Hypoxia increases BK channel activity in the inner mitochondrial membrane
Hypoxia increases BK channel activity in the inner mitochondrial membrane
复制标题
DOI：
10.1016/j.bbrc.2007.04.110
复制
发表时间：
2007-06-22
影响因子：
3.1
通讯作者：
Haddad, Gabriel G.
中科院分区：
文献类型：
--
作者：
Gu, Xiang Q.;Siemen, Detlef;Haddad, Gabriel G.
为了探索生理和缺氧条件下线粒体内膜BK通道的潜在功能，我们使用了线粒体膜上和整个线粒体膜上的膜片。单BK通道在对称K+溶液中的电导为276 +/- 9 pS，具有Ca ~（2+）和电压依赖性，并可被0.1 μ M的Charybdotoxin抑制。在对缺氧的反应中，BK增加了开放概率，使其反转电位（9.3 +/- 2.4 mV）正向移动，但不改变其电导。我们的结论是：（1）该线粒体K+通道在静止时的性质与质膜中的BK通道的性质相似;（2）缺氧诱导该K+通道的开放概率增加，而不是减少（如在质膜中），导致K+从线粒体基质流出到外部。我们推测，这种增加K+流出线粒体进入胞质是重要的缺氧期间，在维持胞质K+。(c)2007年爱思唯尔公司All rights reserved.
To explore the potential function of the BK channel in the inner mitochondrial membrane under physiological and hypoxic conditions, we used on-mitoplast and whole-mitoplast patches. Single BK channels had a conductance of 276 +/- 9 pS under symmetrical K+ solutions, were Ca2+- and volt age-dependent and were inhibited by 0.1 mu M charybdotoxin. In response to hypoxia, BK increased open probability, shifted its reversal potential (9.3 +/- 2.4 mV) in the positive direction and did not change its conductance. We conclude that (1) the properties at rest of this mitoplast K+ channel are similar to those of BK channels in the plasma membrane; (2) hypoxia induces an increase, rather than a decrease (as in the plasmalemma), in the open probability of this K+ channel, leading to K+ efflux from the mitochondrial matrix to the outside. We speculate that this increase in K+ efflux from mitochondria into the cytosol is important during hypoxia in maintaining cytosolic K+. (c) 2007 Elsevier Inc. All rights reserved.