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去甲肾上腺素、血管紧张素II和BAY K 8644对维拉帕米消除肾血流自动调节作用的不同影响。

Different effects of noradrenaline, angiotensin II and BAY K 8644 on the abolition of autoregulation of renal blood flow by verapamil.

作者信息

Ogawa N, Ono H

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 1986 Aug;333(4):445-9. doi: 10.1007/BF00500022.

Abstract

To examine the role of Ca channels in autoregulation of renal blood flow in response to changes of perfusion pressure, experiments were performed with perfused kidney in anesthetized dogs using a Ca channel activator, BAY K 8644, and vasoconstrictors such as noradrenaline and angiotensin II. Control observations usually showed excellent autoregulation of renal blood flow at pressures between 120 and 200 mm Hg, the autoregulatory index being less than 0.2. Verapamil (50 micrograms/min, i.a. infusion) obviously inhibited the renal autoregulation. Simultaneous infusion of 5 micrograms/min of BAY K 8644 with verapamil prevented both the increase of renal blood flow and the impairment of the autoregulation caused by verapamil. Whereas simultaneous infusion of noradrenaline (1 and 3 micrograms/min) or angiotensin II (0.1 and 0.3 micrograms/min) with verapamil dose-dependently reduced renal blood flow, these drugs could not antagonize the inhibitory effect of verapamil on autoregulation. The present experiments show that Ca channels play an important role in establishing renal autoregulation, and that a mere vasoconstriction by noradrenaline and angiotensin II is distinguished from autoregulatory performance.

摘要

为研究钙通道在肾血流自动调节以应对灌注压变化中的作用,在麻醉犬的灌注肾实验中使用钙通道激活剂BAY K 8644以及去甲肾上腺素和血管紧张素II等血管收缩剂进行了实验。对照观察通常显示,在120至200 mmHg的压力下肾血流有良好的自动调节,自动调节指数小于0.2。维拉帕米(50微克/分钟,经动脉输注)明显抑制肾自动调节。维拉帕米与5微克/分钟的BAY K 8644同时输注可防止肾血流增加以及维拉帕米引起的自动调节受损。而维拉帕米与去甲肾上腺素(1和3微克/分钟)或血管紧张素II(0.1和0.3微克/分钟)同时输注会剂量依赖性地降低肾血流,但这些药物不能拮抗维拉帕米对自动调节的抑制作用。本实验表明,钙通道在建立肾自动调节中起重要作用,且去甲肾上腺素和血管紧张素II单纯的血管收缩作用与自动调节功能不同。

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