钾通道在内源性和药理学血管扩张剂血管反应中的作用。

Blood vessels Pub Date : 1991-01-01 DOI:10.1159/000158854
J E Brayden, J M Quayle, N B Standen, M T Nelson
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引用次数: 65

摘要

许多内源性和药理学血管扩张剂使血管平滑肌超极化,这种反应似乎是由于对钾离子的电导增加。超极化可能通过引起电压依赖性钙通道的关闭来促进扩张的机制。最近的证据表明,对超极化血管扩张剂的反应是通过激活atp敏感钾(KATP)通道介导的。cromakalim和降钙素基因相关肽(CGRP)可激活离体血管平滑肌细胞上的单个KATP通道。这种反应被格列本脲抑制。Cromakalim、CGRP和其他血管扩张剂在体外可使动脉超极化和舒张,而这些反应可被格列本脲逆转。这些药物在体内的降压作用被格列本脲所拮抗。我们认为KATP通道的激活和相关的膜超极化是血管舒张的一个重要的一般机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Role of potassium channels in the vascular response to endogenous and pharmacological vasodilators.

Many endogenous and pharmacological vasodilators hyperpolarize vascular smooth muscle and this response appears to be due to an increased conductance to potassium ions. The hyperpolarization may contribute to the mechanism of dilation by causing voltage-dependent calcium channels to close. Recent evidence indicates that the response to hyperpolarizing vasodilators is mediated through activation of ATP-sensitive potassium (KATP) channels. Single KATP channels on isolated vascular smooth muscle cells are activated by cromakalim and calcitonin gene-related peptide (CGRP). This response is inhibited by glibenclamide. Cromakalim, CGRP and other vasodilators hyperpolarize and relax arteries in vitro and these responses are reversed by glibenclamide. The hypotensive effects of these agents in vivo are antagonized by glibenclamide. We propose that activation of KATP channels and the associated membrane hyperpolarization represents an important general mechanism of vasodilation.

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