Role of potassium channels in the vascular response to endogenous and pharmacological vasodilators.
Role of potassium channels in the vascular response to endogenous and pharmacological vasodilators.
复制标题
钾通道在血管对内源性和药理学血管扩张剂的反应中的作用。
DOI：
10.1159/000158854
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Nelson,MT
中科院分区：
文献类型：
--
作者：
Brayden,JE;Quayle,JM;Standen,NB;Nelson,MT
许多内源性和药理性血管扩张剂使血管平滑肌充血，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关闭而参与扩张机制。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敏感性钾（Katp）通道介导的。分离的血管平滑肌细胞上的单Katp通道被cromakalim和降钙素基因相关肽（CGRP）激活。这种反应被格列本奈抑制。Cromakalim，CGRP和其他血管扩张剂在体外使动脉舒张和舒张，这些反应被格列本奈逆转。格列本奈可拮抗这些药物在体内的肿胀作用。我们认为KATP通道的激活和相关的膜超极化是血管舒张的重要机制。
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 glibenclainide. Cromakalim, CGRP and other vasodilators hyperpolarize and relax arteries in vitro and these responses are reversed by glibenclainide. The hypotensive effects of these agents in vivo are antagonized by glibenclainide. We propose that activation of KATPchannels and the associated membrane hyperpolarization represents an important general mechanism of vasodilation.