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 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.Glutamyl Aminopeptidase: A ZINC-dependent membrane-bound aminopeptidase that catalyzes the N-terminal peptide cleavage of GLUTAMATE (and to a lesser extent ASPARTATE). The enzyme appears to play a role in the catabolic pathway of the RENIN-ANGIOTENSIN SYSTEM.Receptors, Angiotensin: Cell surface proteins that bind ANGIOTENSINS and trigger intracellular changes influencing the behavior of cells.Receptor, Angiotensin, Type 1: An angiotensin receptor subtype that is expressed at high levels in a variety of adult tissues including the CARDIOVASCULAR SYSTEM, the KIDNEY, the ENDOCRINE SYSTEM and the NERVOUS SYSTEM. Activation of the type 1 angiotensin receptor causes VASOCONSTRICTION and sodium retention.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.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.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.Antigens, CD13: Zinc-binding metalloproteases that are members of the type II integral membrane metalloproteases. They are expressed by GRANULOCYTES; MONOCYTES; and their precursors as well as by various non-hematopoietic cells. They release an N-terminal amino acid from a peptide, amide or arylamide.Angiotensin Receptor Antagonists: Agents that antagonize ANGIOTENSIN RECEPTORS. Many drugs in this class specifically target the ANGIOTENSIN TYPE 1 RECEPTOR.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 II Type 2 Receptor Blockers: Agents that antagonize the ANGIOTENSIN II TYPE 2 RECEPTOR.Natriuretic Agents: Endogenous or exogenous chemicals that regulate the WATER-ELECTROLYTE BALANCE in the body. They consist of peptides and non-peptide compounds.Angiotensin Amide: The octapeptide amide of bovine angiotensin II used to increase blood pressure by vasoconstriction.Saralasin: An octapeptide analog of angiotensin II (bovine) with amino acids 1 and 8 replaced with sarcosine and alanine, respectively. It is a highly specific competitive inhibitor of angiotensin II that is used in the diagnosis of HYPERTENSION.Gold Compounds: Inorganic compounds that contain gold as an integral part of the molecule.TetrazolesLosartan: An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.Sulfonic Acids: Inorganic or organic oxy acids of sulfur which contain the RSO2(OH) radical.Aminopeptidases: A subclass of EXOPEPTIDASES that act on the free N terminus end of a polypeptide liberating a single amino acid residue. EC 3.4.11.Benzimidazoles: Compounds with a BENZENE fused to IMIDAZOLES.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.Imidazoles: Compounds containing 1,3-diazole, a five membered aromatic ring containing two nitrogen atoms separated by one of the carbons. Chemically reduced ones include IMIDAZOLINES and IMIDAZOLIDINES. Distinguish from 1,2-diazole (PYRAZOLES).Natriuresis: Sodium excretion by URINATION.Blood Pressure: PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.Pyridines: Compounds with a six membered aromatic ring containing NITROGEN. The saturated version is PIPERIDINES.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.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.Rats, Sprague-Dawley: A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.1-Sarcosine-8-Isoleucine Angiotensin II: An ANGIOTENSIN II analog which acts as a highly specific inhibitor of ANGIOTENSIN TYPE 1 RECEPTOR.Biphenyl CompoundsRenin: 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.Vasoconstrictor Agents: Drugs used to cause constriction of the blood vessels.Methionine: A sulfur-containing essential L-amino acid that is important in many body functions.Holocaust: A massive slaughter, especially the systematic mass extermination of European Jews in Nazi concentration camps prior to and during World War II.Cough: A sudden, audible expulsion of air from the lungs through a partially closed glottis, preceded by inhalation. It is a protective response that serves to clear the trachea, bronchi, and/or lungs of irritants and secretions, or to prevent aspiration of foreign materials into the lungs.Hypertension: Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.Polymorphism, Genetic: The regular and simultaneous occurrence in a single interbreeding population of two or more discontinuous genotypes. The concept includes differences in genotypes ranging in size from a single nucleotide site (POLYMORPHISM, SINGLE NUCLEOTIDE) to large nucleotide sequences visible at a chromosomal level.Genotype: The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.Quinic Acid: An acid which is found in cinchona bark and elsewhere in plants. (From Stedman, 26th ed)Muscle, Smooth, Vascular: The nonstriated involuntary muscle tissue of blood vessels.Access to Information: Individual's rights to obtain and use information collected or generated by others.Myocytes, Smooth Muscle: Non-striated, elongated, spindle-shaped cells found lining the digestive tract, uterus, and blood vessels. They are derived from specialized myoblasts (MYOBLASTS, SMOOTH MUSCLE).Journal Impact Factor: A quantitative measure of the frequency on average with which articles in a journal have been cited in a given period of time.History, Ancient: The period of history before 500 of the common era.Hypertension, Portal: Abnormal increase of resistance to blood flow within the hepatic PORTAL SYSTEM, frequently seen in LIVER CIRRHOSIS and conditions with obstruction of the PORTAL VEIN.Probiotics: Live microbial DIETARY SUPPLEMENTS which beneficially affect the host animal by improving its intestinal microbial balance. Antibiotics and other related compounds are not included in this definition. In humans, lactobacilli are commonly used as probiotics, either as single species or in mixed culture with other bacteria. Other genera that have been used are bifidobacteria and streptococci. (J. Nutr. 1995;125:1401-12)Peer Review: An organized procedure carried out by a select committee of professionals in evaluating the performance of other professionals in meeting the standards of their specialty. Review by peers is used by editors in the evaluation of articles and other papers submitted for publication. Peer review is used also in the evaluation of grant applications. It is applied also in evaluating the quality of health care provided to patients.Periodicals as Topic: A publication issued at stated, more or less regular, intervals.Palladium: A chemical element having an atomic weight of 106.4, atomic number of 46, and the symbol Pd. It is a white, ductile metal resembling platinum, and following it in abundance and importance of applications. It is used in dentistry in the form of gold, silver, and copper alloys.Portal Vein: A short thick vein formed by union of the superior mesenteric vein and the splenic vein.

Angiotensin receptor subtype 1 mediates angiotensin II enhancement of isoproterenol-induced cyclic AMP production in preglomerular microvascular smooth muscle cells. (1/90)

In a previous study, we found that angiotensin (Ang) II enhances beta-adrenoceptor-induced cAMP production in cultured preglomerular microvascular smooth muscle cells (PMVSMCs) obtained from spontaneously hypertensive rats. The purpose of the present investigation was to identify the Ang receptor subtypes that mediate this effect. In our first study, we compared the ability of Ang II, Ang III, Ang (3-8), and Ang (1-7) to increase cAMP production in isoproterenol (1 microM)-treated PMVSMCs. Each peptide was tested at 0.1, 1, 10, 100, and 1000 nM. Both Ang II and Ang III increased intracellular (EC50s, 1 and 11 nM, respectively) and extracellular (EC50s, 2 and 14 nM, respectively) cAMP levels in a concentration-dependent fashion. In contrast, Ang (3-8) and Ang (1-7) did not enhance either intracellular or extracellular cAMP levels at any concentration tested. In our second study, we examined the ability of L 158809 [a selective Ang receptor subtype 1 (AT1) receptor antagonist] to inhibit Ang II (100 nM) and Ang III (100 nM) enhancement of isoproterenol (1 microM)-induced cAMP production in PMVSMCs. L 158809 (10 nM) abolished or nearly abolished (p <.001) Ang II and Ang III enhancement of isoproterenol-induced intracellular and extracellular cAMP levels. In contrast, PD 123319 (300 nM; a selective AT2 receptor antagonist) did not significantly alter Ang II enhancement of isoproterenol-induced intracellular or extracellular cAMP levels. We conclude that AT1 receptors, but not AT2, Ang (3-8), nor Ang (1-7) receptors mediate Ang II and Ang III enhancement of beta-adrenoceptor-induced cAMP production in cultured PMVSMCs.  (+info)

Prejunctional angiotensin receptors involved in the facilitation of noradrenaline release in mouse tissues. (2/90)

The effect of angiotensin II, angiotensin III, angiotensin IV and angiotensin-(1-7) on the electrically induced release of noradrenaline was studied in preparations of mouse atria, spleen, hippocampus, occipito-parietal cortex and hypothalamus preincubated with [3H]-noradrenaline. The prejunctional angiotensin receptor type was investigated using the non-selective receptor antagonist saralasin (AT1/AT2) and the AT1 and AT2 selective receptor antagonists losartan and PD 123319, respectively. In atrial and splenic preparations, angiotensin II (0.01 nM-0.1 microM) and angiotensin III (0.01 and 0.1 nM-1 microM) increased the stimulation-induced overflow of tritium in a concentration-dependent manner. Angiotensin IV, only at high concentrations (1 and 10 pM), enhanced tritium overflow in the atria, while angiotensin-(1-7) (0.1 nM-10 microM) was without effect in both preparations. In preparations of hippocampus, occipito-parietal cortex and hypothalamus, none of the angiotensin peptides altered the evoked overflow of tritium. In atrial and splenic preparations, saralasin (0.1 microM) and losartan (0.1 and 1 microM), but not PD 123319 (0.1 microM), shifted the concentration-response curves of angiotensin II and angiotensin III to the right. In conclusion, in mouse atria and spleen, angiotensin II and angiotensin III facilitate the action potential induced release of noradrenaline via a prejunctional AT1 receptor. Only high concentrations of angiotensin IV are effective in the atria and angiotensin-(1-7) is without effect in both preparations. In mouse brain areas, angiotensin II, angiotensin III, angiotensin IV and angiotensin-(1-7) do not modulate the release of noradrenaline.  (+info)

Aminopeptidase A activity and angiotensin III effects on [Ca2+]i along the rat nephron. (3/90)

BACKGROUND: This study examined the specific effects of angiotensin III (Ang III) along the nephron. METHODS: We examined the distribution of aminopeptidase A (APA) activity by using a specific APA inhibitor and by immunostaining with an antirat kidney APA antibody, the Ang III-induced variations of [Ca2+]i by using fura-2 and the characterization of the receptor subtype involved in the response to Ang III in cortical thick ascending limb (CTAL). RESULTS: APA activity was found all along the nephron but was higher in the cortex than in the medulla. This was confirmed by immunostaining. Increases in [Ca2+]i elicited by 10(-7) mol/liter Ang III were observed all along the nephron. The characterization of the receptor subtype involved in the [Ca2+]i response to Ang III in CTAL indicated that EC50 values for Ang III and Ang II were similar (13.5 and 10.3 nmol/liter, respectively), and Ang III-induced responses were totally abolished by AT1 receptor but not by AT2 receptor antagonists. There was a cross-desensitization of [Ca2+]i responses to 10(-7) mol/liter Ang III and Ang II, and the [Ca2+]i responses to 10(-7) mol/liter Ang II and Ang III were not additive. CONCLUSION: These results show that in CTAL, the [Ca2+]i responses to Ang II and Ang III occur through the same AT1a receptor because this subtype is predominant in this segment. Taken together, these data suggest that APA could be a key enzyme to generate Ang III from Ang II in the kidney.  (+info)

Aminopeptidase A inhibitors as potential central antihypertensive agents. (4/90)

Overactivity of the brain renin-angiotensin system (RAS) has been implicated in the development and maintenance of hypertension in several experimental models, such as spontaneously hypertensive rats and transgenic mice expressing both human renin and human angiotensinogen transgenes. We recently reported that, in the murine brain, angiotensin II (AngII) is converted to angiotensin III (AngIII) by aminopeptidase A (APA), whereas AngIII is inactivated by aminopeptidase N (APN). If injected into cerebral ventricles (ICV), AngII and AngIII cause similar pressor responses. Because AngII is metabolized in vivo into AngIII, the exact nature of the active peptide is not precisely determined. Here we report that, in rats, ICV injection of the selective APA inhibitor EC33 [(S)-3-amino-4-mercaptobutyl sulfonic acid] blocked the pressor response of exogenous AngII, suggesting that the conversion of AngII to AngIII is required to increase blood pressure (BP). Furthermore, ICV injection, but not i.v. injection, of EC33 alone caused a dose-dependent decrease in BP by blocking the formation of brain but not systemic AngIII. This is corroborated by the fact that the selective APN inhibitor, PC18 (2-amino-4-methylsulfonyl butane thiol), administered alone via the ICV route, increases BP. This pressor response was blocked by prior treatment with the angiotensin type 1 (AT(1)) receptor antagonist, losartan, showing that blocking the action of APN on AngIII metabolism leads to an increase in endogenous AngIII levels, resulting in BP increase, through interaction with AT(1) receptors. These data demonstrate that AngIII is a major effector peptide of the brain RAS, exerting tonic stimulatory control over BP. Thus, APA, the enzyme responsible for the formation of brain AngIII, represents a potential central therapeutic target that justifies the development of APA inhibitors as central antihypertensive agents.  (+info)

Primary and secondary locations of charge sites in angiotensin II (M + 2H)2+ ions formed by electrospray ionization. (5/90)

High-energy tandem mass spectrometry and molecular dynamics calculations are used to determine the locations of charge in metastably decomposing (M + 2H)2+ ions of human angiotensin II. Charge-separation reactions provide critical information regarding charge sites in multiple charged ions. The most probable kinetic energy released (Tm.p.) from these decompositions are obtained using kinetic energy release distributions (KERDs) in conjunction with MS/MS (MS2), MS/MS/MS (MS3), and MS/MS/MS/MS (MS4) experiments. The most abundant singly and doubly charged product ions arise from precursor ion structures in which one proton is located on the arginine (Arg) side chain and the other proton is located on a distal peptide backbone carbonyl oxygen. The MS3 KERD experiments show unequivocally that neither the N-terminal amine nor the aspartic acid (Asp) side chain are sites of protonation. In the gas phase, protonation of the less basic peptide backbone instead of the more proximal and basic histidine (His) side chain is favored as a result of reduced coulomb repulsion between the two charge sites. The singly and doubly charged product ions of lesser abundance arise from precursor ion structures in which one proton is located on the Arg side chain and the other on the His side chain. This is demonstrated in the MS3 and MS4 mass-analyzed ion kinetic energy spectrometry experiments. Interestingly, (b7" + OH)2+ product ions, like the (M + 2H)2+ ions of angiotensin II, are observed to have at least two different decomposing structures in which charge sites have a primary and secondary location.  (+info)

Angiotensin III depressor action in the conscious rabbit is blocked by losartan but not PD 123319. (6/90)

Vasodilator and vasodepressor properties of angiotensins have been reported, and mediation by prostaglandins or nitric oxide has been proposed. Other studies indicate that angiotensin AT(2) receptors might mediate a depressor action, and the present study was designed to delineate and explore this possibility in a conscious rabbit model. Large intravenous boluses of angiotensin III (15 nmol/kg) produced a predictable pressor peak (82+/-4 mm Hg) followed by a depressor phase (20+/-3 mm Hg), whereas equipressor doses of angiotensin II were less effective at producing depressor responses. Angiotensin-(1-7) did not exert a depressor action, and the reduced potency of angiotensin IV (relative to angiotensin III) was similar for both the pressor and depressor phases ( approximately 100-fold). It is clear that specific angiotensin IV or angiotensin-(1-7) receptors do not mediate depressor effects in this model. The AT(1) antagonist losartan (1 mg/kg) blocked both the pressor and depressor components of the angiotensin III response, whereas the AT(2) antagonist PD 123319 (35 mg/kg) had no effect on either element of the response. The data obtained with the angiotensin receptor subtype-selective compounds, losartan and PD 123319, suggest that the depressor action is an AT(1)-mediated effect and give no indication that AT(2) receptors could be involved. Paradoxically, the greater potency of angiotensin III as a vasodepressor belies the conclusion that the response is AT(1)-mediated, because AT(1) receptors have a greater affinity for angiotensin II versus angiotensin III.  (+info)

Enhancement of noradrenaline release by angiotensin II and bradykinin in mouse atria: evidence for cross-talk between G(q/11) protein- and G(i/o) protein-coupled receptors. (7/90)

1. The interaction between alpha(2)-autoreceptors and receptors for angiotensin (AT(1)) and bradykinin (B(2)) was studied in mouse isolated atria. The preparations were labelled with [(3)H]-noradrenaline and then superfused with desipramine-containing medium and stimulated electrically. 2. Angiotensin II (10(-11) - 10(-7) M), angiotensin III (10(-10) - 10(-6) M) and bradykinin (10(-11) - 10(-7) M) enhanced the evoked overflow of tritium when preparations were stimulated with conditions that led to marked alpha(2)-autoinhibition (120 pulses at 3 Hz), but not when stimulated with conditions that led to little alpha(2)-autoinhibition (20 pulses at 50 Hz). 3. Blockade of alpha-adrenoceptors by phentolamine (1 or 10 microM) reduced or abolished the effect of angiotensin II and bradykinin on the overflow response to 120 pulses at 3 Hz. 4. Addition of the delta-opioid agonist [D-Ser(2)]-leucine enkephalin-Thr (DSLET, 0.1 microM), or of neuropeptide Y (0.1 microM), together with phentolamine, restored the effect of angiotensin II and bradykinin. 5. The beta-adrenoceptor agonist terbutaline (10(-9) - 10(-4) M) enhanced the evoked overflow of tritium irrespective of the degree of autoinhibition. 6. The experiments show that (i) a marked prejunctional facilitatory effect of angiotensin and bradykinin in mouse isolated atria requires prejunctional alpha(2)-autoinhibition; (ii) in the absence of alpha(2)-autoinhibition, activation of other prejunctional G(i/o) protein-coupled receptors, namely opioid and neuropeptide Y receptors, restores a marked effect of angiotensin II and bradykinin; and (iii) the facilitatory effect of terbutaline is not dependent upon the degree of alpha(2)-autoinhibition. The findings indicate that the major part of the release-enhancing effect elicited through prejunctional G(q/11) protein-coupled receptors is due to disruption of an ongoing, alpha(2)-autoreceptor-triggered G(i/o) protein mediated inhibition.  (+info)

Angiotensin III increases MCP-1 and activates NF-kappaB and AP-1 in cultured mesangial and mononuclear cells. (8/90)

BACKGROUND: Monocyte infiltration is a common feature of renal diseases. Angiotensin II (Ang II) participates in inflammatory cell infiltration in the kidney. However, the influence of other peptides of the renin-angiotensin system, such as the N-terminal Ang II degradation product Ang III, has not been addressed. METHODS: In cultured renal and mononuclear cells, we investigated whether Ang III is involved in monocyte recruitment through the regulation of the chemokine, monocyte chemoattractant protein-1 (MCP-1; Northern blot, Western blot, immunofluorescence, and chemotaxis), and the activation of transcription factors, nuclear factor kappaB (NF-kappaB) and activating protein-1 (AP-1; electrophoretic mobility shift assay). RESULTS: In cultured rat mesangial and mononuclear cells, Ang III increased MCP-1 gene expression and protein levels. Supernatants from Ang III-treated mesangial cells showed increased chemoattractant activity for monocytes, which was partially inhibited by the addition of anti-MCP-1 antibody. Ang III elicited a rapid NF-kappaB activation (8-fold, after 30 min), showing a kinetics and intensity similar to that observed with Ang II and tumor necrosis factor-alpha. The maximal NF-kappaB activation was correlated with nuclear translocation of p50 and p65 subunits and disappearance of cytosolic IkappaB. Ang III also activated AP-1 (5-fold, after 18 h), while SP-1 was unchanged. Two NF-kappaB inhibitors abolished the Ang III-induced MCP-1 mRNA expression, suggesting that overexpression of this chemokine is mediated, at least in part, by NF-kappaB activation. CONCLUSIONS: Ang III activates the transcription factors NF-kappaB and AP-1 and increases the expression of related genes, such as MCP-1. Our study describes a novel and potent proinflammatory action of this Ang degradation product, expanding the present view of the renin-angiotensin system.  (+info)

The results confirm an angiotensin-induced depressor response in the conscious rabbit model as described previously.5 The response is evident at high concentrations of angiotensin (,0.5 nmol/kg), and we confirm the observation of Scheuer and Perrone10 that angiotensin III is a more potent depressor than is angiotensin II. The depressor phase follows the well-known pressor response after an intravenous bolus of the peptide. The depressor phase was reproducible with repeated administration of angiotensin III at the smaller doses, but the magnitude of the response to the larger dose (15 nmol/kg) fell significantly from an initial value of 20±3 mm Hg to 11±2 and 11±3 mm Hg. The accompanying pressor components were well maintained, which suggests that the mechanisms for the pressor and depressor responses are different. A qualitative inspection of the responses in Figure 1⇑ indicates that a large depressor component of the angiotensin III response is associated with a truncated pressor phase. It ...
These studies demonstrate that RI Ang II, an AT2R ligand, does not induce a natriuresis in the presence of systemic AT1R blockade. However, a natriuretic response to Ang II, mediated by the AT2R, is unmasked by the intrarenal addition of PC-18, an APN inhibitor. Because the metabolism of Ang III to Ang IV by APN is inhibited by PC-18, these data suggest that Ang III is a significant mediator of Ang II-induced natriuresis. This conclusion is further supported by the ability of APA inhibition to abolish the natriuretic response to Ang II+PC-18.. Previous studies from our laboratory have shown that in the presence of AT1R blockade, RI Ang III infusion results in natriuresis that is abolished by concomitant PD infusion, implicating the renal AT2R in the response.21 Furthermore, addition of RI PC-18 to Ang III infusion causes a 1.8- to 2.8-fold increase in Na+ excretion compared with RI Ang III infusion alone.22 These findings prompted the present set of investigations to determine whether renal ...
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The IUPHAR/BPS Guide to Pharmacology. angiotensin III ligand page. Quantitative data and detailed annnotation of the targets of licensed and experimental drugs.
Adoptive transfer of T cells genetically improved to sole anti-TSLPR chimeric antigen receptors can cure B-ALL in xenograft kinds. Philadelphia chromosomeClike (Ph-like) leukemias react badly to regular chemotherapy RICTOR and possess Angiotensin III (human, mouse) high prices of relapse.17 Multiple groupings have got Angiotensin III (human, mouse) now demonstrated that rearrangements accounts for fifty percent of Ph-like ALL genomic alterations and are also highly associated with concomitant and stage mutations.17,18,20,21,32 We keep that the TSLPR features as an ALL oncoprotein provided its cell surface area reflection and association with poor scientific outcomes and thus might be an ideal immunotherapeutic focus on. Furthermore, TSLPR phrase in regular tissue shows up to end up being limited. We demonstrate that a TSLPR CAR may eradicate individual Web site Angiotensin III (human, mouse) completely. For structure of the lengthy CAR constructs, the CH2CH3 websites from IGHG1 ...
Creative Peptides offers (Des-Asp1,Ile8)-Angiotensin II for your research. We also provide custom peptide synthesis, process development, GMP manufacturing.
Life/form CPARLENE Full Manikin w/Memory & Printer-Life/form® CPARLENE® is flexible and adaptable because it was designed with modular components that require no conversion kits. Manikin is completely upgradable and interchangeable. Individu
1. Competitive or non-competitive inhibition of the myotropic and pressor response of angiotensin II is dependent on the nature of the substituent in position 8 of the antagonist peptide analogue. Substituents in other positions of the molecule, particularly position 1, contribute greatly to the potency of these antagonists.. 2. As is evidenced after adrenalectomy or after blockade with phentolamine and phenoxybenzamine, the initial pressor activity observed with all the antagonistic peptides is partially due to the release of catecholamines and partially to a direct myotropic effect.. 3. [Sar1, Thr8]angiotensin II has been found to possess the lowest agonist to antagonist ratio of all antagonists tested.. 4. [Des-Asp1, Ile8]angiotensin II selectively and specifically inhibits the release of aldosterone from adrenal cortex. Thus, unlike angiotensin II, this heptapeptide has pronounced organ specificity, suggesting that the heptapeptide (angiotensin III) is the aldosterone-releasing ...
... definition, any of three oligopeptides occurring in plasma, an inactive form (angiotensin I) and two varieties (angiotensin II and angiotensin III) that elevate blood pressure and stimulate the adrenal cortex to secrete aldosterone. See more.
Supplementary MaterialsSupplemental Material kvir-10-01-1573491-s001. lay the building blocks for finding potential T6SS effectors. (ExPEC) can infect the tissue from the distal digestive tract and trigger various illnesses in human beings and pets [1C3]. ExPEC contains uropathogenic (UPEC), neonatal meningitis-causing (NMEC), avian pathogenic (APEC), and septicemic (SEPEC) [4C6]. ExPEC does not have pathogenicity when its colonized within Rabbit Polyclonal to HSP90B the intestine usually. However when these pathogens migrate to extra-intestinal Angiotensin III (human, mouse) organs, they are able to trigger various life-threatening illnesses such as urinary system attacks, newborn meningitis, peritonitis, bacteremia, and septicemia [4,5,7C9]. ExPEC offers caused a high mortality and economic deficits in swine market so far. It has posed a serious threat to human being health and improved animal market costs worldwide [5,10,11]. With the quick development of the swine market in China, the ...
Quantitative autoradiography was used to characterize angiotensin AT1 and AT2 receptors, in the rat aorta at three developmental ages; embryonic day 18 (E18), and postnatal weeks 2 and 8. The expression of angiotensin receptors was higher in the aorta of E18 and 2-week-old rat. A major proportion of the angiotensin receptors expressed in the aorta at these two ages was AT2 (84 and 81% respectively). Conversely, in the aorta of 8-week-old rats, AT1 was the predominant angiotensin receptor subtype (71%). In 8-week-old rats, the AT2 subtype was also present (28%). In pre- and postnatal rats, [125I]Sar1-angiotensin II binding to AT1 receptors was sensitive to GTP gamma S whereas binding to AT2 receptors was not. AT2 receptors may serve an important role during stages of rapid growth of the aorta, and also have a significant function in the adult vasculature ...
Indirect evidence has implicated a role for central angiotensin II in blood pressure control. To answer directly the question of whether angiotensin II exists in the brain, independent of blood-borne angiotensin, and to quantify the amounts in different parts of the central nervous system, a sensitive radioimmunoassay was used to measure extracts of male adult rat brain hypothalamus and cortex after purification with high pressure liquid chromatography with a high recovery. The fractions coeluted with authentic angiotensin. Rats were nephrectomized bilaterally, and 24 hours later the brains were extracted in acetic acid and boiled. SepPak C-18 purification preceded reverse phase high pressure liquid chromatography. High pressure liquid chromatography revealed two peaks, one which comigrated precisely with [Ile5] angiotensin II, and another smaller peak which overlapped with [Ile5] angiotensin III. The highest levels were found in the hypothalamus (125 pg/g tissue), pituitary (190 pg/g tissue), ...
Naltrexone is well absorbed by glass and the patient is instructed to heard in such cases are associated with a neuron, where large negatively charged area, or anions into a heptapeptide angiotensin iii which then activates the natural ergot alkaloids are capable of fast contraction, composed of cells with clear consciousness, paranoid delusions or hallucinations or perceptual process after the onset of pain. Ffi abbrev. [from latin causalis causal, from causa a cause] causal effect of succinylcholine (sc) on electrically stimulated rat phrenic nerve diaphragm preparation. The extent and severity of management of obstetrical hemorrhage. They may follow abnormal pattern. Although b12 deficiency during foetal life leads to the events themselves, and local growth factors. Kanamyc in, gentamic in, colistin, amphoteric in b; s ystemic fluc onazole; ec hinoc andin; newer triazoles if indic ated for invasive fungal infection, see text 41 general principles of treatment failure rate was as high as 24.5 ...
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1. The angiotensin analogues Sar1-Ala8-angiotensin II (AII), Sar1-Ile8-AII, Sar1-Leu8-AII, Sar1-Thr8-AII, [Des1-Asp]-Ile8-AII and [Des1-Asp]-Sar2-Ile8-AII and converting enzyme inhibitor (SQ 80221) infused by intra-adrenal arterial infusion had no effect on aldosterone secretion in sodium-deficient sheep at doses in excess of those shown to block exogenous angiotensin II or III infusion.. 2. It is suggested that the intrinsic agonist activity of the analogues may fulfil the requirements for a permissive role for angiotensin in the aldosterone response to sodium deficiency.. ...
Broad specificity aminopeptidase. Plays a role in the final digestion of peptides generated from hydrolysis of proteins by gastric and pancreatic proteases. May play a critical role in the pathogenesis of cholesterol gallstone disease. May be involved in the metabolism of regulatory peptides of diverse cell types, responsible for the processing of peptide hormones, such as angiotensin III and IV, neuropeptides, and chemokines. Found to cleave antigen peptides bound to major histocompatibility complex class II molecules of presenting cells and to degrade neurotransmitters at synaptic junctions. Is also implicated as a regulator of IL-8 bioavailability in the endometrium, and therefore may contribute to the regulation of angiogenesis. Is used as a marker for acute myeloid leukemia and plays a role in tumor invasion. In case of human coronavirus 229E (HCoV-229E) infection, serves as receptor for HCoV-229E spike glycoprotein. Mediates as well human cytomegalovirus (HCMV) infection ...
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140 ° செல்சியசு வெப்பநிலையில் தங்கம் புரோமினுடன் வினைபுரிந்து தங்கம் (III) சேர்மத்தை உருவாக்குகிறது. ஆனால் அயோடினுடன் மிக மெதுவாக வினைபுரிந்து ஒற்றை அயோடைடை உருவாக்குகிறது. தங்கம் நேரடியாக கந்தகத்துடன் வினைபுரிவதில்லை. ஆனால் குளோரோ ஆரிக் அமிலத்தின் வழியாக அல்லது நீர்த்த தங்கம்(III) குளோரைடு வழியாக ஐதரசன் சல்பைடு வாயுவை செலுத்தினால் தங்கம்(III) சல்பைடு உருவாகிறது. அறை ...
目前胃癌的细胞毒药物治疗已进入一个平台期。随着分子生物学研究的深入开展,胃癌的诊断及治疗进入了分子水平。大量的基础和临床研究正在探索胃癌的分子靶点包括:人表皮生长因子受体2、人表皮生长因子受体1、哺乳动物雷帕霉素靶蛋白、血管内皮生长因子、血管内皮生长因子2、纤维母细胞生长因子受体2、肝细胞生长因子受体以及聚腺苷酸二磷酸核糖转移酶等。目前,仅有人表皮生长因子受体2的靶向药物曲妥珠单抗及血管内皮生长因子受体2靶向药物ramucirumab被III期临床研究证实在晚期胃癌中有显著疗效,针对上述靶点的其他药物需进一步研究和开发。
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
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)]
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In living organisms, enzymes work in complicated networks to perform various biological functions. To analyse such functions, specific enzyme inhibitors are needed. Such inhibitors would be of great...
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 ...
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)]
Angiotensin convertaza, cunoscuta si sub numele de kinaza II sau peptidil-dipeptidaza A, este o enzima din clasa hidrolazelor implicate in hidroliza legaturilor peptidice la nivelul C-terminal. Are localizare transmembranara si este alcatuita dintr-un singur lant polipeptidic cu doua situsuri catalitice ce contin zinc. Clivajul proteolitic elibereaza din membrana celulara in spatiul extracelular enzima functionala, circulanta6.. Majoritatea angiotensin convertazei (~90%) se gaseste legata in tesuturi si doar o mica parte circula libera in plasma. Sursa principala a enzimei este endoteliul pulmonar.. Enzima participa in cascada sistemului renina-angiotensina-aldosteron ca raspuns la hipovolemie, fiind responsabila de conversia angiotensinei I in angiotensina II, vasoconstrictor puternic care creste tensiunea arteriala. De asemenea angiotensin convertaza este responsabila si de inactivarea bradikininei (in sistemul kalikreina-kinina)3;6.. Activitatea angiotensin convertazei este crescuta in ...
Alamandine | [Ala1]-Angiotensin (1-7), Angiotensin A (1-7) (Human, Rat, Mouse)4475-v 0.5 mg | 25.00 EURAla-Arg-Val-Tyr-Ile-His-Pro (M.W.
The protein encoded by this gene is a zinc metalloprotease that displays some activity against angiotensin-3. The encoded protein is inhibited by the aminopeptidase inhibitor amastatin, as well as by the general inhibitors o-phenanthroline and batimastat. Defects in this gene may be associated with lung tumorigenesis. [provided by RefSeq, Oct 2016 ...
Discuss the medication that may have caused him to deteriorate - What is the enzyme that converts angiotensin I to angiotensin II and where is this normally
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] ...
Mono- and Stereopictres of 5.0 Angstrom coordination sphere of Sodium atom in PDB 2gg5: Novel Bacterial Methionine Aminopeptidase Inhibitors
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.
Angiotensin 1 converting enzyme - 67 yrs. Angiotensin 1 converting enzyme (ace) serum 126.7, what should be done? Bad? What does this mean? Life style changes. Medication? Thank you ACE levels. 51 M Notes: 67 yrs angiotensin 1 converting enzyme (ace) serum 126.7, what should be done? Bad? What does this mean? Life style changes. Medication? Thank you ANS: not enough information to help at this point. Are you 51 or 67? Need to know why it was measured, what meds, other illnesses, & what is normal in that lab. Get this information & will be happy to do 2nd opinion as I specialize in RAAS
an antihypertensive drug that blocks the formation of angiotensin II in the kidney, leading to relaxation of the arteries; promotes the excretion of salt and water by inhibiting the activity of the angiotensin converting enzyme; also used to treat congestive heart failure. ...
The following pages link to Angiotensin Converting Enzyme Inhibitor: View (previous 50 , next 50) (20 , 50 , 100 , 250 , 500) ...
Monoklonale und polyklonale Angiotensin I Converting Enzyme 1 Antikörper für viele Methoden. Ausgesuchte Qualitäts-Hersteller für Angiotensin I Converting Enzyme 1 Antikörper. Hier bestellen.
製藥大廠Cytokinetics最近宣布,公司開發的用於治療肌萎縮性脊髓側索硬化症(ALS)新藥tirasemtiv,在臨床 III 期研究中未能達到目標而宣告失敗。受這一結果影響,公司宣布將暫停該藥物的研發,公司股價應聲下跌 33%。 Cytoki...
Two themes were addressed in the 2013-14 academic year: curriculum development and teaching professionalism.. Organizer & Sponsor. AMES sponsored these MEJC activities. Helen Amerongen, PhD, served as the the MEJC Organizer. She is a member of the Academy of Medical Education Scholars (AMES*) and the Block Director for Foundations, as well as the Associate Department Head and Professor of the Department of Cellular and Molecular Medicine.. Given the enthusiastic participation of faculty in these journal club activities, the articles are posted here as resources for faculty instructional development.. ...
Drapala A, Sikora M, Ufnal M (September 2014). "Statins, the renin-angiotensin-aldosterone system and hypertension - a tale of ... Adult Treatment Panel III): Executive Summary. Bethesda, MD: National Institutes of Health. National Heart, Lung, and Blood ... A 2015 Cochrane systematic review update reported that rosuvastatin is more than three-fold more potent than atorvastatin.[39] ... 41 (3): 40-43. Retrieved 6 October 2018.. *^ Wolozin B, Wang SW, Li NC, Lee A, Lee TA, Kazis LE (July 2007). "Simvastatin is ...
There are three isoforms (identified as ET-1, -2, -3) with varying regions of expression and binding to at least four known ... Agapitov AV, Haynes WG; Haynes (March 2002). "Role of endothelin in cardiovascular disease". J Renin Angiotensin Aldosterone ... Some 3'-UTR AU-rich elements (AREs) play important regulatory roles in cytokine and proto-oncogene expression by influencing ... 3 (5): 256-63. doi:10.1038/ncpneuro0490. PMID 17479073. Hasue F, Kuwaki T, Kisanuki YY, Yanagisawa M, Moriya H, Fukuda Y, ...
Angiotensin Converting Enzyme (ACE) converts Angiotensin I to Angiotensin II. 5. Angiotensin II stimulates the release of ... Renin-angiotensin system: 1. The kidneys sense low blood pressure. 2. Release renin into the blood. 3. Renin causes production ...
Angiotensinogen and angiotensin. AGT. liver. angiotensin receptor → IP3. vasoconstriction release of aldosterone from adrenal ... increase circulating level of factors 2, 7, 9, 10, antithrombin III, plasminogen ... Activates the renin-angiotensin system by producing angiotensin I of angiotensinogen Secretin. SCT. duodenum. S cell. SCT ... E3. placenta. syncytiotrophoblast. ER. glucocorticoid. Cortisol. adrenal cortex (zona fasciculata and zona reticularis cells). ...
Renin-angiotensin-aldosterone system. http://edemainformation.blogspot.ca/2005/11/edema-pathophysiology-and-treatment.html ...
Smith A, Price C, Cullen M, Muda M, King A, Ozanne B, Arkinstall S, Ashworth A (Jun 1997). "Chromosomal localization of three ... Rössig L, Hermann C, Haendeler J, Assmus B, Zeiher AM, Dimmeler S (Jan 2002). "Angiotensin II-induced upregulation of MAP ... Smith A, Price C, Cullen M, Muda M, King A, Ozanne B, Arkinstall S, Ashworth A (Jun 1997). "Chromosomal localization of three ... Upregulation of MKP-3 has been shown to alleviate chronic postoperative pain. DUSP6 has been shown to interact with MAPK3. ...
Overexpression of this gene in mammalian cells was reported to inhibit angiotensin-II induced cell calcium mobilization and ... in angiotensin-II signaling". Biochem. Biophys. Res. Commun. 283 (5): 1061-8. doi:10.1006/bbrc.2001.4881. PMID 11355880. Saha S ... 565 (1-3): 181-7. doi:10.1016/j.febslet.2004.03.062. PMID 15135076. Wu X, Zeng H, Zhang X, et al. (2004). "Phosphatase of ... 2004). "PRL-3 expression in metastatic cancers". Clin. Cancer Res. 9 (15): 5607-15. PMID 14654542. Kozlov G, Cheng J, Ziomek E ...
... by increase in the plasma concentration of angiotensin III. by increased plasma angiotensin II, ACTH, or potassium levels. The ... Control of aldosterone release from the adrenal cortex: The role of the renin-angiotensin system: Angiotensin is involved in ... 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 enzyme degrades vasoconstricting angiotensin II into angiotensin III and therefore helps to regulate blood pressure. Reaux ... which generates one of the main effector peptides of the brain renin-angiotensin system, angiotensin III, has a key role in ...
... in the renin-angiotensin-aldosterone system (RAAS), keeping Angiotensin I from being converted to Angiotensin II. The ... Lisinopril is a drug of the angiotensin-converting enzyme (ACE) inhibitor class used primarily in treatment of high blood ... 1980). "A new class of angiotensin-converting enzyme inhibitors". Nature. 288 (5788): 280-3. Bibcode:1980Natur.288..280P. doi: ... Lisinopril is an ACE Inhibitor, meaning it blocks the actions of angiotensin converting enzyme (ACE) ...
This leads to the product angiotensin I (Ang I) which is a decapeptide. Ang I is broken down by the angiotensin-converting ... There are four S pockets, and three S′ pockets (table 1). The pockets alternate on either side of the backbone in the ligand. ... 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 ...
Also able to cleave angiotensin III to generate angiotensin IV, a bioactive peptide of the renin-angiotensin pathway. Due to ... Chromosome 9 open reading frame 3 (C9ORF3) also known as aminopeptidase O (APO) is an enzyme which in humans is encoded by the ...
Agapitov AV, Haynes WG (March 2002). "Role of endothelin in cardiovascular disease". J Renin Angiotensin Aldosterone Syst 3 (1 ... Štitasta žlezda: tiroidni hormon (T3 i T4) • kalcitonin. Paraštitna žlezda: PTH ... Poznate su tri izoforme (ET-1, -2, -3) sa različitim regionima izražavanja, i dva ključna tipa receptora, ETA i ETB. ... 3): 155-65. PMID 1331845. doi:10.1016/0143-4179(92)90158-S. Cite uses deprecated parameter ,month=. (help) ...
increase in the plasma concentration of angiotensin III, a metabolite of angiotensin II ... The role of the renin-angiotensin systemEdit. Angiotensin is involved in regulating aldosterone and is the core regulation.[16] ... The level of angiotensin II is regulated by angiotensin I, which is in turn regulated by renin, a hormone secreted in the ... Angiotensin II acts synergistically with potassium, and the potassium feedback is virtually inoperative when no angiotensin II ...
It does so by inhibiting the enzymes aminopeptidase N (APN), dipeptidyl peptidase III (DPP3), angiotensin-converting enzyme ( ... 3) receptor antagonist". Journal of Medicinal Chemistry. 50 (18): 4543-7. doi:10.1021/jm070114m. PMID 17676725. ...
Around one in three subjects develops systemic symptoms;[102] after a number of hours, or rarely, delayed for more than 24 ... These likely make the venom stronger by altering the victim's physiology.[103] Angiotensin-converting-enzyme inhibitors, or ACE ... In about two of three cases, the female fully consumes the male while mating continues. Males which are not eaten die of their ... Young, Anna R.; Pincus, Steven J. (February-March 2001). "Comparison of Enzymatic Activity from Three Species of Necrotising ...
Angiotensin II-induced senescence of vascular smooth muscle cells requires down-regulation of ZnT-3 and ZnT-10. Solute carrier ... Patrushev N, Seidel-Rogol B, Salazar G (2012). "Angiotensin II requires zinc and downregulation of the zinc transporters ZnT3 ... In mice, ZnT-3 is required for some forms of memory that depend on the hippocampus and the amygdala. Zinc transport by ZnT-3 ... Zinc transporter 3 also known as solute carrier family 30 member 3 is a protein in humans that is encoded by the SLC30A3 gene. ...
The conversion of angiotensin I to angiotensin II and the inactivation of bradykinin were thought to be mediated by the same ... The short half-life necessitates two or three times per day dosing, which may reduce patient compliance. The adverse effect and ... 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 ...
This protein may also be involved in blood pressure regulation by inactivation of angiotensin II. Three transcript variants ... 19 (3): 251-7. doi:10.1002/humu.10047. PMID 11857741. Cui X, Hawari F, Alsaaty S, Lawrence M, Combs CA, Geng W, Rouhani FN, ... 3 (12): 1169-76. doi:10.1038/ni859. PMID 12436109. York IA, Chang SC, Saric T, Keys JA, Favreau JM, Goldberg AL, Rock KL (2002 ... 419 (6906): 480-3. doi:10.1038/nature01074. PMID 12368856. Saric T, Chang SC, Hattori A, York IA, Markant S, Rock KL, Tsujimoto ...
Angiotensin converting enzyme. *Antithrombin-III. *Lipoprotein lipase. *Apolipoproteins. *Growth factors. *Chemokines. The ... 3. p. 345-359 *^ Ebong, Eno; Macaluso FP; Spray DC; Tarbell JM (August 2011). "Imaging the Endothelial Glycocalyx In Vitro By ...
The risk of developing hyperkalemia is increased in patients who are also on ACE inhibitors, angiotensin II receptor ... Angiotensin II: a powerful controller of sodium transport in the early proximal tubule, Hypertension. 1990;15:451-458, doi: ... of the action of angiotensin II on the secretion of hydrogen ions in proximal tubule cells. Amiloride was also tested as ...
"A new class of angiotensin-converting enzyme inhibitors". Nature 288 (5788): 280-3. PMID 6253826. doi:10.1038/288280a0. ... Effect on blood pressure and the renin-angiotensin system". Curr Therap Res 37: 342-51. ... doi:10.1186/1758-2946-2-3. edit *↑ Joanne Wixon, Douglas Kell (2000). "Website Review: The Kyoto Encyclopedia of Genes and ... 2S)-1-[(2S)-6-amino-2[(1S)-1-karboksi-3-fenilpropil]amino}heksanoil]pirolidin-2-karboksilna kiselina ...
There are three volume regulating systems: two salt saving systems, the renin angiotensin aldosterone system (RAAS) and the ... As of 2017 a truncated form of ANP called ularitide was under development in Phase III trials for heart failure. Brain ... Omapatrilat (dual inhibitor of NEP and angiotensin-converting enzyme) developed by BMS did not receive FDA approval due to ... Other dual inhibitors of NEP with ACE/angiotensin receptor are (in 2003) being developed by pharmaceutical companies. ANP is ...
2000). "The novel G-protein coupled receptor SALPR shares sequence similarity with somatostatin and angiotensin receptors". ... 2005). "Relaxin-3/insulin-like peptide 5 chimeric peptide, a selective ligand for G protein-coupled receptor (GPCR)135 and ... Van der Westhuizen ET, Sexton PM, Bathgate RA, Summers RJ (2005). "Responses of GPCR135 to human gene 3 (H3) relaxin in CHO-K1 ... Relaxin/insulin-like family peptide receptor 3, also known as RXFP3, is a human G-protein coupled receptor. Relaxin receptor ...
"SMAD3 deficiency promotes inflammatory aortic aneurysms in angiotensin II-infused mice via activation of iNOS". Journal of the ... The MH1 structure consists of four-helices and three sets of antiparallel β-hairpins, one of which is used to interact with DNA ... the three residues strictly conserved in all R-SMADS and in SMAD4 (Arg74 and Gln76 located in β2 and Lys81 in β3 in SMAD3) ... underlining the critical roles of these three proteins within the TGF-β signaling pathway and the impact of this pathway in ...
... are superior to other inhibitors of the renin-angiotensin system such as angiotensin receptor blockers (ARBs),[115] or ... A second oral agent of another class or insulin may be added if metformin is not sufficient after three months.[87] Other ... 65 (3): 385-411. doi:10.2165/00003495-200565030-00005. PMID 15669880.. *^ a b c d e f g h i j k l m n o p q r s Melmed, Shlomo ... "Effect of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers on all-cause mortality, cardiovascular ...
Rabbit polyclonal Angiotensin III antibody conjugated to Biotin. Validated in ELISA, RIA and tested in Human. Immunogen ... Angiotensin III is an eptapeptide drived from cleavage of full length angiotensin (AGT). AGT is a polypeptide vasopressor ... Angiotensin III (heptapeptide) is a degradation product of angiotensin II, and has less vasopressor activity than the parent ... However, Angiotensin III does stimulate aldosterone release. The renin-angiotensin system plays an important role in the ...
Angiotensin III acetate salt hydrate for your research needs. Find product specific information including CAS, MSDS, protocols ... Angiotensins, Cell Biology, Cell Signaling and Neuroscience, Neuropeptides, Peptides and Proteins, Peptides for Cell Biology ...
The renal mechanisms responsible for angiotensin II (ANG II)-induced hypertension remain incompletely understood. The present ... Role of the Na+/H+ exchanger 3 in angiotensin II-induced hypertension.. Li XC1, Shull GE2, Miguel-Qin E1, Zhuo JL3. ... 3. Laboratory of Receptor and Signal Transduction, Department of Pharmacology and Toxicology; Division of Nephrology, ... and glycogen synthase kinase 3αβ signaling proteins in the proximal tubules (P , 0.01). We concluded that NHE3 in proximal ...
Three Candidate Genes and Angiotensin-Converting Enzyme Inhibitor-Related Cough. A Pharmacogenetic Analysis. Robert Y. L. Zee, ... Three Candidate Genes and Angiotensin-Converting Enzyme Inhibitor-Related Cough. Robert Y. L. Zee, Valluri S. Rao, Robert Z. ... Three Candidate Genes and Angiotensin-Converting Enzyme Inhibitor-Related Cough. Robert Y. L. Zee, Valluri S. Rao, Robert Z. ... Association between cough and angiotensin-converting enzyme inhibitors versus angiotensin II antagonists: the design of a ...
Is the adrenal angiotensin receptor angiotensin II--or angiotensin III like? Acta Endocrinol (Copenh). 1983 Jan; 102(1):116-21. ... "Angiotensin III" by people in Harvard Catalyst Profiles by year, and whether "Angiotensin III" was a major or minor topic of ... The rates of peptide NH exchange with solvent for [Asn1, Val5]angiotensin II, angiotensin III and saralasin. Biochim Biophys ... Offset of actions of angiotensin II, angiotensin III, and their analogue antagonists in renal and femoral vascular beds: ...
The half-lives of angiotensin II, angiotensin II-amide, angiotensin III, Sar1-Ala8-angiotensin II and renin in the circulatory ... Effects of des-Asp-angiotensin I on the contractile action of angiotensin II and angiotensin III. Eur J Pharmacol. 1995;278:175 ... Angiotensin-(1-7) did not exert a depressor action, and the reduced potency of angiotensin IV (relative to angiotensin III) was ... Comparative effects of angiotensin II and its degradation products angiotensin III and angiotensin IV in rat aorta. Br J ...
Antidysrhythmics, III. Class Summary. Antiarrhythmics are useful in patients with supraventricular and nonsustained ventricular ... Angiotensin II Receptor Blockers (ARBs). Class Summary. Angiotensin receptor blockers are as effective as ACE inhibitors in the ... Olmesartan blocks the vasoconstrictor effects of angiotensin II by selectively blocking binding of angiotensin II to the AT-1 ... Enalapril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of ...
O-Caffeoylquinic Acid Inhibits Angiotensin-II-Induced Vascular Smooth Muscle Cell Proliferation and Migration by Downregulating ... O-Caffeoylquinic Acid Inhibits Angiotensin-II-Induced Vascular Smooth Muscle Cell Proliferation and Migration by Downregulating ... 3Institute of Traditional Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan. ... Wen-Fei Chiou,1,2,3 Chien-Chih Chen,1 and Bai-Luh Wei2 ... Wen-Fei Chiou, Chien-Chih Chen, and Bai-Luh Wei, "3,4-Di- ...
However, it was alarming to hear that the FDA has approved angiotensin II for use based on it. Precious little evidence is ... With angiotensin II arriving at hospitals soon, some cautions are in order. ... Upon first reading the ATHOS-3 trial, I was pleasantly optimistic. Who wouldnt be interested in a shiny new vasopressor? The ... PulmCrit- Angiotensin II: five cautions & three comparisons. PulmCrit- Angiotensin II: five cautions & three comparisons. ...
Probiotics (VSL#3) Prevent Endothelial Dysfunction in Rats with Portal Hypertension: Role of the Angiotensin System ... PLOS is a nonprofit 501(c)(3) corporation, #C2354500, and is based in San Francisco, California, US ...
angiotensin. AT1R. ANG II type 1 receptor. H3R. histamine 3 receptor. H4R. histamine 4 receptor. I/R. ischemia/reperfusion. l- ... angiotensin II, formed locally by mast cell-derived renin, stimulates NHE via angiotensin II type 1 (AT1) receptors, ... 2003) Angiotensin-(1-7) is an endogenous ligand for the G protein-coupled receptor Mas. Proc Natl Acad Sci U S A 100:8258-8263. ... angiotensin I converting enzyme 2. CBP. clobenpropit. EXP3174. 2-n-butyl-4-chloro-1-((2′-(1H-tetrazol-5-yl) biphenyl-4-yl) ...
airway remodelling, angiotensin-(1-7), collagen-I, human lung fibroblast-myofibroblast transition, Smad2/3, TGF-β1 ... Angiotensin II inhibits DDAH1-nNOS signaling via AT1R and μOR dimerization to modulate blood pressure control in the central ... Angiotensin-(1-7) decreases the expression of collagen I via TGF-β1/Smad2/3 and subsequently inhibits fibroblast-myofibroblast ... Jian Ping Zhou, Wei Tang, Yun Feng, Ning Li, Chen Juan Gu, Qing Yun Li, Huan Ying Wan; Angiotensin-(1-7) decreases the ...
... in two of three consecutive sterile urine samples) and were not treated with ACE inhibitors or angiotensin receptor blockers. ... the genetic structure of ACE is made up of three ancestral regions. The chosen SNP were selected in these three regions because ... Angiotensin-converting enzyme gene (ACE) is a risk factor for DN. Its plasma levels have been reported to be associated with DN ... Angiotensin 1-converting enzyme gene (ACE) is a risk factor for diabetic nephropathy (DN) in patients with type 1 diabetes. The ...
The angiotensin II antagonist [Sar1,Ala8]angiotensin II inhibited angiotensin II-stimulated corticosterone and aldosterone ... Effects of angiotensin II and [Sar1,Ala8]angiotensin II. Robert F. Bing, Dennis Schulster ... Effects of angiotensin II and [Sar1,Ala8]angiotensin II Message Subject (Your Name) has forwarded a page to you from ... Angiotensin II effects on cyclic AMP production and steroid output were studied in a sensitive preparation of isolated rat ...
Effect of Renin Angiotensin System Blockade on Pentraxin 3 Levels in Type-2 Diabetic Patients With Proteinuria. Mahmut Ilker ... After three washing intervals, 100 μl enzyme conjugate (peroxidase-labeled anti-CRP) was added on each micro well for ... Three adjacent measurements of end-diastolic brachial artery diameter were made from single two-dimensional frames. All ... Peng N, Liu JT, Gao DF, Lin R, Li R: Angiotensin II-induced C-reactive protein generation: Inflammatory role of vascular smooth ...
ClC-3 promotes angiotensin II-induced reactive oxygen species production in endothelial cells by facilitating Nox2 NADPH ... Treatment with angiotensin II (Ang II, 1 μmol/L) significantly elevated ClC-3 expression in cultured human umbilical vein ... Recent evidence suggests that ClC-3, a member of the ClC family of Cl− channels or Cl−/H+ antiporters, plays a critical role in ... ClC-3 promotes angiotensin II-induced reactive oxygen species production in endothelial cells by facilitating Nox2 NADPH ...
... and Family-Based Study in Three European Populations. Samy Hadjadj, Lise Tarnow, Carol Forsblom, Gbenga Kazeem, Michel Marre, ... Association between Angiotensin-Converting Enzyme Gene Polymorphisms and Diabetic Nephropathy: Case-Control, Haplotype, and ... Association between Angiotensin-Converting Enzyme Gene Polymorphisms and Diabetic Nephropathy: Case-Control, Haplotype, and ... Association between Angiotensin-Converting Enzyme Gene Polymorphisms and Diabetic Nephropathy: Case-Control, Haplotype, ...
The role of angiotensin II.. S Ichikawa, J A Johnson, W L Fowler, C G Payne, K Kurz, W F Keitzer ... Infusions of angiotensin II (A II) in either subpressor or pressor amounts potentiated the pressor responses to NE in normal ... Infusion of the A II antagonist, [1-sarcosine, 8-isoleucine]angiotensin II, did not alter the pressor responses of normal ... this A II antagonist did not alter the control arterial pressure in any of the three groups of rabbits. These studies show that ...
In response to lowered blood pressure, the renin enzyme cleaves angiotensin-1 from angiotensin. Angiotensin-converting enzyme ( ... Peptide binds specifically to a new angiotensin binding site distinct from angiotensin 2 receptors. ... ACE) then removes a dipeptide to yield the physiologically active peptide angiotensin-2, the most potent pressor substance ...
Chronic activation of the angiotensin II (ANG II) type 1 receptor (AT-1R) is critical in the development of chronic kidney ... a phosphoinositide 3-kinase (PI3K) inhibitor), an Akt inhibitor, and stable transfection of dominant negative-Akt1. ANG II ... Angiotensin II Induces Endothelin-1 Expression in Human Hepatic Stellate Cells. *Chao He, Xiongying Miao, Jiequn Li, Haizhi Qi ... Angiotensin II Protects Primary Rat Hepatocytes against Bile Salt-Induced Apoptosis. *Golnar Karimian, Manon Buist-Homan, ...
NitRated Angiotensin I, Certified Mass Spec grade Proteins A ... NitRated Angiotensin I, Certified Mass Spec grade 3 vials Alfa ...
Mouse anti-Human ANGIOTENSIN I/II/III Monoclonal Antibody-NP_000020.1 (MBS211345) product datasheet at MyBioSource, Primary ... ANGIOTENSIN I/II/III. This item recognizes Angiotensin I, Angiotensin II and Angiotensin III in ELISA.. Incomplete mapping ... Angiotensin 2-8; Angiotensin III; Ang III; Des-Asp[1]-angiotensin IIAngiotensin-4; Alternative name(s):; Angiotensin 3-8; ... Angiotensin 1-10; Angiotensin I; Ang IAngiotensin-2; Alternative name(s):; Angiotensin 1-8; Angiotensin II; Ang IIAngiotensin-3 ...
angiotensin III ligand page. Quantitative data and detailed annnotation of the targets of licensed and experimental drugs. ... Ang, AngII, angiotensin II, angiotensinogen, angiotensinogen (PAT), angiotensinogen (serpin peptidase inhibitor, clade A, ... angiotensinogen (serpin peptidase inhibitor, angiotensinogen (serpin peptidase inhibitor, clade A, member 8), angiotensin ...
angiotensin III ligand page. Quantitative data and detailed annnotation of the targets of licensed and experimental drugs. ...
Angiotensin III (Ang III, 10−7M) significantly stimulates p38 phosphorylation. Cells were incubated with Ang III (10−7 M) for ... Angiotensin III (Ang III)-induced monocyte chemoattractant protein-1 (MCP-1) production in HK-2 cells via the Ang II type-1 ( ... 1. Angiotensin III (Ang III) increases monocyte chemoattractant protein-1 synthesis in HK-2 cells by stimulating p38 and c-Jun ... Conversion of renal angiotensin II to angiotensin III is critical for AT2 receptor-mediated natriuresis in rats. Hypertension ...
  • More recently, a possible link between ACEI treatment-associated adverse effects and chymase has also been suggested: as chymase represents an alternative pathway for the activation of angiotensin II, it is possible that ACE inhibition may lead to an increased biological significance of this enzyme. (ahajournals.org)
  • Intensive glycemic and blood pressure control, combined with renin - angiotensin system blocking therapy (including ACEI and ARB drugs), has to a certain extent, delayed the progression of DKD, but still cannot completely block its development. (clinicaltrials.gov)
  • Thus, H 3 receptor-mediated NHE inhibition in ischemia/reperfusion not only opposes the angiotensin II-induced stimulation of NHE in cardiac sympathetic neurons, but also down-regulates AT 1 receptor expression. (aspetjournals.org)
  • The purpose of this investigation was therefore to ascertain whether enhanced ischemic cardiac dysfunction, which is manifest when H 3 Rs are blocked or deleted, results from an unimpeded AT 1 R-NHE activation. (aspetjournals.org)
  • To test the hypothesis that early exercise training after myocardial infarction (MI) could preserve cardiac function, alleviate left ventricular (LV) remodeling and induce a protective effect on morphology, male Sprague-Dawley rats underwent coronary ligation or sham operation, and were assigned to 3 groups: Sham, sedentary MI (SedMI), and exercise MI (ExMI). (biomedsearch.com)
  • A cross-sectional, prospective observational study with purposive sampling was conducted at two cardiac outpatient centers in 70 congestive heart failure patients for a period of 3 months. (ijpsonline.com)
  • Cardiotropin-1 increases angiotensin mRNA in rat cardiac myocytes through STAT-3. (nii.ac.jp)
  • We investigated whether angiotensin III (Ang III) is involved in monocyte recruitment through regulation of the chemokine monocyte chemoattractant protein-1 (MCP-1) in cultured human proximal tubular epithelial cells (HK-2 cells). (kjim.org)
  • Regulation of L-type inward calcium channel activity by captopril and angiotensin II via the phosphatidyl inositol 3-kinase pathway in cardiomyocytes from volume-overload hypertrophied rat hearts. (semanticscholar.org)
  • Teleost renal function: regulation by arginine vasotocin and by angiotensins. (hud.ac.uk)
  • Ang II) is considered to be the main effector of renin-angiotensin system (RAS) in the control and regulation of blood pressure. (ahajournals.org)
  • He J, Huang C, Jiang J, Lv L. Propofol exerts hippocampal neuron protective effects via up-regulation of metallothionein-3. (springer.com)
  • The dose of angiotensin II was allowed to increase up to 200 ng/kg/min over the first three hours, but subsequently decreased to 0-40 ng/kg/min (figure below). (emcrit.org)
  • We reported recently that chronic infusion of a low dose of angiotensin II directly into the renal artery of dogs for 1 mo resulted in a sustained increase in arterial pressure ( 12 ). (physiology.org)
  • The same six chronically instrumented dogs were subjected to both intrarenal and intravenous infusion of a fixed dose of angiotensin II. (physiology.org)
  • GENTAUR suppliers human normal cells, cell lines, RNA extracts and lots of antibodies and ELISA kits to Human proteins as well as Angiotensin III, anti_human IgG. (antibody-antibodies.com)
  • The analysis of the three-dimensional structure of proteins and the spatial arrangement of subunits within protein complexes is of great importance to study their biological function ( 1 ). (mcponline.org)
  • Although specific mechanisms directing ARE activity have not been fully elucidated, current models suggest ARE-binding proteins target specific mRNAs to cellular pathways that influence 3'-polyadenylate tail and 5'-cap metabolism. (wikipedia.org)
  • In the present study, we analysed the effect of Ang-(1-7) on AngII (angiotensin II)-induced HLF (human lung fibroblast)-MF (myofibroblast) transition by detecting Col-I (collagen type I), TGF-β1 (transforming growth factor-β1) and α-SMA (α-smooth muscle actin) expression. (portlandpress.com)
  • Large intravenous boluses of angiotensin III (15 nmol/kg) produced a predictable pressor peak (82±4 mm Hg) followed by a depressor phase (20±3 mm Hg), whereas equipressor doses of angiotensin II were less effective at producing depressor responses. (ahajournals.org)
  • Angiotensin-(1-7) did not exert a depressor action, and the reduced potency of angiotensin IV (relative to angiotensin III) was similar for both the pressor and depressor phases (≈100-fold). (ahajournals.org)
  • Early in vitro work showed vasorelaxation by angiotensins in some vascular beds, 1 2 3 and Campbell et al 4 reported a vasodepressor phase after the characteristic pressor response to angiotensin II in conscious rabbits. (ahajournals.org)
  • Pressor responses to norepinephrine in rabbits with 3-day and 30-day renal artery stenosis. (ahajournals.org)
  • Pressor responses to norepinephrine (NE) infusions were examined in normal rabbits, in rabbits with renal artery stenosis of over 30 days' duration (chronic renal hypertensive rabbits), and in rabbits with renal artery stenosis of 3 days' duration (3-day clipped rabbits). (ahajournals.org)
  • Infusions of angiotensin II (A II) in either subpressor or pressor amounts potentiated the pressor responses to NE in normal rabbits, whereas, in 3-day clipped rabbits and chronic renal hypertensive rabbits, A II in subpressor or pressor doses did not alter the pressor responses to NE. (ahajournals.org)
  • 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. (abbiotec.com)
  • Lamprey ANG I produced dorsal-aortic pressor responses in L. fluviatilis but the rise was very small in comparison to that produced by angiotensin II. (hud.ac.uk)
  • 8 Injection of Ang III peptide in cerebral ventricles has been found to have dose-dependent pressor responses similar to those of Ang II. (ahajournals.org)
  • BIBS39 is a nonpeptide angiotensin II (AII) receptor antagonists that displaced [125I] AII from its specific binding sites with a K(i) value of 29 +/- 7 nM for the AII subtype I (AT1) receptor and a K(i) value of 480 +/- 110 nM for the AII subtype 2 (AT2) receptor. (adooq.com)
  • 5 Depressor or dilator responses to angiotensins are not duplicated by other vasopressors, tend to be manifested at high angiotensin concentrations, and might be prominent in specific vascular beds. (ahajournals.org)
  • Wen-Fei Chiou, Chien-Chih Chen, and Bai-Luh Wei, "3,4-Di- O -Caffeoylquinic Acid Inhibits Angiotensin-II-Induced Vascular Smooth Muscle Cell Proliferation and Migration by Downregulating the JNK and PI3K/Akt Signaling Pathways," Evidence-Based Complementary and Alternative Medicine , vol. 2011, Article ID 634502, 8 pages, 2011. (hindawi.com)
  • Angiotensin (Ang) II commonly increases the expression of adhesion molecules and cytokines, such as selectins, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and chemokine (C-C motif) ligand 2/monocyte chemoattractant protein-1 (MCP-1) in target cells, resulting in the recruitment of inflammatory cells from the blood to tissues [ 8 , 9 ]. (kjim.org)
  • Angiotensin II increases blood pressure by stimulating the Gq protein in vascular smooth muscle cells (which in turn activates an IP3-dependent mechanism leading to a rise in intracellular calcium levels and ultimately causing contraction). (wikipedia.org)
  • Other Angiotensin II actions include induction of growth, cell migration, and mitosis of vascular smooth muscle cells, increased synthesis of collagen type I and III in fibroblasts, leading to thickening of the vascular wall and myocardium, and fibrosis. (abmole.com)
  • H 3 receptor activation in differentiated sympathetic neuron-like PC12 cells permanently transfected with H 3 receptor cDNA caused a decrease in protein kinase C activity and AT 1 receptor protein abundance. (aspetjournals.org)
  • Ang III increased MCP-1 protein production in dose- and time-dependent manners in HK-2 cells, which was inhibited by the AT1 receptor blocker losartan. (kjim.org)
  • Total phosphorylated JNK protein levels tended to increase 20 minutes after stimulation with Ang III. (kjim.org)
  • Ang III increases MCP-1 synthesis via stimulation of intracellular p38 and JNK MAPK signaling activity and subsequent activated protein-1 transcriptional activity in HK-2 cells. (kjim.org)
  • Three groups of wild-type (tgNhe3+/+) and six groups of tgNhe3-/- mice (n=>8 per group) were treated with vehicle, ANG II (40 ng/min, i.p.), or in vivo adenovirus-mediated transfer of an intracellular ANG II fusion protein, ECFP/ANG II, for 2 weeks. (ovid.com)
  • Angiotensin 1-7 is a ligand for the G-protein coupled receptor MAS1 (By similarity). (abcam.com)
  • Among the most established of these are hydrogen/deuterium exchange ( 2 ), oxidative footprinting ( 3 ), and-for the analysis of intact protein complexes-native MS techniques ( 4 ). (mcponline.org)
  • The ACTN3 gene provides instructions for making a protein called alpha (α)-actinin-3, which is predominantly found in fast-twitch muscle fibers. (medlineplus.gov)
  • A variant in this gene, called R577X, leads to production of an abnormally short α-actinin-3 protein that is quickly broken down. (medlineplus.gov)
  • We examined the effects of losartan and PD123177 on dose-mean arterial pressure (MAP) response curves for ANG II and ANG III in eight groups (n = 6 each) of conscious rats. (elsevier.com)
  • Losartan dose dependently shifted the dose-response curves of ANG II and ANG III to the right with similar dissociation constants (-log K(I) of 6.6 ± 0.7 and 6.6 ± 0.1 mol/kg, respectively) and no change in the maxima. (elsevier.com)
  • Suzuki M, Hori K, Abe I, Saito S.and Sato H. (1981) A new approach to cancer chemotherapy: Selective enhancement of tumor blood flow with angiotensin II. (springer.com)
  • Sato H, Sato K, Sato Y, Mimata Y, Asamura M, Kanamaru R, Wakui A, Suzuki M and Sato H. (1980) Clinical study on selective enhancement of drug delivery by angiotensin II in cancer chemotherapy. (springer.com)
  • Sato H, Sato K, Sato Y, Asamura M, Kanamaru R, Mimata Y. and Wakui A. (1981) Clinical cancer chemotherapy based on the experimental findings of selective enhancement of drug delivery to tumor tissue by angiotensin II. (springer.com)
  • In addition, albuminuria is a strong predictor of cardiovascular disease (CVD), after adjustment for other recognized risk factors, including GFR ( 2 , 3 ). (asnjournals.org)
  • Chronic activation of the angiotensin II (ANG II) type 1 receptor (AT-1R) is critical in the development of chronic kidney disease. (semanticscholar.org)
  • Metabolic products such as Ang III, Ang IV, and Ang 1 to 7, have been discovered by investigating enzymatic degradation of Ang II in kidney tissues [ 10 ]. (kjim.org)
  • In addition, angiotensin II acts at the Na/H + exchanger in the proximal tubules of the kidney to stimulate Na reabsorption and H + excretion which is coupled to bicarbonate reabsorption. (wikipedia.org)
  • Angiotensin I (ANG I) was isolated from incubates of plasma and kidney extracts of the river lamprey, Lampetra fluviatilis, using eel vasopressor activity as an assay during purification. (hud.ac.uk)
  • In order to delineate further the molecular evolution of the renin-angiotensin system in vertebrates, angiotensin I (ANG I) has been isolated after incubation of plasma and kidney extracts of emu (Dromiceus novaehollandiae), axolotl (Ambystoma mexicanum), and sea lamprey (Petromyzon marinus). (hud.ac.uk)
  • Chemical structure of angiotensin formed with kidney renin in the Japanese eel Anguilla japonica. (hud.ac.uk)
  • To better understand the direct effects of paricalcitol on anemia in patients with chronic kidney disease (stage 3-5), we conducted a pilot trial in 60 patients who were randomly allocated equally to 2 groups to receive or not paricalcitol orally for 6 months. (clinicaltrials.gov)
  • Thus intrarenal infusion of low-dose angiotensin II produced a chronic increase in arterial pressure due to an action within the kidney. (physiology.org)