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钾通道开放剂通过激活ATP敏感性钾通道诱导线粒体基质体积变化。

Potassium channel openers induce mitochondrial matrix volume changes via activation of ATP-sensitive K+ channel.

作者信息

Szewczyk A, Mikołajek B, Pikuła S, Nałecz M J

机构信息

Nencki Institute of Experimental Biology, Department of Muscle Biochemistry, Warszawa, Poland.

出版信息

Pol J Pharmacol. 1993 Jul-Aug;45(4):437-43.

PMID:8118486
Abstract

Recently, using patch-clamp method, an ATP-sensitive potassium channel in rat liver mitochondrial inner membrane was identified. In this report we investigated the effects of different potassium channel openers on potassium ion permeability of rat liver mitochondria. For that purpose we employed light scattering technique, reflecting mitochondrial volume changes linked to solute transport. Among various potassium channel openers RP 66471, pinacidil, minoxidil sulfate and KRN 2391 were found to stimulate mitochondrial swelling with high efficiency. P1060, aprykalim and diazoxide had only a slight effect, while Ro 31-6930 and nicorandil were found ineffective. Activation by the K+ openers was abolished by the antidiabetic sulfonylurea, glibenclamide (the well known blocker of ATP-sensitive potassium channels). These findings may suggest that mitochondrial ATP-dependent K+ channel is involved in regulation of mitochondrial matrix volume.

摘要

最近,利用膜片钳技术,在大鼠肝线粒体内膜中鉴定出一种ATP敏感性钾通道。在本报告中,我们研究了不同钾通道开放剂对大鼠肝线粒体钾离子通透性的影响。为此,我们采用光散射技术,该技术反映了与溶质转运相关的线粒体体积变化。在各种钾通道开放剂中,发现RP 66471、匹莫齐特、硫酸米诺地尔和KRN 2391能高效刺激线粒体肿胀。P1060、阿普卡林和二氮嗪只有轻微作用,而Ro 31-6930和尼可地尔无效。抗糖尿病磺酰脲类药物格列本脲(众所周知的ATP敏感性钾通道阻滞剂)可消除钾通道开放剂的激活作用。这些发现可能表明线粒体ATP依赖性钾通道参与线粒体基质体积的调节。

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