Navegando por Palavras-chave "angiotensin converting enzyme"

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    ACE activity during the hypotension produced by standardized aqueous extract of Cecropia glaziovii Sneth: A comparative study to captopril effects in rats
    (Elsevier B.V., 2007-05-01) Ninahuaman, M. F. M. L.; Souccar, C.; Lapa, A. J.; Lima-Landman, M. T. R.; Universidade Federal de São Paulo (UNIFESP)
    To evaluate the effect of the standardized aqueous extract (AE) of Cecropia glaziovii Sneth on the plasma angiotensin I converting enzyme (ACE-EC 3.4.15. 1) activity, rats were treated with a single dose of AE (1 g/kg, p.o.) or repeatedly (0.5 g/kg/bid, p.o.) for 60 days. Captopril (50 mg/kg, p.o.) was used as positive control on the same animals. the effects on the blood pressure were recorded directly from the femoral artery (single dose), or indirectly by the tail cuff method (repeated doses) in conscious rats. the plasma ACE activity was determined spectrofluorimetrically using Hypuril-Hystidine-Leucine as substrate. the arterial blood pressure, heart rate and plasma ACE activity were not significantly modified within 24 h after a single dose administration of AE. Comparatively, blood pressure in captopril treated rats was reduced by 7-16% and heart rate was increased by 10-20% from 30 min to 24 h after drug administration. ACE activity after captopril presented a dual response: an immediate inhibition peaking at 30 min and a slow reversal to 32% up-regulation after 24 h. To correlate the drug effects upon repeated administration of either compound, normotensive rats were separated in three groups: animals with high ACE (48.8 +/- 2.6 nmol/min/ml), intermediate ACE (39.4 +/- 1.4 nmol/min/ml) and low ACE (23.5 +/- 0.6 nmol/min/ml) activity, significantly different among them. Repeated treatment with AE reduced the mean systolic blood pressure (121.7 +/- 0.5 min Hg) by 20 min Hg after 14 days. the hypotension was reversed upon washout 60 days afterwards. Likely, repeated captopril administration decreased blood pressure by 20mm Hg throughout treatment in all groups. After 30 days treatment with AE (0.5 g/kg/bid, p.o.) the plasma ACE activity was unchanged in any experimental group. After captopril (50 mg/ kg/bid, p.o.) administration the plasma ACE activity was inhibited by 50% within I h treatment but it was up-regulated by 120% after 12 h in all groups. It is concluded that the hypotension produced by prolonged treatment with AE of C. glaziovii is unrelated to ACE inhibition. (C) 2006 Elsevier GmbH. All rights reserved.
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    Caracterização fisiopatológica do sistema renina-angiotensina durante o status epilepticus induzido pela pilocarpina em camundongos transgênicos que expressam tonina de rato
    (Universidade Federal de São Paulo (UNIFESP), 2013-12-20) Iha, Higor Alves [UNIFESP]; Mazzacoratti, Maria da Graca Naffah Mazzacoratti [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    Objectives: To evaluate the influence of pilocarpine induced long-term convulsive seizure in transgenic mice with overexpressed plasma and brain Ang II. Methods: Using a 320mg/kg pilocarpine dose to induce SE. Following the injection protocol of CAVALHEIRO (1995). We conducted an investigation of both strains (TGM (rTon) and WT C57Black/6) of the following groups: a) saline group; b) 3 hour in SE group; and c) Tonic-clonic seizure group. The last group was created upon the greater incidence of such crises in rTon when compared with WT. During the SE, we accessed several parameters such as latency for the first seizure, tonic-clonic seizure susceptibility and mortality. In their hippocampi was assessed by western-blot, real-time RT-PCR, respectively, protein and RNAm expression levels of AT1, AT2, B1 and B2 receptors as well as of the ACE ACE2, iNOS and eNOS enzymes. The same was made to AT1 receptor in heart. It was also assessed the enzymatic activity of hippocampal, cardiac and plasmatic ECA. Results: In an assessment of how both strains reacted to the pilocarpine induced SE we found no difference on first seizure latency time, but a significant higher frequency of death during the generalized tonic-clonic seizure in rTon mice, 66% in rTon and 34% in WT. In RAS, KKS and NO analyzed parameters we found in studied mice groups strain comparison that rTon showed: a) Saline group: in mRNA hippocampal expression, greater transcript level for iNOS and lower for B1 receptor, in protein quantifying, greater for hippocampal AT1 receptor and lower for cardiac AT1 receptor, thereafter, on ECA enzymatic activity evaluation, greater in hippocampi and heart a and on ACE activity, in heart on AT1 receptor protein levels and in plasma on ACE activity; b) in Tonic-Clonic group: mRNA levels were reduced transcripts of eNOS and iNOS, protein quantification showed raised in hippocampi raised ECA2 and lowered B1 receptor and in heart raised AT1 receptor, thereafter, in ECA enzymatic activity assessment, increased in hippocampal and in plasmatic forms. c) 3h of SE group: in hippocampi mRNA levels were upkeeped for ECA transcript, raised for ECA2 and eNOS transcript and reduced for iNOS transcript, protein analysis showed greater raised hippocampal and heart AT1 receptor and hippocampal lowered B2 receptor. Thereafter, on ECA enzymatic activity evaluation, showed raised activity on hippocampal and plasmatic forms. Conclusion: Transgenic mice showed in assessed tissues differences on RAS, KKS and iNOS expression. These differences resulted in a differentiated response to pilocarpine induced seizure in RAS, KKS, iNOS and eNOS which culminated in a greater propensity to tonic-clonic seizures and greater frequency of death throughout the SE, but didn´t affected the latency period for the first seizure.
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    Disruption of the kinin B-1 receptor gene affects potentiating effect of captopril on BK-induced contraction in mice stomach fundus
    (Elsevier B.V., 2006-12-01) Barbosa, Ana M. R. B.; Felipe, Sandra A.; Pesquero, Joao B.; Paiva, Antonio C. M.; Shimuta, Suma I.; Universidade Federal de São Paulo (UNIFESP)
    A transgenic mouse model, deficient in kinin B-1 receptor (B-1(-/-)) was used to evaluate the role of B-2 receptor in the smooth muscle stomach fundus. the results showed that the potency of bradykinin (BK) to induce contraction in the gastric tissue was maintained whereas the efficacy was markedly reduced. the angiotensin converting enzyme (ACE) inhibitor captopril potentiated BK-induced effect in wild type (WT) but not in B-1(-/-) fundus. However, ACE activity detected by the convertion of Ang I to Ang II was inhibited by captopril in both types of gastric tissues. Taking into account the hypothesis that captopril and ACE bind to the B2 receptor, we suggest that this complex was not formed in the stomach deficient in B-1 receptor. Therefore, our finding strongly support the hypothesis that in smooth muscles that constitutively express the kinin B1 and B2 receptors, an interaction between captopril and ACE, B1 and B2 receptors should occur forming a complex protein interaction for the potentiating effect of ACE on kinin receptors. (c) 2006 Elsevier Inc. All rights reserved.
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    Fate of bradykinin on the rat liver when administered by the venous or arterial route
    (Blackwell Publishing Asia, 2005-03-01) Gioli-Pereira, L.; Nascimento, E. A.; Santos, E. L.; Bracht, A.; Juliano, M. A.; Pesquero, J. B.; Borges, D. R.; Kouyoumdjian, M.; Universidade Federal de São Paulo (UNIFESP); Maringa State Univ
    Background and Aim: Bradykinin (BK) infused into the portal vein elicits a hypertensive response via the B2 receptor (B2R) and is efficiently hydrolyzed by the liver. Our purpose was to characterize the mechanism of interaction between BK and the liver.Method: BK, HOE-140 (a B2R antagonist), des-R-9-BK (a BIR agonist) and enzyme inhibitors were used in monovascular or bivascular perfusions and in isolated liver cell assays.Results: Des-R-9-BK did not elicit a portal hypertensive response (PHR); BK infused into the hepatic artery elicited a calcium-dependent PHR and a calcium-independent arterial hypertensive response (HAHR), with the latter being almost abolished by naproxen. BK has a predominant distribution in the extracellular space and an average hepatic extraction of 8% in the steady state. Hydrolysis products of infused BK (R-1-F-5 and R-1-P-7) did not elicit PHR. Angiotensin converting enzyme (ACE) is concentrated in the perivenous region and B2R in the periportal region. Microphysiometry showed that BK (and not a B1 agonist) interacts with stellate cells and the endothelial sinusoidal/Kupffer cell fraction. This effect was inhibited by the B2R antagonist.Conclusions: Events can be summarized as: the hypertensive action of BK on sinusoidal cells of the periportal region is followed by its hydrolysis by ACE which is primarily present in the perivenous region; there is no functional B1R in the normal liver; BK induces HAHR via eicosanoid release and PHR by a distinct pathway on the B2R. Our data suggest that BK may participate in the modulation of sinusoidal microvasculature tonus both in the portal and the arterial routes. (C) 2005 Blackwell Publishing Asia Pty Ltd.