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卡托普利对去甲肾上腺素血管收缩性的影响。

Effect of captopril on norepinephrine vascular contractility.

作者信息

Ubeda M, Fenoy F, Carbonell L F, Salazar F J, García-Estañ J, Salom M G, Quesada T

出版信息

Gen Pharmacol. 1985;16(3):303-6. doi: 10.1016/0306-3623(85)90091-6.

Abstract

In isolated aortic rings and in vitro perfused mesenteric arteries of Wistar rats the vasoconstrictor responses to norepinephrine (NE) were not affected by captopril (2 X 10(-4) M). However, captopril (1 mg/kg i.v.) in pithed Wistar rats attenuated significantly the increases in diastolic blood pressure induced by NE. In pithed rats the effect of captopril on NE diastolic blood pressure responses disappeared either in the presence of an angiotensin II (5 ng X kg-1 X min) infusion or when the rats were previously nephrectomized. These findings suggest that the effect of captopril on vascular responses to norepinephrine is mediated by an inhibition of the renin-angiotensin system and not by an antagonistic effect on alpha-adrenergic receptors.

摘要

在Wistar大鼠的离体主动脉环和体外灌注肠系膜动脉中,卡托普利(2×10⁻⁴ M)不影响去甲肾上腺素(NE)引起的血管收缩反应。然而,在脊髓横断的Wistar大鼠中,静脉注射卡托普利(1 mg/kg)可显著减弱NE引起的舒张压升高。在脊髓横断的大鼠中,无论是在输注血管紧张素II(5 ng·kg⁻¹·min)时,还是在大鼠预先肾切除后,卡托普利对NE舒张压反应的作用均消失。这些发现表明,卡托普利对血管对去甲肾上腺素反应的作用是通过抑制肾素-血管紧张素系统介导的,而不是通过对α-肾上腺素能受体的拮抗作用。

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