Opening of potassium channels modulates mitochondrial function in rat skeletal muscle
Opening of potassium channels modulates mitochondrial function in rat skeletal muscle
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DOI：
10.1016/s0005-2728(02)00340-7
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发表时间：
2002-12-02
影响因子：
4.3
通讯作者：
Kunz, WS
中科院分区：
文献类型：
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作者：
Debska, G;Kicinska, A;Kunz, WS
我们研究了大鼠骨骼肌中二氮嗪和尼可地尔激活的K+通道的存在。在大鼠骨骼肌成肌细胞系L 6中，钾转运的激活引起细胞耗氧量的刺激，这意味着线粒体效应。与分离的大鼠骨骼肌线粒体一起工作，两种钾通道开放剂（KCO）都刺激呼吸，使线粒体内膜脱钙，并以严格的钾依赖性方式导致线粒体NAD系统的氧化。这是KCO介导的线粒体内膜钾转运刺激的强烈指示。此外，二氮嗪和尼可地尔对骨骼肌线粒体氧化磷酸化的钾特异性作用被抗糖尿病磺酰脲衍生物格列本脲（一种众所周知的ATP调节钾通道（K-ATP通道）抑制剂）完全消除。由于二氮嗪和尼可地尔在相同浓度下均促进KSCN缓冲液中失能线粒体的肿胀，因此我们的结果表明大鼠骨骼肌中存在线粒体ATP调节的钾通道（mitoK（ATP）通道），其可调节线粒体氧化磷酸化。(C)2002 Elsevier Science B. V.保留所有权利。
We have investigated the presence of diazoxide- and nicorandil-activated K+ channels in rat skeletal muscle. Activation of potassium transport in the rat skeletal muscle myoblast cell line L6 caused a stimulation of cellular oxygen consumption, implying a mitochondrial effect. Working with isolated rat skeletal muscle mitochondria, both potassium channel openers (KCOs) stimulate respiration, depolarize the mitochondrial inner membrane and lead to oxidation of the mitochondrial NAD-system in a strict potassium-dependent manner. This is a strong indication for KCO-mediated stimulation of potassium transport at the mitochondrial inner membrane. Moreover, the potassium-specific effects of both diazoxide and nicorandil on oxidative phosphorylation in skeletal muscle mitochondria were completely abolished by the antidiabetic sulfonylurea derivative glibenclamide, a well-known inhibitor of ATP-regulated potassium channels (K-ATP channels). Since both diazoxide and nicorandil facilitated swelling of de-energised mitochondria in KSCN buffer at the same concentrations, our results implicate the presence of a mitochondrial ATP-regulated potassium channel (mitoK(ATP) channel) in rat skeletal muscle which can modulate mitochondrial oxidative phosphorylation. (C) 2002 Elsevier Science B.V. All rights reserved.