Patricia Castro-Moreno

Universidad Nacional Autónoma de México, Ciudad de México, The Federal District, Mexico

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Publications (3)0 Total impact

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    ABSTRACT: We investigated captopril effects, an ACE inhibitor, on hypertension development, on Ang II and Ang-(1-7) plasma concentrations, on Ang II-induced contraction in isolated kidneys, and on kidney AT1R from spontaneously hypertensive (SHR) rats. Five weeks-old SHR and Wistar Kyoto (WKY) rats were treated with captopril at 30 mg/kg/day, in drinking water for 2 or 14 weeks. Systolic blood pressure (SBP) was measured, and isolated kidneys were tested for perfusion pressure and AT1R expression; while Ang II and Ang-(1-7) concentrations were determined in plasma. Captopril did not modify SBP in WKY rats and avoided its increase as SHR aged. Plasma Ang-II concentration was ∼4-5 folds higher in SHR rats, and captopril reduced it (P < 0.05); while captopril increased Ang-(1-7) by ∼2 fold in all rat groups. Captopril increased Ang II-induced pressor response in kidneys of WKY and SHR rats, phenomenon not observed in kidneys stimulated with phenylephrine, a α(1) -adrenoceptor agonist. Captopril did not modify AT1R in kidney cortex and medulla among rat strains and ages. Data indicate that captopril increased Ang II-induced kidney perfusion pressure but not AT(1) R density in kidney of WKY and SHR rats, due to blockade of angiotensin II synthesis; however, ACE inhibitors may have other actions like activating signaling processes that could contribute to their diverse effects.
    Autonomic &amp Autacoid Pharmacology 10/2012; 32(3 Pt 4):61-9.
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    ABSTRACT: The renal renin angiotensin system modulates blood pressure via the action of angiotensin II at type 1 (AT1) and type 2 (AT2) angiotensin receptors. It has been proposed that there is an increased pressor response to angiotensin II (ANG II) in the hypertensive rat kidney. We determined the role of the AT1 receptor in L-NAME-induced hypertension. Male Wistar rats (250-300 g) were divided into control (tap water) and L-NAME (50 mg/kg/day/2 weeks) treated groups. Concentration-response curves to ANG II were constructed in isolated perfused kidneys and AT1 receptor expression was determined by Western blot in the renal cortex, medulla and papilla. ANG II evoked an increase in perfusion pressure in kidneys of both control and L-NAME-treated rats in a concentration-related manner. In L-NAME-treated rats, a greater maximal effect was observed compared to control rats (160 +/- 13 vs. 138 +/- 8 mmHg; p<0.05, respectively), suggesting that L-NAME promoted ANG II hypersensitivity. In both, control and L-NAME groups, the response to ANG II was blocked by the selective AT1 receptor antagonist losartan (1 x 10(-8) and 3.16 x 10(-8) M). AT1 receptor expression in kidney cortex, medulla and papilla did not show significant differences between groups. Our results demonstrate that AT1 receptor stimulation is related to renal vasculature hypersensitivity in L-NAME-induced hypertension.
    Proceedings of the Western Pharmacology Society 01/2009; 52:47-9.
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    ABSTRACT: The blockade of renin-angiotensin system by pharmacological interventions with angiotensin converting-enzyme (ACE) inhibitors or AT1 receptor antagonists in the juvenile critical age may attenuate or even prevent the development of hypertension. In this work, we determined the Ang II type 1 (AT1) receptor role in L-NAME-induced hypertension in pithed rats. Male Wistar rats (250-300 g) were used. Rats were divided into the following groups: Control (tap water) and N(omega)-Nitro-L-arginine methyl ester (L-NAME, 60 mg/kg/day/2 weeks). Dose-response curves to Ang II were constructed in the pithed rat. The results show that Ang II evoked blood pressure increase in pithed rats in a dose-related manner. In L-NAME-treated rats a greater maximal effect was observed, indicating that L-NAME promotes Ang II hypersensitivity. In L-NAME-treated rats, Ang II response was blocked by losartan (1 and 3 mg/kg), a selective AT1 receptor antagonist, indicating that AT1 receptor influence L-NAME hypertensive mechanism. Our results suggest that Ang II hypersensitivity in L-NAME-induced hypertension can be due to increased AT1 receptor expression or sensitivity changes.
    Proceedings of the Western Pharmacology Society 01/2009; 52:54-6.