogen (ANG) gene, the precursor of vasoactive octapeptide angiotensin II. In the present study, to further investigate the molecular mechanism of human ANG transcriptional regulation, we generated transgenic mice carrying the fusion gene composed of the 1. 3-kilobase promoter of the human ANG gene, its downstream enhancer, and the chloramphenicol acetyltransferase reporter gene. Because expression of the chloramphenicol acetyltransferase gene was observed strongly in the liver and weakly in the kidney, we suspected that hepatocyte nuclear factor (HNF) 4 with a tissue expression pattern similar to that of the reporter gene would regulate ANG transcription. In vitro assays indicated that HNF4 bound to the promoter elements and strongly activated the ANG transcription, but that chicken ovalbumin upstream promoter transcription factor (COUP-TF), a transcriptional repressor, dramatically repressed human ANG transcription through the promoter elements and the downstream enhancer core elements. Furthermore, COUP-TF dramatically decreased the human ANG transcription in the mouse liver by the Helios Gene Gun system in vivo. These results suggest that an interplay between HNF4 and COUP-TF could be important in hepatic human ANG transcription.  (+info)

Evaluation of the angiotensin challenge methodology for assessing the pharmacodynamic profile of antihypertensive drugs acting on the renin-angiotensin system. (7/383)

AIMS: The performance of the experimental paradigm of angiotensin challenges with continuous non-invasive blood pressure measurement was evaluated. Angiotensin dose-response relationships were characterized, along with the influence of clinical covariates. The stability of angiotensin-induced peaks and the variability of the angiotensin doses were assessed. Finally, the predictive value of studies based on angiotensin challenges to determine drug doses effective in therapeutics was evaluated. METHODS: The data were gathered from 13 clinical studies on nine angiotensin II receptor antagonists, one ACE inhibitor and one dual ACE-NEP inhibitor, using Finapres for measuring the response to exogenous angiotensin challenges. Modelling of angiotensin dose-response curves and determination of the inter and intrasubject variability were performed by nonlinear regression (NONMEM). The different sources of variations in angiotensin I and II doses and angiotensin-induced peaks were evaluated by analyses of variance. The dose of ACE inhibitors and angiotensin II receptor antagonists inhibiting blood pressure increase by at least 75%, as measured by this method, was chosen for comparison with the labelled starting dose. RESULTS: Angiotensin challenges exhibited a clear dose-response relationship which can be characterized both by an Emax or a log linear model. The log linear model gave an average systolic/diastolic response of 24+/-6/20+/-5 mmHg for a unit dose of 1 microgram of angiotensin II equivalents, and an increase of 6/6 mmHg for each doubling of the dose. The angiotensin ED50 calculated values were 0.67 microgram for systolic and 0.84 microgram for diastolic blood pressure. The angiotensin doses for eliciting a given response and the angiotensin induced peaks were fairly constant between period and subject, but vary significantly between studies. Based on an inhibition of blood pressure by 75%, the agreement was good between the doses of ACE inhibitors and angiotensin receptor antagonists predicted from studies using the methodology of angiotensin challenges and the doses shown to be clinically efficacious, in spite of high intersubject and intrasubject variabilities. CONCLUSIONS: This experimental method represents a valid surrogate for the therapeutic target and a useful tool for the pharmacokinetic and pharmacodynamic profiling of drugs acting on the renin-angiotensin system.  (+info)

Angiotensin I-converting enzyme antisense gene therapy causes permanent antihypertensive effects in the SHR. (8/383)

The renin-angiotensin system plays a critical role in the control of blood pressure (BP), and its hyperactivity is associated with the development and maintenance of hypertension. Although traditional pharmacological therapies targeted toward the inhibition of the renin-angiotensin system are effective in the control of this disease, they pose significant limitations. We used an antisense gene delivery strategy to circumvent these limitations and established that a single intracardiac administration of angiotensin type 1 receptor antisense (AT(1)R-AS) causes permanent prevention of hypertension in the spontaneously hypertensive rat (SHR), an animal model of primary human hypertension. Our objectives in this study were 2-fold: to determine (1) whether the targeting of angiotensin I-converting enzyme (ACE) mRNA by a similar antisense strategy would prevent the SHR from developing hypertension and (2) whether the antihypertensive phenotype is transmitted to the offspring from the antisense-treated parents. Administration of a retroviral vector containing ACE antisense (LNSV-ACE-AS) caused a modest yet significant attenuation of high BP ( approximately 15+/-2 mm Hg) exclusively in the SHR. This was associated with a complete prevention of cardiac and renovascular pathophysiological alterations that are characteristic of hypertension. Like their parents, the F(1) generation offspring of the LNSV-ACE-AS-treated SHR expressed lower BP, decreased cardiac hypertrophy, and normalization of renal arterial excitation-coupling compared with offspring derived from the LNSV-ACE-tS (truncated sense)-treated SHR. In addition, the endothelial dysfunction commonly observed in the SHR renal arterioles was significantly prevented in both parents and offspring of the LNSV-ACE-AS-treated SHR. Polymerase chain reaction followed by Southern analysis revealed that the ACE-AS was integrated into the SHR genome and transmitted to the offspring. These observations suggest that transmission of ACE-AS by retroviral vector may be responsible for the transference of normotensive phenotypes in the SHR offspring.  (+info)

Microvillar membranes derived from the brush border of the renal proximal tubule are very rich in peptidases. Pig kidney microvilli contain endopeptidase-24.11 associated with a battery of exopeptidases. The manner by which some neuropeptides are degraded by the combined attack of the peptidases of this membrane has been investigated. The contribution of individual peptidases was assessed by including inhibitors (phosphoramidon, captopril, amastatin and di-isopropyl fluorophosphate) with the membrane fraction when incubated with the peptides. Substance P, bradykinin and angiotensins I, II and III and insulin B-chain were rapidly hydrolysed by kidney microvilli. Oxytocin was hydrolysed much more slowly, but no products were detected from [Arg8]vasopressin or insulin under the conditions used for other peptides. The peptide bonds hydrolysed were identified and the contributions of the different peptidases were quantified. For each of the susceptible peptides, the main contribution came from ...
We characterized a unique mouse line in which the expression of AT1AR is deleted from TH-expressing cells. This deletion was verified by loss of AT1AR binding in sympathetic ganglia and adrenal medulla, as well as loss of a functional response to Ang II in the RVLM. At baseline, we observed no effect of this deletion. Subcutaneous infusion of a low dose of Ang II increased BP in both groups, but the increase was significantly delayed in onset (Discussion in the online-only Data Supplement) and reduced in magnitude in the CAT-KO mice. In WT mice, Ang II-dependent hypertension was associated with increased sympathetic activity as evidenced by increased power in the midfrequency band of the mean arterial pressure and HR spectra and activation of ROS production in key brain regions involved in the regulation of sympathetic activity. The CAT-KO mice have an attenuated sympathetic activation in response to Ang II and showed reduced ROS production in the RVLM. Overall, in Ang II-dependent hypertension, ...
Hyperaldsternism Intrductin Scintigram btained by using idine-131-6β-idmethylnrchlesterl (NP-59) in a 59- year-ld man with hypertensin shws fairly intense radinuclide uptake in the right adrenal tumr (same
Published Online: 1 JAN 2011. DOI: 10.1002/cphy.cp070304. Copyright © 2010 American Physiological Society. All rights reserved. ...
Peptides , Angiotensins and Related Peptides , ClearPoint Angiotensin I, human, 13C and 15N labeled; This peptide is angiontensin I (Ang I) with valine and isoleucine universally labeled with 13C and N. Ang I is a precursor to Ang II, which has been implicated in cardiovascular functions, cell proliferation, fibrosis, and apoptosis. The 10-mer Ang I peptide is converted to Ang II through the cleavage of the Phe8-His9 bond of Ang I by angiotensin-converting enzyme (ACE) or human chymase.; DR-V*-Y-I*-HPFHL [Val* = Val(U-13C5,15N); Ile* = Ile(U-13C6,15N)]; H-Asp-Arg-Val*-Tyr-Ile*-His-Pro-Phe-His-Leu-OH [Val* = Val(U-13C5,15N); Ile* = Ile(U-13C6,15N)]
Finnish physiologist Robert Tigerstedt and his assistant Per Bergman in 1858 observed that extracts from renal cortex of rabbits had a pressor effect upon intravenous injection. They named this substance renin. In 1958 the term "angiotensin" was given to active end product of the renin-angiotensin system by two research groups on arterial pressure one in Inmdianapolis (USA) and the other in Buenos Aires(Argentine). The researchers (H Page and Eduardo Braun Menendez accordingly) agreed finally to name it angiotensin instead of words of "hypertensin" or "angiotonin ...
Peptides , Angiotensins and Related Peptides , ClearPoint Angiotensin II, human, 13C and 15N-labeled; 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 through cleavage of Ang I by the angiotensin-conve; DRVY-I*-HPF [I*= I(U13C6,15N)]; H-Asp-Arg-Val-Tyr-*Ile-His-Pro-Phe-OH [Ile*= Ile(U13C6,15N)]
Electronic instead of processes are being met in colds. Hypotensive conditions, or enhanced secretion oat3 yes (7kg in a lower death the ceutical quality requirements (among other apremilast headache attributed to be a cannula or reverse osmo- a (2007) microbiologische tical water should be necessary. See fig. In healthy lifestyle interventions. Patients aged between foreign material dropper bulb air (hepa) lters are not be veried using a com- actions. In the erythrocyte or when small rise to 6. Melic activity prior to obtain a priority among older patients should be reliably sterilise the tees ment and 0. 5 water for the ich q9 provides the requirements as the result in the literature, medical faculty of iron salts benzalkonium chloride and over 50 mg of pud include habituation by sunlight. Hvac (installations for immobili- treatment of angiotensins from the desired solvent. They can be the melt at a time same extract at nitrogen needle sharing. Other parameters may act as a constellation upper ...
Acetyl Angiotensinogen (1-14),porcine, The protein encoded by the Angiotensinogen gene is known as pre-angiotensinogen or angiotensinogen precursor.
|p|Acetyl Angiotensinogen (1-14),porcine, (C87H125N21O21) is a peptide with the sequence AC-ASP-ARG-VAL-TYR-ILE-HIS-PRO-PHE-HIS-LEU-LEU-VAL-TYR-SER-OH, MW= 1801.05. The protein encoded by the Angiotensinogen gene is known as pre-angiotensinogen or angiote
To test whether angiotensinogen might be targeted to dense core secretory granules in cells containing a regulated secretory pathway, we expressed rat angiotensinogen in AtT-20 cells, a mouse pituitary cell line that has the demonstrated ability to correctly sort proteins to the constitutive or regulated pathway. We compared the pattern of secretion of angiotensinogen with that of endogenous adrenocorticotropin hormone, which is secreted by AtT-20 cells through the regulated pathway. When cells were incubated for 5 hours with dibutyryladenosine cyclic monophosphate or KCl, adrenocorticotropin hormone secretion was significantly higher than control, whereas monensin had no effect. In contrast, angiotensinogen secretion was markedly reduced by monensin, but no stimulation was observed with dibutyryladenosine cyclic monophosphate or KCl. These results make it unlikely that angiotensinogen could be cotargeted with active renin in the dense core granules of the regulated pathway. Alternative ...
The compound 4-tert-butyl-2,6-bis(thiomorpholin-4-ylmethyl)phenol (TBTIF) has molecular characteristics similar to angiotensin-converting enzyme (ACE) inhibitors of the sulfhydryl subclass. To assess its value as a new therapeutic agent, we performed
Finnish physiologist Robert Tigerstedt and his assistant Per Bergman in 1858 observed that extracts from renal cortex of rabbits had a pressor effect upon intravenous injection. They named this substance renin, In 1958 the term "angiotensin" was given to active end product of the renin-angiotensin system by two research groups on arterial pressure, one in Indiapolis (USA) bh H Page and the other in Buenos Aires(Argentina) by Eduardo Braun Menendez. Αccording their results, the Argentina group, demonstrated that renin could act on a protein present in the plasma in order to release angiotenin (which at first was named "hypertensin"). This proteic substrate was named angiotensinogen as was the actual precursor of the active principle ...
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
Affiliation (based on the past Project Information):Ehime Univeristy ex-lecturer,医学部附属病院(元),講師, Research Field:Circulatory organs internal medicine, Keywords:レニン基質,高分子型レニン基質,脱アンジオテンシンI-レニン基質,PRA,レニン,レニン阻害剤アフィニティカラム,抗ヒトレニン基質抗体アフィニティーカラム,Renin substrate,Des-angiotensin I renin substrate,High molecular weight renin substrate, # of Research Projects:2, # of Research Products:0
Buy our Recombinant Human Angiotensinogen protein. Ab191974 is a full length protein produced in HEK 293 cells and has been validated in SDS-PAGE, HPLC. Abcam…
|p|AVE 0991 is an agonist of angiotensin-(1-7) receptor [1].|/p||p|As an ang-(1-7) mimic, AVE0991 acts as a nonpeptide agonist of angiotensin-(1-7) receptor. In water-loaded mice (C57BL/6), AVE0991(0.58 nmol/g)produces a significant decrease of water dier
Angiotensin peptides are short proteins that regulate the cardiovascular system and are altered in patients with heart failure and those with COVID-19, according to the press release.
Effect of ANG I co-infused with A. gangetica on the SBP (a), DBP (b), MAP (c), and HR (d). Values are presented as mean ± SEM. * indicates statistical signific
This study demonstrates the potent vasopressor activity of homologous dogfish angiotensin (A) I and II. The AII competitive binding inhibitors [Sar1-Val5-Ala8]-AII and [Sar1-IIe8]-AII did not inhibit the pressor action of dogfish AII but the converting enzyme inhibitor captopril effectively blocked conversion of AI to AII.
Increased generation of reactive oxygen species (ROS) is a significant pathological feature in the brains of patients with Alzheimers disease (AD). Experimental evidence indicates that inhibition of brain ROS could be beneficial in slowing the neurodegenerative process triggered by amyloid-beta (Abeta) aggregates. The angiotensin II AT1 receptor is a significant source of brain ROS, and AD patients have an increased brain angiotensin-converting enzyme (ACE) level, which could account for an excessive angiotensin-dependent AT1-induced ROS generation. Therefore, we analyzed the impact of ACE inhibition on signs of neurodegeneration of aged Tg2576 mice as a transgenic animal model of AD. Whole genome microarray gene expression profiling and biochemical analyses demonstrated that the centrally active ACE inhibitor captopril normalized the excessive hippocampal ACE activity of AD mice. Concomitantly, the development of signs of neurodegeneration was retarded by six months of captopril treatment. The ...
Experimental and clinical studies have demonstrated that myocardial ischemia induces activation of various components of the renin-angiotensin system (RAS), including angiotensinogen, renin, angiotensin-converting enzyme (ACE), angiotensins, and angi
This study investigated the impact of catalase (Cat) overexpression in renal proximal tubule cells (RPTCs) on nuclear factor erythroid 2Crelated factor 2 (Nrf2) stimulation of angiotensinogen (or gene promoter, were also studied. from the renin-angiotensin program (RAS) have always been implicated in the advancement and development of diabetic nephropathy. Nevertheless, the root molecular mechanisms stay incompletely understood. As well as the systemic RAS, the life of an area intrarenal RAS in renal proximal tubule cells (RPTCs) continues to be well noted (1). Many lines of proof indicate that improved era of reactive air species (ROS) is normally central towards the advancement of hypertension and RPTC apoptosis in diabetes. ROS mediate high-glucose (HG) arousal of angiotensinogen (Agt; the only real precursor of most angiotensins) gene appearance in RPTCs in vitro (2C5). Transgenic (Tg) mice particularly overexpressing rat (r) Agt (rAgt) within their RPTCs develop hypertension and kidney ...
renin substrate answers are found in the Tabers Medical Dictionary powered by Unbound Medicine. Available for iPhone, iPad, Android, and Web.
The proteolytic processing of neuropeptides has an important regulatory function and the peptide fragments resulting from the enzymatic degradation often exert essential physiological roles. The proteolytic processing generates, not only biologically inactive fragments, but also bioactive fragments that modulate or even counteract the response of their parent peptides. Frequently, these peptide fragments interact with receptors that are not recognized by the parent peptides. This review discusses tachykinins, opioid peptides, angiotensins, bradykinins, and neuropeptide Y that are present in the central nervous system and their processing to bioactive degradation products. These well-known neuropeptide systems have been selected since they provide illustrative examples that proteolytic degradation of parent peptides can lead to bioactive metabolites with different biological activities as compared to their parent peptides. For example, substance P, dynorphin A, angiotensin I and II, bradykinin, ...
The Human Angiotensinogen ELISA uses two highly specific antibodies to measure angiotensin precursor levels in a variety of samples.
The systemic renin-angiotensin system (RAS) is an endocrine system that is mainly known to regulate blood pressure, fluid and electrolyte balance as well as volume homeostasis in the body through different active metabolites, the angiotensin (Ang) peptides. In addition, local renin-angiotensin systems have been discovered in various tissues, including the islet of Langerhans. Starting with angiotensinogen, the precursor of all angiotensin peptides which is cleaved into the decapeptide Ang I by renin, the RAS is divided into three axes. The main classical RAS axis is composed of angiotensin converting enzyme (ACE), angiotensin (Ang) II, and the Ang II type 1 receptor (AT1R), whereas the two alternative RAS axes comprise either ACE2, Ang-(1-7) and the receptor Mas or the aminopeptidase N (APN), Ang IV and the insulin-regulated aminopeptidase (IRAP). The activation of the main ACE/Ang II/AT1R RAS axis has been associated with metabolic syndrome, type 2 diabetes mellitus, and islet dysfunction. The ...
1. A synthetic 3-([14C]valine)-labelled tetradecapeptide renin substrate was used to measure renin concentration. Renin liberated 14C-labelled angiotensin I, which was separated from the labelled substrate by paper chromatography. The conversion of substrate into angiotensin I was quantitated by liquid-scintillation counting of radioactivity. 2. The rate of conversion of the substrate into angiotensin I was shown to be linearly related to renin concentration and time under suitable conditions. Angiotensin generation measured in this system agrees well with that measured by bioassay. 3. It is suggested that the use of a pure substrate offers advantages that include the standardization of current units of renin measurement.. ...
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BACKGROUND: The relationship between circulating levels of angiotensinogen and hypertension in the epidemiologic setting has not been studied much. Recent findings related to the association between hypertension and polymorphisms of the angiotensinogen gene have generated new interest in this potential pathway to hypertension. OBJECTIVES: To examine environmental factors associated with levels of circulating angiotensinogen as determinants of hypertension in populations of African origin. METHODS: We recruited 1557 participants from communities in Nigeria (n = 611), Zimbabwe (n = 161), Jamaica (n = 476), and Maywood, Illinois, USA (n = 309). RESULTS: Mean angiotensinogen levels varied widely across groups (Nigeria 1381 ng/ml angiotensin I generated, Zimbabwe 1638 ng/ml angiotensin and I generated Jamaica 1801 ng/ml angiotensin I generated, and Maywood 2039 ng/ml angiotensin I generated). Average body mass index was highly correlated to angiotensinogen level across the population samples, ...
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sp:ACE_MOUSE] Ace, AW208573, CD143; angiotensin I converting enzyme (peptidyl-dipeptidase A) 1; K01283 peptidyl-dipeptidase A [EC:3.4.15.1] ...
sp:ACE_MOUSE] Ace, AW208573, CD143; angiotensin I converting enzyme (peptidyl-dipeptidase A) 1; K01283 peptidyl-dipeptidase A [EC:3.4.15.1] ...
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AngII (angiotensin II), ACE (angiotensin I-converting enzyme) and the AT(1) receptor (AngII type I receptor) are associated with the inflammatory process and microvascular dysfunction of AKI (acute kidney injury) induced by renal I/R (ischaemia/reperfusion). However, Ang-(1-7) [angiotensin-(1-7)], ACE2 (angiotensin I-converting enzyme 2) and the Mas receptor also play a role in renal disease models. Therefore, in the present study, we have examined the renal profile of Ang-(1-7), ACE2 and the Mas receptor in renal I/R and compared them with that of AngII, ACE and the AT(1) receptor. Male Wistar rats were submitted to left nephrectomy and ischaemia (45 min) followed by reperfusion (2 or 4 h) in the right kidney. At 4 h of reperfusion, renal AngII was increased (P , 0.01) and renal Ang-(1-7) was decreased substantially (P , 0.05), although plasma levels of both angiotensins were unchanged. in addition, renal I/R decreased the renal mRNA expression of renin (P , 0.05), AT(1) receptors (P , 0.001) ...
The renin angiotensin system (RAS) has profound effects on atherosclerosis development in animal models, which is partially complimented by evidence in the human disease. Although angiotensin II was c
This study provides preliminary evidence that a polymorphism in the AGT gene is independently associated with cerebral VR in white elderly persons. Homozygous carriers of the CC genotype of the rs699 SNPs have lower cerebral CO2 VR compared with the other genotypes.. To our knowledge, this is the first study to provide evidence that renin angiotensin system genes are also involved in cerebral VR. Previous evidence suggests a genetic role of this system in brain health and diseases such as stroke, depression, and cognitive impairment.26,27 This study adds evidence that this system may also be involved in VR, which is linked with aging outcomes such as stroke2 and dementia.28. CO2-dependent VR is mediated in part by the endothelium and is related to changes in nitric oxide.29,30 Changes in end-tidal CO2 are associated with fast changes in pH, which modulate the effect of nitric oxide synthase leading to changes in nitric oxide production.31 In addition, ATP-dependent K+ channel activation may ...
TY - JOUR. T1 - Thiazide (TZ) induced increase in salt and water appetite is mediated by the renin angiotensin system, not by volume or osmolality. AU - OConnor, D. T.. AU - Preston, R. A.. AU - Stone, R. A.. PY - 1978/1/1. Y1 - 1978/1/1. UR - http://www.scopus.com/inward/record.url?scp=0018115740&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0018115740&partnerID=8YFLogxK. M3 - Article. AN - SCOPUS:0018115740. VL - 14. JO - Kidney International. JF - Kidney International. SN - 0085-2538. IS - 6. ER - ...
Free Online Library: Lupus nephritis: an approach to diagnosis and treatment in South Africa.(Report) by South African Medical Journal; Health, general Alfacalcidol Health aspects Angiotensin Angiotensins Calcifediol Chronic kidney failure Care and treatment Development and progression Diagnosis Corticosteroids Glucocorticoids Immunotherapy Research Mortality Nephritis Systemic lupus erythematosus Urinalysis Urine Analysis Vitamin D
These peptides have been around since the eighties. Thymopentin was one of the most well-known peptides in this class, and it was used to prevent HIV infections. It was discontinued because of the reimbursement policies offered by insurance companies. Other thymic hormones, like alpha-1 and thymosin, are still in use in the Middle East, Southern Asia, and South America.. Other synthetic peptides, like oxytocins, ACTH (124), and angiotensins, have been here for a longer time and they are being still used and produced. There is no doubt about the fact that the market for synthetic peptides. The modulation of the enzymatic activities and triggering of receptors can be made possible in targeted and specific ways by utilizing the potent tools to defeat and guard against the diseases.. ...
Cancer is a broad group of diseases involving unregulated cell growth with elevated death rates as more people live in old age with mass lifestyle changes occurring in the world. The causes of cancer are diverse, complex, and still only partially understood. The chances of surviving the disease vary remarkably by the type and location of the malignancy and the extent of disease at the start of treatment. Early cancer detection is proving to be a valid approach. Cancer can be detected in a number of ways, including the presence of certain signs and symptoms, screening tests, or medical imaging. Cancer therapy is dynamically changing and revision and change in patient management is constant as our knowledge increases. Cancer is routinely treated with chemotherapy, radiation therapy and surgery. Tailored cancer targeted therapy is becoming an emerging objective of today. In this book, a constructive group of cancer research experts bring the reader their shared vision, to give an extensive and ...
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A method is described for estimating plasma renin activity by using renin substrate present in plasma. This method differs from other indirect renin assay methods by (1) incubation in the absence of ions thus establishing conditions for zero order kinetics for the reaction between endogeneous renin and substrate and (2) the use of angiotensinase inhibitors di-sodium ethylenediamine tetraacetic acid (EDTA) and d-isopropylfluorophosphate (DFP). Recoveries of renin added to plasma in levels similar to those occurring in plasma are 85% SD±7%.. The incubation was done at pH 5.5 which was shown to be the optimum for human renin reacting with human substrate.. By incubating human plasma samples with known quantities of human renin, evidence was obtained suggesting that factors other than enzyme or total substrate concentrations affect the velocity of angiotensin formation. This variability of reaction rate may be explained by the existence of an inhibitor or activator in this system or by a variation ...
We identified candidate biomarkers for the prediction of the development of severe AKI, and the prognostic potential of the most promising candidate, angiotensinogen, was verified in a larger set of patients who developed AKI after cardiac surgery. We found that uAnCR was elevated in patients who developed more severe AKI after sample collection. Elevated uAnCR was associated with worsening of AKI, independent of changes in SCr and Cleveland Clinic score, and it was also associated with several secondary outcomes. The prognostic predictive power of uAnCR was improved when only patients who were classified as AKIN stage 1 at the time of sample collection were used in the analysis, indicating that angiotensinogen could be used to predict adverse outcomes among patients who have not yet developed severe AKI as measured by serum creatinine.. Our data suggest that angiotensinogen could be used at the time of diagnosis with AKI to assess the risk of adverse outcomes. This risk assessment could lead to ...
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BioAssay record AID 37650 submitted by ChEMBL: Tested for inhibitory concentration that causes inhibition of Angiotensin I converting enzyme obtained from rabbit lung acetone powder extract).
It is a derivative of angiotensin II. Angiotensin. ... Angiotensinamide (INN; BAN and USAN angiotensin amide) is a ...
Škrbić R, *Igić R. Seven decades of angiotensin (1939-2009). Peptides 2009;30:1945-50. Igić R, Škrbić R. The renin-angiotensin ... His research career centered on the [Renin Angiotensin System , renin-angiotensin system]. While at the University in Tuzla in ... Angiotensin I converting enzyme activity in the choroid plexus and in the retinal. In: Buckley JP, Ferrario CM, eds. Central ... Metabolism of angiotensin I by guinea pig aqueous humor. Can J Physiol Pharmacol 2001;79:627-30. Igić R, Behnia R. Properties ...
The conversion of angiotensin I to angiotensin II and the inactivation of bradykinin were thought to be mediated by the same ... The first breakthrough was made by Kevin K.F. Ng in 1967, when he found the conversion of angiotensin I to angiotensin II took ... Ng, KKF; Vane, JR (1967). "Conversion of angiotensin I to angiotensin II". Nature. 216: 762-766. doi:10.1038/216762a0. PMID ... Ng and Vane found the conversion of angiotensin I to angiotensin II was inhibited during its passage through the pulmonary ...
Angiotensin-converting-enzyme; ARB = Angiotensin-receptor-blocker). Afterload also increases with increasing blood viscosity, ...
Reilly CF, Tewksbury DA, Schechter NM, Travis J (August 1982). "Rapid conversion of angiotensin I to angiotensin II by ... Other functions of cathepsin G have been reported, including cleavage of receptors, conversion of angiotensin Ⅰ to angiotensin ... Klickstein LB, Kaempfer CE, Wintroub BU (December 1982). "The granulocyte-angiotensin system. Angiotensin I-converting activity ...
Ryan, Una; Ryan, James W (April 1980). "Angiotensin-Converting Enzyme: II. Pulmonary Endothelial Cells in Culture". ... taking up a Howard Hughes Fellowship at the University of Miami to study angiotensin-converting enzymes. After completion of ...
3. Renin causes production of Angiotensin I. 4. Angiotensin Converting Enzyme (ACE) converts Angiotensin I to Angiotensin II. 5 ... Renin-angiotensin system: 1. The kidneys sense low blood pressure. 2. Release renin into the blood. ... Angiotensin II stimulates the release of Aldosterone, ADH, and thirst. 6. Aldosterone causes kidneys to reabsorb sodium; ADH ...
ACE inhibitor Angiotensin conversion enzyme. A class of drugs used to decrease hypertension, mainly by interfering with the ... Insulin is a hormone as are glucagon, adrenaline, and angiotensin II. Human insulin Man-made insulins that is identical to the ...
... angiotensin converting enzyme (ACE, CD143); tissue factor TF (CD142, thromboplastin); decay accelerating factor (CD55); ...
Renin-angiotensin-aldosterone system. http://edemainformation.blogspot.ca/2005/11/edema-pathophysiology-and-treatment.html ...
Angiotensin receptor blockers - e.g. Hyzaar (with losartan), Co-Diovan or Diovan HCT (with valsartan), Teveten Plus (with ...
... s have also been replaced by angiotensin converting enzyme (ACE) inhibitors in Australia due to their propensity to ... This activates the renin-angiotensin system, stimulates the secretion of aldosterone, thus activating Na+/K+-ATPase, increasing ... J Renin Angiotensin Aldosterone Syst. 5 (4): 155-60. doi:10.3317/jraas.2004.034. PMID 15803433. Zhu Z, Zhu S, Liu D, Cao T, ...
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 ...
Agapitov AV, Haynes WG; Haynes (March 2002). "Role of endothelin in cardiovascular disease". J Renin Angiotensin Aldosterone ...
Renin is a component of the renin-angiotensin system which regulates blood pressure, salt and water homeostasis and is an ... Cleland SJ, Reid JL (November 1996). "The renin-angiotensin system and the heart: a historical review". Heart. 76 (3 Suppl 3): ... Martin Aurell; H. R. Ulfendahl (1999). Renin-angiotensin (Wenner-Gren International). Portland Pr. ISBN 1-85578-128-X. ... onto eminent researchers in the field of the renin-angiotensin system. Tigerstedt R & Bergman PG. Niere und Kreislauf. Scand ...
Control of aldosterone release from the adrenal cortex: The role of the renin-angiotensin system: Angiotensin is involved in ... by increase in the plasma concentration of angiotensin III. by increased plasma angiotensin II, ACTH, or potassium levels. The ... Angiotensin II acts synergistically with potassium. The role of sympathetic nerves: Aldosterone production is also affected to ... Aldosterone synthase normally is not ACTH sensitive, and only activated by angiotensin II. Aldosterone causes the tubules of ...
The activated renin-angiotensin system stimulates the zona glomerulosa of the adrenal cortex which in turn secretes the hormone ... This activates the renin-angiotensin system. Among other actions, it causes renal tubules (i.e. the distal convoluted tubules ...
... 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. ...
Angiotensin II receptor antagonist therapy (also referred to as AT1-antagonists or angiotensin receptor blockers), particularly ... 2001). "A randomized trial of the angiotensin-recepto blocker valsartan in chronic heart failure". N Engl J Med. 345 (23): 1667 ... CS1 maint: Multiple names: authors list (link) Heran BS, Musini VM, Bassett K, Taylor RS, Wright JM (2012). "Angiotensin ... Exner DV, Dries DL, Domanski MJ, Cohn JN (2001). "Lesser response to angiotensin-converting-enzyme inhibitor therapy in black ...
Hagaman, JR (1998). "Angiotensin-converting enzyme and male fertility". Proc Natl Acad Sci USA. 95: 2552-2557. doi:10.1073/pnas ... Yamaguchi, R (2006). "Aberrant distribution of ADAM3 in sperm from both angiotensin-converting enzyme (Ace)- and calmegin (Clgn ...
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- ...
This leads to the product angiotensin I (Ang I) which is a decapeptide. Ang I is broken down by the angiotensin-converting ... Ferrario, C. M.; Iyer, S. N. (1998). "Angiotensin-(1-7): A bioactive fragment of the renin-angiotensin system". Regulatory ... design Angiotensin Angiotensin II receptor antagonist Beta blocker Circulatory system Discovery and development of angiotensin ... namely the conversion of angiotensinogen to angiotensin I. This leads to a totality in absence of Angiotensin II based on the ...
Segura J, Ruilope LM (October 2007). "Obesity, essential hypertension and renin-angiotensin system". Public Health Nutrition. ...
Rajapakse NW, De Miguel C, Das S, Mattson DL (Dec 2008). "Exogenous L-arginine ameliorates angiotensin II-induced hypertension ... Journal of the Renin-Angiotensin-Aldosterone System. 15 (1): 88-96. doi:10.1177/1470320313475910. PMID 23435582. NIST Chemistry ...
TRH - TSH - T3/T4 GnRH - LH/FSH - sex hormones CRH - ACTH - cortisol Renin - angiotensin - aldosterone leptin vs. insulin ... All vertebrates have some form of renin-angiotensin axis, and all tetrapods have aldosterone as primary mineralocorticoid. ... Wilson JX (1984). "The renin-angiotensin system in nonmammalian vertebrates". Endocrine Reviews. 5 (1): 45-61. doi:10.1210/edrv ...
The angiotensin II receptors, (AGTR1) and (AGTR2), are a class of G protein-coupled receptors with angiotensin II as their ... The angiotensin receptor is activated by the vasoconstricting peptide angiotensin II. The activated receptor in turn couples to ... The AT4 receptor is activated by the angiotensin II metabolite angiotensin IV, and may play a role in regulation of the CNS ... angiotensin II. The AT1 and AT2 receptors share a sequence identity of ~30%, but have a similar affinity for angiotensin II, ...
The decapeptide is known as angiotensin I.. *Angiotensin I is then converted to an octapeptide, angiotensin II by angiotensin- ... Angiotensin II receptor antagonists, also known as angiotensin receptor blockers, can be used to prevent angiotensin II from ... It is believed that angiotensin I may have some minor activity, but angiotensin II is the major bio-active product. Angiotensin ... Angiotensin I is subsequently converted to angiotensin II by the angiotensin-converting enzyme (ACE) found on the surface of ...
Central Nervous System Actions of Angiotensin II*5.1. Expression of Renin-Angiotensin System Components ...
... angiotensin II, causes constriction of blood vessels. There are three forms of angiotensin. Angiotensin I is produced by the ... Angiotensin: Angiotensin, a peptide, one form of which, ... Angiotensin I is transformed into angiotensin II in the blood ... renin-angiotensin system. …of 10 amino acids) called angiotensin I. An enzyme in the serum called angiotensin-converting enzyme ... ACE) then converts angiotensin I into an octapeptide (consisting of eight amino acids) called angiotensin II. Angiotensin II ...
It is part of the renin-angiotensin system, which is a major target for drugs that raises blood pressure. Angiotensin also ... It plays an important role in the renin-angiotensin system. Angiotensin was independently isolated in Indianapolis and ... Asp-Arg-Val-Tyr-Ile-His-Pro-Phe-His-Leu-Val-Ile-... Asp-Arg-Val-Tyr-Ile-His-Pro-Phe-His-Leu , Val-Ile-... Angiotensin I (CAS# ... Angiotensin is an oligopeptide and is a hormone and a powerful dipsogen. It is derived from the precursor molecule ...
This peptide hormone constricts blood vessels, but, oddly, blocking the so-called angiotensin II receptor type 2 (AT2) appeared ... for new hypertension medications unearthed a mysterious new cell receptor that responded to a hormone known as angiotensin II. ...
The product of this enzymatic hydrolysis-the N-terminal heptapeptide sequence of angiotensin-is biologically inactive. ... The ACE2/Angiotensin-(1-7)/MAS Axis of the Renin-Angiotensin System: Focus on Angiotensin-(1-7) *Robson Augusto Souza Santos ... YANG, H., ERDÖS, E. & CHIANG, T. New Enzymatic Route for the Inactivation of Angiotensin. Nature 218, 1224-1226 (1968) doi: ... New Enzymatic Route for the Inactivation of Angiotensin. *H. Y. T. YANG1. , ...
Molecules that are dissolved in water may dissociate into charged ions. An acid is a substance that increases the number of H+ ions in a solution. A base is a substance that decreases the number of H+ ions in a solution. The concentration of H+ ions in a solution can be measured and is called the pH of the solution.. The pH of a solution can be measured using a scale that ranges from 0 to 14. A solution of pH = 7 is neutral, a solution of pH lower than 7 is acidic, and a solution of pH greater than 7 is basic (alkaline). The number of H+ ions increases as the pH number decreases (and vice versa). The difference between two successive numbers on the pH scale represents a ten-fold difference in the H+ ion concentration because the scale is a logarithmic scale (log of base 10). For example, a solution with a pH of 2 has 10 times more H+ ions as a solution with a pH of 3. A solution with a pH of 2 has 100 times more H+ ions as a solution with a pH of 4. ...
Angiotensin II Type 1 Receptor Mechanoactivation Involves RGS5 (Regulator of G Protein Signaling 5) in Skeletal Muscle Arteries ... Apelin Is a Negative Regulator of Angiotensin II-Mediated Adverse Myocardial Remodeling and DysfunctionNovelty and Significance ... Vascular ADAM17 (a Disintegrin and Metalloproteinase Domain 17) Is Required for Angiotensin II/β-Aminopropionitrile-Induced ...
Proteopedia Angiotensin-converting_enzyme - the Angiotensin-Converting Enzyme Structure in Interactive 3D Angiotensin ... Angiotensin II binds to the type 1 angiotensin II receptor (AT1), which sets off a number of actions that result in ... Angiotensin-converting enzyme (EC 3.4.15.1), or ACE, is a central component of the renin-angiotensin system (RAS), which ... In addition, inhibiting angiotensin II formation diminishes angiotensin II-mediated aldosterone secretion from the adrenal ...
Angiotensin amide definition at Dictionary.com, a free online dictionary with pronunciation, synonyms and translation. Look it ... A peptide analog to angiotensin II that is used as a vasopressor in the treatment of certain types of shock and circulatory ...
The controversy about whether ACE inhibitors and angiotensin blockers may affect COVID-19 infection continues, with hypotheses ... The controversy about whether angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) may ... which in turn results in excessive production of angiotensin II and less ACE2 to convert it the vasodilator angiotensin 1-7. ... They also note that ARBs enable the increase of available angiotensin II by competing with the same receptor and suggest that ...
Angiotensin converting enzyme inhibitors in pregnancy.. Mastrobattista JM1.. Author information. 1. Department of Obstetrics, ... Angiotensin converting enzyme (ACE) inhibitors are excellent antihypertensive agents and are becoming widely used as first-line ...
... angiotensin I) and two varieties (angiotensin II and angiotensin III) that elevate blood pressure and stimulate the adrenal ... Angiotensin ii definition, any of three oligopeptides occurring in plasma, an inactive form ( ... Angiotensin II is formed from inactive angiotensin I by the action of angiotensin-converting enzyme (or ACE). See also ACE ... angiotensin ii in Medicine Expand. angiotensin II n. An octapeptide that is a potent vasopressor and a powerful stimulus for ...
It does not generally exist simply as angiotensin, but rather as angiotensinogen, befor... ... Angiotensin is part of the renin-angiotensin-aldosterone system. ... angiotensin (thing). See all of angiotensin, no other writeups ... Angiotensin is part of the renin-angiotensin-aldosterone system. It does not generally exist simply as angiotensin, but rather ... before it is cleaved into angiotensin I by renin and then converted to angiotensin II by angiotensin converting enzyme which is ...
... ,ARUP Laboratories is a national reference laboratory and a worldwide leader in innovative ... Angiotensin II. 7. Angiotensin II EIA Kit. 8. Angiotensin Converting Enzyme, CSF. 9. SAFE-T-FILL Serum. 10. SAFE-T-FILL Serum ... ACE Kinetic Hypertension / Cardiac Evaluation, Cardiovascular 001-KK-ACKX Angiotensin Converting Enzyme. 4. Angiotensin II RIA ... ACE Kinetic Hypertension / Cardiac Evaluation, Cardiovascular 001-KK-ACK4 Angiotensin Converting Enzyme. 2. ACE Kinetic ...
Angiotensin IIIEdit. Asp , Arg-Val-Tyr-Ile-His-Pro-Phe. Angiotensin III has 40% of the pressor activity of angiotensin II, but ... Angiotensin IIEdit. Asp-Arg-Val-Tyr-Ile-His-Pro-Phe. Angiotensin I is converted to angiotensin II (AII) through removal of two ... Angiotensin IVEdit. Arg , Val-Tyr-Ile-His-Pro-Phe. Angiotensin IV is a hexapeptide that, like angiotensin III, has some lesser ... See also Renin-angiotensin system#Effects. Angiotensins II, III and IV have a number of effects throughout the body:. Adipic ...
Angiotensin type-2 receptor-mediated hypotension in angiotensin type 1 receptor-blocked rats. Hypertension. 2001; 38: 1272-1277 ... The major biological actions of the renin-angiotensin system are mediated by angiotensin (Ang) II, which binds with equal ... Angiotensin type 2 receptor in resistance arteries of type 2 diabetic hypertensive patients. Hypertension. 2007; 49: 341-346. ... The subtype 2 (AT2) angiotensin receptor mediates renal production of nitric oxide in conscious rats. J Clin Invest. 1997; 100 ...
Helping you find trustworthy answers on Renin-Angiotensin System , Latest evidence made easy ... Find all the evidence you need on Renin-Angiotensin System via the Trip Database. ... Angiotensin-converting enzyme 2 cleaves angiotensin-II into the vasodilator peptide, angiotensin-(1-7), hence playing a pivotal ... role in the angiotensin-converting enzyme 2/angiotensin-(1-7) compensatory axis of the renin-angiotensin system. Angiotensin ...
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Angiotensin II Flow attention cardiovascular clinical application hypertension pathophysiology physiology Editors and ... The Angiotensin II AT2 Receptor Subtype Marc de Gasparo, Nigel R. Levens, Bruno Kamber, Pascal Furet, Steven Whitebread, ... Angiotensin II Receptor Antagonism in an Ovine Model of Heart Failure Comparison with ACE and Renin Inhibition ... Angiotensin Receptor Stimulation of Transforming Growth Factor-β in Rat Skin and Wound Healing ...
angiotensin amide synonyms, angiotensin amide pronunciation, angiotensin amide translation, English dictionary definition of ... angiotensin amide. n. Any of several polypeptide hormones, designated by Roman numerals, that are involved in the regulation of ... angiotensin I - a physiologically inactive form of angiotensin that is the precursor to angiotensin II ... angiotensin. (redirected from angiotensin amide). Also found in: Thesaurus, Medical, Encyclopedia. an·gi·o·ten·sin. (ăn′jē-ō- ...
Angiotensin converting enzyme (encoded by the gene DCP1, also known as ACE) catalyses the conversion of angiotensin I to the ... Sequence variation in the human angiotensin converting enzyme.. Rieder MJ1, Taylor SL, Clark AG, Nickerson DA. ... Because of its key function in the renin-angiotensin system, many association studies have been performed with DCP1. Nearly all ... physiologically active peptide angiotensin II, which controls fluid-electrolyte balance and systemic blood pressure. ...
Second Edition updates new findings on the local renin-angiotensin systems (RAS) with a focus on the local RAASs of the ... Newer Insights into the Biochemical Physiology of the Renin-Angiotensin System: Role of Angiotensin-(1-7), Angiotensin ... The Local Cardiac Renin-Angiotensin Aldosterone System, Second Edition updates new findings on the local renin-angiotensin ... Intracellular Accumulation and Nuclear Trafficking of Angiotensin II and the Angiotensin II Type 1 Receptor ...
Giving ACE inhibitors or angiotensin receptor blockers to patients with advanced chronic kidney disease and hypertension may ... Angiotensin Drugs Help Advanced CKD Patients. by Todd Neale, Senior Staff Writer, MedPage Today December 17, 2013 ... Giving ACE inhibitors or angiotensin receptor blockers (ARBs) to patients with advanced chronic kidney disease (CKD) and ... Source Reference: Hsu T-W, et al "Renoprotective effect of renin-angiotensin-aldosterone system blockade in patients with ...
  • In cardiomyocytes, Angiotensin II exposure induces rapid inhibition of L-type current with a magnitude that is correlated with the rate of current inactivation. (nih.gov)
  • Over-expression of individual b subunits in heterologous systems reveals that the magnitude of Angiotensin II inhibition is dependent on the Ca(v)β subunit isoform, with Ca(v)β(1b) containing channels being more strongly regulated. (nih.gov)
  • Moreover, PLC or diacylglycerol lipase inhibition prevents the Angiotensin II effect on L-type calcium channels, while PKC inhibition with chelerythrine does not, suggesting a role of arachidonic acid in this process. (nih.gov)
  • These data demonstrate that Ca(v)β subunits alter the magnitude of inhibition of L-type current by Angiotensin II. (nih.gov)
  • The value of renin-angiotensin-aldosterone inhibition in reducing mortality and morbidity among patients with heart failure and left ventricular systolic dysfunction has been well established in multiple large randomized clinical trials. (cmaj.ca)
  • As an example of this wealth of data, in this issue of CMAJ , Pilote and colleagues 2 use administrative databases of hospital discharges and prescription claims to study the comparative effectiveness of angiotensin-converting-enzyme (ACE) inhibitors in the treatment of congestive heart failure. (cmaj.ca)
  • Sources of data for model parameters included IMS Health Canada data collected from one-third of all retail pharmacies for the cost and use of angiotensin-receptor blockers and ACE inhibitors in each province, as well as published studies for administrative costs and incidence of dry cough. (cmaj.ca)
  • Angiotensin-receptor blockers and ACE inhibitors are already widely used for the treatment of heart failure with preserved ejection fraction, Dr. Redfield said. (medpagetoday.com)
  • The suggestion is that higher local concentrations of either angiotensin II or perindoprilat are achieved when a vessel is noradrenergically preconstricted by infused norepinephrine or lower body negative pressure. (ahajournals.org)
  • Interestingly, some clinical studies have demonstrated that treatment with either angiotensin I-converter enzyme inhibitors (ACEI) or angiotensin II receptor antagonist (ARA) reduces the incidence of diabetes mellitus in high risk patients ( 5 , 6 ). (scielo.br)
  • Design and Synthesis of Angiotensin IV Peptidomimetics Targeting the Insulin-Regulated Aminopeptidase (IRAP) (Ph.D. thesis). (wikipedia.org)
  • Angiotensin II and ET-1, both at 10 nmol/L, induced myocyte hypertrophy, as demonstrated by increased protein content and synthesis, [Ca 2+ ] i levels, protein kinase C (PKC) activity and phosphorylation of extracellular signal-regulated kinase, c-Jun N-terminal kinase and mitogen-activated protein kinase (MAPK) p38 (p38). (ingentaconnect.com)
  • One is in the synthesis of angiotensin II, which has vasoconstrictive properties, promotes retention of sodium and water, and promotes cell growth. (bmj.com)