An ANGIOTENSIN II analog which acts as a highly specific inhibitor of ANGIOTENSIN TYPE 1 RECEPTOR.
An amino acid intermediate in the metabolism of choline.
A FLAVOPROTEIN, this enzyme catalyzes the oxidation of SARCOSINE to GLYCINE; FORMALDEHYDE; and HYDROGEN PEROXIDE (H2O2).
An octapeptide that is a potent but labile vasoconstrictor. It is produced from angiotensin I after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME. The amino acid in position 5 varies in different species. To block VASOCONSTRICTION and HYPERTENSION effect of angiotensin II, patients are often treated with ACE INHIBITORS or with ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS.
An essential branched-chain aliphatic amino acid found in many proteins. It is an isomer of LEUCINE. It is important in hemoglobin synthesis and regulation of blood sugar and energy levels.
A LIVER mitochondrial matrix flavoenzyme that catalyzes the oxidation of SARCOSINE to GLYCINE and FORMALDEHYDE. Mutation in the enzyme causes sarcosinemia, a rare autosomal metabolic defect characterized by elevated levels of SARCOSINE in BLOOD and URINE.
An angiotensin receptor subtype that is expressed at high levels in a variety of adult tissues including the CARDIOVASCULAR SYSTEM, the KIDNEY, the ENDOCRINE SYSTEM and the NERVOUS SYSTEM. Activation of the type 1 angiotensin receptor causes VASOCONSTRICTION and sodium retention.
Cell surface proteins that bind ANGIOTENSINS and trigger intracellular changes influencing the behavior of cells.
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.
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.
Agents that antagonize ANGIOTENSIN RECEPTORS. Many drugs in this class specifically target the ANGIOTENSIN TYPE 1 RECEPTOR.
A decapeptide that is cleaved from precursor angiotensinogen by RENIN. Angiotensin I has limited biological activity. It is converted to angiotensin II, a potent vasoconstrictor, after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME.
An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.
Agents that antagonize the ANGIOTENSIN II TYPE 2 RECEPTOR.
A heptapeptide formed from ANGIOTENSIN II after the removal of an amino acid at the N-terminal by AMINOPEPTIDASE A. Angiotensin III has the same efficacy as ANGIOTENSIN II in promoting ALDOSTERONE secretion and modifying renal blood flow, but less vasopressor activity (about 40%).
A FLAVOPROTEIN enzyme that catalyzes the oxidative demethylation of dimethylglycine to SARCOSINE and FORMALDEHYDE.
A family of sodium chloride-dependent neurotransmitter symporters that transport the amino acid GLYCINE. They differ from GLYCINE RECEPTORS, which signal cellular responses to GLYCINE. They are located primarily on the PLASMA MEMBRANE of NEURONS; GLIAL CELLS; EPITHELIAL CELLS; and RED BLOOD CELLS where they remove inhibitory neurotransmitter glycine from the EXTRACELLULAR SPACE.
An enzyme that catalyzes the METHYLATION of GLYCINE using S-ADENOSYLMETHIONINE to form SARCOSINE with the concomitant production of S-ADENOSYLHOMOCYSTEINE.
A branched-chain essential amino acid that has stimulant activity. It promotes muscle growth and tissue repair. It is a precursor in the penicillin biosynthetic pathway.
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.
An octapeptide analog of angiotensin II (bovine) with amino acids 1 and 8 replaced with sarcosine and alanine, respectively. It is a highly specific competitive inhibitor of angiotensin II that is used in the diagnosis of HYPERTENSION.
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.
Compounds containing 1,3-diazole, a five membered aromatic ring containing two nitrogen atoms separated by one of the carbons. Chemically reduced ones include IMIDAZOLINES and IMIDAZOLIDINES. Distinguish from 1,2-diazole (PYRAZOLES).
A 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.
Compounds with a BENZENE fused to IMIDAZOLES.
Drugs used to cause constriction of the blood vessels.
PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.
Oligopeptides which are important in the regulation of blood pressure (VASOCONSTRICTION) and fluid homeostasis via the RENIN-ANGIOTENSIN SYSTEM. These include angiotensins derived naturally from precursor ANGIOTENSINOGEN, and those synthesized.
A non-essential amino acid. It is found primarily in gelatin and silk fibroin and used therapeutically as a nutrient. It is also a fast inhibitory neurotransmitter.
Drugs used in the treatment of acute or chronic vascular HYPERTENSION regardless of pharmacological mechanism. Among the antihypertensive agents are DIURETICS; (especially DIURETICS, THIAZIDE); ADRENERGIC BETA-ANTAGONISTS; ADRENERGIC ALPHA-ANTAGONISTS; ANGIOTENSIN-CONVERTING ENZYME INHIBITORS; CALCIUM CHANNEL BLOCKERS; GANGLIONIC BLOCKERS; and VASODILATOR AGENTS.
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.
Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.

Regulation of angiotensin II receptors and PKC isoforms by glucose in rat mesangial cells. (1/50)

It has been shown that glomerular angiotensin II (ANG II) receptors are downregulated and protein kinase C (PKC) is activated under diabetic conditions. We, therefore, investigated ANG II receptor and PKC isoform regulation in glomerular mesangial cells (MCs) under normal and elevated glucose concentrations. MCs were isolated from collagenase-treated rat glomeruli and cultured in medium containing normal or high glucose concentrations (5.5 and 25.0 mM, respectively). Competitive binding experiments were performed using the ANG II antagonists losartan and PD-123319, and PKC analysis was conducted by Western blotting. Competitive binding studies showed that the AT1 receptor was the only ANG II receptor detected on MCs grown to either subconfluence or confluence under either glucose concentration. AT1 receptor density was significantly downregulated in cells grown to confluence in high-glucose medium. Furthermore, elevated glucose concentration enhanced the presence of all MC PKC isoforms. In addition, PKCbeta, PKCgamma and PKCepsilon were translocated only in cells cultured in elevated glucose concentrations following 1-min stimulation by ANG II, whereas PKCalpha, PKCtheta, and PKClambda were translocated by ANG II only in cells grown in normal glucose. Moreover, no changes in the translocation of PKCdelta, PKCiota, PKCzeta, and PKCmu were detected in response to ANG II stimulation under euglycemic conditions. We conclude that MCs grown in high glucose concentration show altered ANG II receptor regulation as well as PKC isoform translocation compared with cells grown in normal glucose concentration.  (+info)

Cloning and characterization of ATRAP, a novel protein that interacts with the angiotensin II type 1 receptor. (2/50)

The carboxyl-terminal cytoplasmic domain of the angiotensin II type 1 (AT1) receptor has recently been shown to interact with several classes of cytoplasmic proteins that regulate different aspects of AT1 receptor physiology. Employing yeast two-hybrid screening of a mouse kidney cDNA library with the carboxyl-terminal cytoplasmic domain of the murine AT1a receptor as a bait, we have isolated a novel protein with a predicted molecular mass of 18 kDa, which we have named ATRAP (for AT1 receptor-associated protein). ATRAP interacts specifically with the carboxyl-terminal domain of the AT1a receptor but not with those of angiotensin II type 2 (AT2), m3 muscarinic acetylcholine, bradykinin B2, endothelin B, and beta2-adrenergic receptors. The mRNA of ATRAP was abundantly expressed in kidney, heart, and testis but was poorly expressed in lung, liver, spleen, and brain. The ATRAP-AT1a receptor association was confirmed by affinity chromatography, by specific co-immunoprecipitation of the two proteins, and by fluorescence microscopy, showing co-localization of these proteins in intact cells. Overexpression of ATRAP in COS-7 cells caused a marked inhibition of AT1a receptor-mediated activation of phospholipase C without affecting m3 receptor-mediated activation. In conclusion, we have isolated a novel protein that interacts specifically with the carboxyl-terminal cytoplasmic domain of the AT1a receptor and affects AT1a receptor signaling.  (+info)

Dynamic Ca2+ signalling in rat arterial smooth muscle cells under the control of local renin-angiotensin system. (3/50)

1. We visualized the changes in intracellular Ca2+ concentration ([Ca2+]i), using fluo-3 as an indicator, in individual smooth muscle cells within intact rat tail artery preparations. 2. On average in about 45 % of the vascular smooth muscle cells we found spontaneous Ca2+ waves and oscillations ( approximately 0.13 Hz), which we refer to here as Ca2+ ripples because the peak amplitude of [Ca2+]i was about one-seventh of that of Ca2+ oscillations evoked by noradrenaline. 3. We also found another pattern of spontaneous Ca2+ transients often in groups of two to three cells. They were rarely observed and are referred to as Ca2+ flashes because their peak amplitude was nearly twice as large as that in noradrenaline-evoked responses. 4. Sympathetic nerve activity was not considered responsible for the Ca2+ ripples, and they were abolished by inhibitors of either the Ca2+ pump in the sarcoplasmic reticulum (cyclopiazonic acid) or phospholipase C (U-73122). 5. Both angiotensin antagonists ([Sar1,Ile8]-angiotensin II and losartan) and an angiotensin converting enzyme inhibitor (captopril) inhibited the Ca2+ ripples. 6. The extracellular Ca2+-dependent tension borne by unstimulated arterial rings was reduced by the angiotensin antagonist by approximately 50 %. 7. These results indicate that the Ca2+ ripples are generated via inositol 1,4, 5-trisphosphate-induced Ca2+ release from the intracellular Ca2+ stores in response to locally produced angiotensin II, which contributes to the maintenance of vascular tone.  (+info)

Overexpression of angiotensin II type I receptor in cardiomyocytes induces cardiac hypertrophy and remodeling. (4/50)

Angiotensin II (AII) is a major determinant of arterial pressure and volume homeostasis, mainly because of its vascular action via the AII type 1 receptor (AT1R). AII has also been implicated in the development of cardiac hypertrophy because angiotensin I-converting enzyme inhibitors and AT1R antagonists prevent or regress ventricular hypertrophy in animal models and in human. However, because these treatments impede the action of AII at cardiac as well as vascular levels, and reduce blood pressure, it has been difficult to determine whether AII action on the heart is direct or a consequence of pressure-overload. To determine whether AII can induce cardiac hypertrophy directly via myocardial AT1R in the absence of vascular changes, transgenic mice overexpressing the human AT1R under the control of the mouse alpha-myosin heavy chain promoter were generated. Cardiomyocyte-specific overexpression of AT1R induced, in basal conditions, morphologic changes of myocytes and nonmyocytes that mimic those observed during the development of cardiac hypertrophy in human and in other mammals. These mice displayed significant cardiac hypertrophy and remodeling with increased expression of ventricular atrial natriuretic factor and interstitial collagen deposition and died prematurely of heart failure. Neither the systolic blood pressure nor the heart rate were changed. The data demonstrate a direct myocardial role for AII in the development of cardiac hypertrophy and failure and provide a useful model to elucidate the mechanisms of action of AII in the pathogenesis of cardiac diseases.  (+info)

Molecular cloning of a ferret angiotensin II AT(1) receptor reveals the importance of position 163 for Losartan binding. (5/50)

A complementary DNA for the angiotensin II (AngII) type 1 (AT(1)) receptor from Mustela putorius furo (ferret) was isolated from a ferret atria cDNA library. The cDNA encodes a protein (fAT(1)) of 359 amino acids having high homologies (93-99%) to other mammalian AT(1) receptor counterparts. When fAT(1) was expressed in COS-7 cells and photoaffinity labeled with the photoactive analogue (125)I- inverted question markSar(1), Bpa(8)AngII, a protein of 100 kDa was detected by autoradiography. The formation of this complex was specific since it was abolished in the presence of the AT(1) non-peptidic antagonist L-158,809. Functional analysis indicated that the fAT(1) receptor efficiently coupled to phospholipase C as demonstrated by an increase in inositol phosphate production following stimulation with AngII. Binding studies revealed that the fAT(1) receptor had a high affinity for the peptide antagonist inverted question markSar(1), Ile(8)AngII (K(d) of 5. 8+/-1.4 nM) but a low affinity for the AT(1) selective non-peptidic antagonist DuP 753 (K(d) of 91+/-15.6 nM). Interestingly, when we substituted Thr(163) with an Ala residue, which occupies this position in many mammalian AT(1) receptors, we restored the high affinity of this receptor for Dup 753 (11.7+/-5.13 nM). These results suggest that position 163 of the AT(1) receptor does not contribute to the overall binding of peptidic ligands but that certain non-peptidic antagonists such as Dup 753 are clearly dependent on this position for efficient binding.  (+info)

The luminal membrane of rat thick limb expresses AT1 receptor and aminopeptidase activities. (6/50)

BACKGROUND: Endogenous intratubular angiotensin II (Ang II) supports an autocrine tonic stimulation of NaCl absorption in the proximal tubule, and its production may be regulated independently of circulating Ang II. In addition, endogenous Ang II activity may be regulated at the brush border membrane (BBM), by the rate of aminopeptidase A and N (APA and APN) activities and the rate of Ca2+-independent phospholipase A2 (PLA2-dependent endocytosis and recycling of the complex Ang II subtype 1 (AT1) receptor (AT1-R). The aim of the present study was to look for subcellular localization of AT1-R, and APA and APN activities in the medullary thick ascending limb of Henle (mTAL), as well as search for an asymmetric coupling of AT1-R to signal transduction pathways. METHODS: Preparations of isolated basolateral membrane (BLMV) and luminal (LMV) membrane vesicles from rat mTAL were used to localize first, AT1-R by 125I-[Sar1, Ile8] Ang II binding studies and immunoblot experiments with a specific AT1-R antibody, and second, APA and APN activities. Microfluorometric monitoring of cytosolic Ca2+ with a Fura-2 probe was performed in mTAL microperfused in vitro, after apical or basolateral application of Ang II. RESULTS: AT1-R were present in both LMV and BLMV, with a similar Kd (nmol/L range) and Bmax. Accordingly, BLMV and LMV preparations similarly stained specific AT1-R antibody. APA and APN activities were selectively localized in LMV, although to a lesser extent than those measured in BBM. In the in vitro microperfused mTAL, basolateral but not apical Ang II induced a transient increase in cytosolic [Ca2+]. CONCLUSIONS: Besides the presence of basolateral AT1-R in mTAL coupled to the classical Ca2+-dependent transduction pathways, AT1-R are present in LMV, not coupled with Ca2+ signaling, and co-localized with APA and APN activities. Thus, apical APA and APN may play an important role in modulating endogenous Ang II activity on NaCl reabsorption in mTAL.  (+info)

AT1 receptors in the RVLM mediate pressor responses to emotional stress in rabbits. (7/50)

In this study, we examined the role of angiotensin type 1 (AT1) receptors in the rostral ventrolateral medulla (RVLM) in mediating the pressor action of emotional stress in conscious rabbits. Rabbits were chronically instrumented with guide cannulas for bilateral microinjections into the RVLM and an electrode for measuring renal sympathetic nerve activity (RSNA). Airjet stress evoked increases in arterial pressure, heart rate, and RSNA, which reached a maximum (+9+/-1 mm Hg, +20+/-5 beats/min, and +93+/-17%, respectively) in the first 2 minutes of stress exposure. Then RSNA rapidly returned to prestress values, while arterial pressure and heart rate remained close to the maximal level until the conclusion of the 7-minute airjet exposure. Microinjections of the nonselective angiotensin receptor antagonist sarile (0.5 nmol, n=8) or AT1 receptor antagonists losartan (2 nmol, n=6) or candesartan (0.2 nmol, n=6) into the RVLM did not alter resting cardiovascular parameters. By contrast, the antagonists attenuated the sustained phase (4 to 7 minutes) of the pressor stress response by 55% to 89%. However, only sarile decreased the onset of this response. The antagonists affected neither the stress-induced tachycardia nor the pressor response to glutamate microinjections. Microinfusion of angiotensin II (4 pmol/min, n=8) into the RVLM did not change the pressor response to airjet stress but attenuated tachycardic response by 47%. Microinjections of vehicle did not alter the cardiovascular stress response. Sarile, losartan, and angiotensin II did not affect the sympathoexcitatory response to baroreceptor unloading. These results suggest that AT1 receptors in the RVLM are important in mediating the pressor effects of emotional stress in conscious rabbits.  (+info)

Autocrine angiotensin system regulation of bovine aortic endothelial cell migration and plasminogen activator involves modulation of proto-oncogene pp60c-src expression. (8/50)

Rapid endothelial cell migration and inhibition of thrombosis are critical for the resolution of denudation injuries to the vessel wall. Inhibition of the endothelial cell autocrine angiotensin system, with either the angiotensin-converting enzyme inhibitor lisinopril or the angiotensin II receptor antagonist sar1, ile8-angiotensin II, leads to increased endothelial cell migration and urokinase-like plasminogen activator (u-PA) activity (Bell, L., and J. A. Madri. 1990. Am. J. Pathol. 137:7-12). Inhibition of the autocrine angiotensin system with the converting-enzyme inhibitor or the receptor antagonist also leads to increased expression of the proto-oncogene c-src: pp60c-src mRNA increased 7-11-fold, c-src protein 3-fold, and c-src kinase activity 2-3-fold. Endothelial cell expression of c-src was constitutively elevated after stable infection with a retroviral vector containing the c-src coding sequence. Constitutively increased c-src kinase activity reconstituted the increases in migration and u-PA observed with angiotensin system interruption. Antisera to bovine u-PA blocked the increase in migration associated with increased c-src expression. These data suggest that increases in endothelial cell migration and plasminogen activator after angiotensin system inhibition are at least partially pp60c-src mediated. Elevated c-src expression with angiotensin system inhibition may act to enhance intimal wound closure and to reduce luminal thrombogenicity in vivo.  (+info)

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.. ...
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The angiotensin II (AII) antagonist, losartan, increases uric acid excretion when administered to humans. However, the active metabolite of losartan, EXP 3174, and other nonpeptide AII antagonists such as eprosartan and SB 203220 are devoid of uricosuric activity. To investigate the mechanism of losartan-induced uricosuria, we examined the effects of losartan, EXP 3174, eprosartan and SB 203220 on OH- -dependent [14C]urate uptake into rat proximal tubule brush-border membrane vesicles. Losartan (10 microM) inhibited [14C]urate uptake at all time points examined, except at equilibrium (2 hr). Losartan had no effect on urate uptake in the absence of an OH- gradient. The inhibitory effect of losartan on urate uptake was concentration dependent (IC50 = 9.5 +/- 1.4 microM) and competitive in nature. The other AII antagonists also inhibited urate uptake but were 6-8-fold less potent than losartan with IC50 values of EXP 3174 (65 +/- 13 microM), eprosartan (60 +/- 7.0 microM) and SB 203220 (74 +/- 12.5 ...
Green vehicles include electric vehicles, natural gas vehicles, fuel cell vehicles (FCV), and vehicles running on fuel such as a biodiesel or an ethanol blend. An FCV is equipped with a cylinder valve installed in an ultra-high pressure vessel to control the hydrogen flow. For this purpose, an optimum design of the solenoid actuator is necessary to ensure reliability when driving an FCV. In this study, an electromagnetic field analysis for ensuring reliable operation of the solenoid actuator was conducted by using Maxwell V15. The electromagnetic field analysis was performed by magneto static technique, according to the distance between magnetic poles, in order to predict the attraction force. Finally, the attraction force was validated through comparison between the Maxwell results and measurement results. From the results, the error of attraction force ranged from 2.33 to 3.85 N at testing conditions.
Buy cheap Generic Cozaar online without prescription. Cozaar is an angiotensin II antagonist used to decrease high blood pressure.
During candesartan infusion, the AERP was no longer shortened by rapid pacing (Figure 1A⇑). The AERP at baseline (131±5, 142±9, and 148±10 ms at BCLs of 200, 300, and 400 ms, respectively) was not significantly different from the corresponding AERP after the termination of rapid pacing (136±9, 147±12, and 153±13 ms at BCLs of 200, 300, and 400 ms respectively) (Table 1⇑). The percent change in AERP in the candesartan group was significantly less than that in the saline group (+4.1±7.7% versus −11.3±8.9%, +3.7±8.3% versus −10.6±11.0% at BCLs of 300 and 400 ms, respectively, P,0.01) (Figure 2⇑).. In the captopril-treated group, the time course of electrical remodeling was similar to that in the candesartan-treated group and the AERP was not shortened during rapid pacing (baseline versus after 180 minutes of pacing: from 140±15 to 137±11, from 153±15 to 153±14, and from 166±22 to 174±20 ms at BCLs of 200, 300, and 400 ms, respectively) (Table 1⇑, Figure 1A⇑). In ...
Animal research is an emotional subject, inspiring passionate debate on both sides Important to understand why animals like mice are used for medical science.
The aminopeptide sequence for saralasin differs from angiotensin II at three sites. At position 1, sarcosine is replaced by ... isoleucine is replaced by valine, and at position 8, phenylalanine is replaced by alanine which leads to a smaller stimulatory ... Ip S, Tsang S, Wong T, Che C, Leung P (2003). "Saralasin, a nonspecific angiotensin II receptor antagonist, attenuates ... Saralasin is a competitive angiotensin II receptor antagonist with partial agonist activity. ...
... angiotensin i MeSH D23.469.050.050.050 - angiotensin ii MeSH D23.469.050.050.050.050 - angiotensin amide MeSH D23.469.050.050. ... type ii MeSH D23.101.100.110.925 - e-selectin MeSH D23.101.100.110.930 - p-selectin MeSH D23.101.100.110.970 - vascular cell ... type ii MeSH D23.050.301.264.035.915 - p-selectin MeSH D23.050.301.264.035.920 - vascular cell adhesion molecule-1 MeSH D23.050 ... histocompatibility antigens class ii MeSH D23.050.301.500.410.400 - hla-d antigens MeSH D23.050.301.500.410.400.420 - HLA-DP ...
... angiotensin i MeSH D12.644.456.073.041 - angiotensin ii MeSH D12.644.456.073.041.050 - angiotensin amide MeSH D12.644.456.073. ... angiotensin i MeSH D12.644.400.070.078 - angiotensin ii MeSH D12.644.400.070.080 - angiotensin iii MeSH D12.644.400.085 - ... casein kinase ii MeSH D12.644.360.200 - cyclic nucleotide-regulated protein kinases MeSH D12.644.360.200.125 - cyclic amp- ... interferon type ii MeSH D12.644.276.174.440.893.510 - interferon-gamma, recombinant MeSH D12.644.276.174.480 - lymphokines MeSH ...
... type II: EC 5.99.1.3) 6-carboxytetrahydropterin synthase Category:EC 6.1.1 FARSB (EC 6.1.1.20) EC 6.2.1.1: Acetate-CoA ligase ... L-allo-isoleucine--holo-CmaA peptidyl-carrier protein ligase EC 6.2.1.47: Medium-chain-fatty-acid-(acyl-carrier-protein) ligase ... EC 3.4.15 Angiotensin converting enzyme Category:EC 3.4.21 Serine protease Chymotrypsin (EC 3.4.21.1) Trypsin (EC 3.4.21.4) ... Sarcosine oxidase EC 1.5.3.1 Dihydrobenzophenanthridine oxidase EC 1.5.3.12 Category:EC 1.5.4 (with a disulfide as acceptor) ...
Inhibition of adenylate cyclase by angiotensin II in rat renal cortex. abstract::Adenylate cyclase of rat renal cortex was ... inhibited by angiotensin II (AII). Inhibition required Na+ (100-200 mM) and GTP (10(-8)-10(-4) M) and was opposed by the ... abstract::Two experiments tested whether serotonergic neurons participate in the acute feedback effects of estradiol on LH and ... abstract::The seasonal changes in response to the negative feedback action of estradiol on LH secretion were studied in two ...
Angiotensin II, Ile(5)- Angiotensin II, Isoleucine(5)- Angiotensin II, Val(5)- Angiotensin II, Valine(5)- Angiotensin-(1-8) ... Isoleucine(5)-Angiotensin Isoleucyl(5)-Angiotensin II Valyl(5)-Angiotensin II Pharm Action. Vasoconstrictor Agents. Registry ... see ANGIOTENSIN AMIDE 1966-1973); ANGIOTENSIN II, ILE(5)- was indexed under ANGIOTENSIN II 1981-1999, and ISOLEUCINE 1975-1981 ... Angiotensins [D12.644.456.073] * Angiotensin I [D12.644.456.073.021] * Angiotensin II [D12.644.456.073.041] * Angiotensin Amide ...
Angiotensin II, Iodine Isotopes, Metalloendopeptidases, Knockout Mice, Prosencephalon, Angiotensin Type 2 Receptor, Renin- ... The recent identification of a novel binding site for angiotensin (Ang) II as the peptidase neurolysin (E.C. 3.4.24.16) has ... angiotensin II in neurolysin knockout mouse brains. Creators Name:. Speth, R.C. and Carrera, E.J. and Bretón, C. and Linares, A ... non-neurolysin Ang II binding site in the mouse brain. Binding of 125I-SI Ang II to neurolysin in the presence of PCMB was ...
Angiotensin II, Iodine Isotopes, Metalloendopeptidases, Knockout Mice, Prosencephalon, Angiotensin Type 2 Receptor, Renin- ... The recent identification of a novel binding site for angiotensin (Ang) II as the peptidase neurolysin (E.C. 3.4.24.16) has ... angiotensin II in neurolysin knockout mouse brains. Creators Name:. Speth, R.C. and Carrera, E.J. and Bretón, C. and Linares, A ... non-neurolysin Ang II binding site in the mouse brain. Binding of 125I-SI Ang II to neurolysin in the presence of PCMB was ...
The aminopeptide sequence for saralasin differs from angiotensin II at three sites. At position 1, sarcosine is replaced by ... isoleucine is replaced by valine, and at position 8, phenylalanine is replaced by alanine which leads to a smaller stimulatory ... Ip S, Tsang S, Wong T, Che C, Leung P (2003). "Saralasin, a nonspecific angiotensin II receptor antagonist, attenuates ... Saralasin is a competitive angiotensin II receptor antagonist with partial agonist activity. ...
Inhibition of adenylate cyclase by angiotensin II in rat renal cortex. abstract::Adenylate cyclase of rat renal cortex was ... inhibited by angiotensin II (AII). Inhibition required Na+ (100-200 mM) and GTP (10(-8)-10(-4) M) and was opposed by the ... abstract::Two experiments tested whether serotonergic neurons participate in the acute feedback effects of estradiol on LH and ... abstract::The seasonal changes in response to the negative feedback action of estradiol on LH secretion were studied in two ...
Angiotensin II, Ile(5)- Angiotensin II, Isoleucine(5)- Angiotensin II, Val(5)- Angiotensin II, Valine(5)- Angiotensin-(1-8) ... Isoleucine(5)-Angiotensin Isoleucyl(5)-Angiotensin II Valyl(5)-Angiotensin II Pharm Action. Vasoconstrictor Agents. Registry ... see ANGIOTENSIN AMIDE 1966-1973); ANGIOTENSIN II, ILE(5)- was indexed under ANGIOTENSIN II 1981-1999, and ISOLEUCINE 1975-1981 ... Angiotensins [D12.644.456.073] * Angiotensin I [D12.644.456.073.021] * Angiotensin II [D12.644.456.073.041] * Angiotensin Amide ...
... and 1,1-diphenyl-2-picrylhydrazyl (DPPH) radicals, as well as ferric-reducing antioxidant power ,i,in vitro,/i,, but exerts ... isoleucine; Leu: leucine; Tyr: tyrosine; Phe: phenylalanine; His: histidine; Lys: lysine; Arg: arginine; Pro: proline. Two ... Vaštag, L. Popović, S. Popović, L. Petrović, and D. Peričin, "Antioxidant and angiotensin-I converting enzyme inhibitory ... sarcosine oxidase method), and BUN (urease/glutamate dehydrogenase method) using an AU2700 Beckman coulter chemistry analyzer ( ...
angiotensin I (1-7) (Supplementary Concept). *aprikalim (Supplementary Concept). *Atenolol (MeSH Term) ... 1-Sarcosine-8-Isoleucine Angiotensin II (MeSH Term). *2-(4-(2-carboxyethyl)phenethylamino)-5-N-ethylcarboxamidoadenosine ( ... 1-(1-acetyl-piperidine-4-yl)-3-adamantan-1-yl-urea (Supplementary Concept) ... L-proline, N2-((1S)-1-carboxy-3-phenylpropyl)-N6-((4-hydroxyphenyl)iminomethyl)-L-lysyl- (Supplementary Concept) ...
Sarcosine (1968-1974)/analogs & derivatives (1975-1979). Public MeSH Note. 91; was see under ANGIOTENSIN II 1980-90. History ... Angiotensin II (1966-1974)/analogs & derivatives (1975-1979). Glycine (1966-1967). Isoleucine (1966-1974)/analogs & derivatives ... Angiotensins [D12.644.456.073] * Angiotensin II [D12.644.456.073.041] * Angiotensin Amide [D12.644.456.073.041.050] ... Angiotensins [D23.469.050.050] * Angiotensin II [D23.469.050.050.050] * Angiotensin Amide [D23.469.050.050.050.050] ...
Sarcosine (1968-1974)/analogs & derivatives (1975-1979). Public MeSH Note. 91; was see under ANGIOTENSIN II 1980-90. History ... Angiotensin II (1966-1974)/analogs & derivatives (1975-1979). Glycine (1966-1967). Isoleucine (1966-1974)/analogs & derivatives ... Angiotensins [D12.644.456.073] * Angiotensin II [D12.644.456.073.041] * Angiotensin Amide [D12.644.456.073.041.050] ... Angiotensins [D23.469.050.050] * Angiotensin II [D23.469.050.050.050] * Angiotensin Amide [D23.469.050.050.050.050] ...
Angiostatins N0000171050 Angiotensin Amide N0000171051 Angiotensin I N0000171047 Angiotensin II N0000171052 Angiotensin III ... Reticulum Calcium-Transporting ATPases N0000170214 Sarcosine N0000167884 Sarcosine Dehydrogenase N0000169064 Sarcosine Oxidase ... N0000006307 Isoflurane N0000006308 Isoflurophate N0000178808 Isoindoles N0000006312 Isoleucine N0000167786 Isoleucine-tRNA ... Angiotensin II N0000167982 11-beta-Hydroxysteroid Dehydrogenase Type 1 N0000167981 11-beta-Hydroxysteroid Dehydrogenase Type 2 ...
2,/sub,R and D,sub,3,/sub,R), we find that eticlopride binds D,sub,2,/sub,R in a pose very similar to that in the D,sub,3,/sub, ... 2,/sub, and D,sub,3,/sub, receptors (D,sub, ... Angiotensin (Ang) II (SD Ang II) and Sarcosine1 , Isoleucine8 - ... Ang II (SI Ang II) and their radioiodinated congeners binding to rat liver membrane AT1 receptors. Noto NM, Restrepo YM, Pang ... J Robert Lane 1 2 , Ara M Abramyan 3 , Pramisha Adhikari 3 , Alastair C Keen 1 2 4 , Kuo-Hao Lee 3 , Julie Sanchez 1 2 , Ravi ...
ISOLEUCINE ANGIOTENSIN II ANGIOTENSIN-CONVERTING ENZYME INHIBITOR ANGIOTENSIN-CONVERTING ENZYME INHIBITOR ANGIOTENSIN- ... ANTIRHEUMATIC ANGIOTENSIN I ANTI-INFLAMMATORY AGENTS, ANTIRHEUMATIC ANGIOTENSIN II ANTI-INFLAMMATORY AGENTS, ANTIRHEUMATIC ... CARDIOVASCULAR AGENTS ANGIOTENSIN AMIDE CARDIOVASCULAR AGENTS ANGIOTENSIN II CARDIOVASCULAR AGENTS ANISTREPLASE CARDIOVASCULAR ... EPOXYMETHA VASOCONSTRICTOR AGENTS ANGIOTENSIN AMIDE VASOCONSTRICTOR AGENTS ANGIOTENSIN II VASOCONSTRICTOR AGENTS ARGIPRESSIN ...
Angiotensin II Angiotensin II ,Angiotensin II Angiotensin II Receptor,Angiotensin II Receptor Angiotensin II, 1-(N- ... 8A-L-threonine-10A-L-isoleucine-30B-L-threonine-,Insulin (ox), 8A-L-threonine-10A-L-isoleucine-30B-L-threonine- Insulin A Chain ... Des Asp Angiotensin II Des Aspartyl Angiotensin II,Des Aspartyl Angiotensin II Des-Asp Angiotensin II,Des-Asp Angiotensin II ... angiotensin ,angiotensin angiotensin II,angiotensin II angiotensin converting enzyme,angiotensin converting enzyme antithrombin ...
Sarcosine Monosodium Salt use Sarcosine Sarcosine N Demethylase use Sarcosine Dehydrogenase Sarcosine N-Demethylase use ... SAPS II use Simplified Acute Physiology Score SAPS III use Simplified Acute Physiology Score ... SAMHD1 dNTPase use SAM Domain and HD Domain-Containing Protein 1 SAMHD1 Protein use SAM Domain and HD Domain-Containing Protein ... S-(N-(3-Aminopropyl)-2-aminoethyl)thiophosphoric Acid use Amifostine S-100 Calcium-Binding Protein beta Subunit use S100 ...
Angiotensin II Angiotensin II ,Angiotensin II Angiotensin II Receptor,Angiotensin II Receptor Angiotensin II, 1-(N- ... 8A-L-threonine-10A-L-isoleucine-30B-L-threonine-,Insulin (ox), 8A-L-threonine-10A-L-isoleucine-30B-L-threonine- Insulin A Chain ... Des Asp Angiotensin II Des Aspartyl Angiotensin II,Des Aspartyl Angiotensin II Des-Asp Angiotensin II,Des-Asp Angiotensin II ... angiotensin ,angiotensin angiotensin II,angiotensin II angiotensin converting enzyme,angiotensin converting enzyme antithrombin ...
  • The recent identification of a novel binding site for angiotensin (Ang) II as the peptidase neurolysin (E.C. 3.4.24.16) has implications for the renin-angiotensin system (RAS). (mdc-berlin.de)
  • At position 5, isoleucine is replaced by valine, and at position 8, phenylalanine is replaced by alanine which leads to a smaller stimulatory effect. (wikipedia.org)
  • This report describes the distribution of specific binding of 125I-Sarcosine1, Isoleucine8 Ang II (125I-SI Ang II) in neurolysin knockout mouse brains compared to wild-type mouse brains using quantitative receptor autoradiography. (mdc-berlin.de)
  • Saralasin is a competitive angiotensin II receptor antagonist with partial agonist activity. (wikipedia.org)
  • To block VASOCONSTRICTION and HYPERTENSION effect of angiotensin II, patients are often treated with ACE INHIBITORS or with ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS . (nih.gov)
  • 125I-SI Ang II binding was substantially higher by an average of 85% in wild-type mouse brains compared to neurolysin knockout brains, suggesting the presence of an additional non-AT1, non-AT2, non-neurolysin Ang II binding site in the mouse brain. (mdc-berlin.de)
  • At position 1, sarcosine is replaced by aspartic acid increasing the affinity for vascular smooth muscle receptors and making the peptide resistant to degradation by aminopeptidases Pals et al (1979). (wikipedia.org)