Hypoxia increases BK channel activity in the inner mitochondrial membrane

被引:32
作者
Gu, Xiang Q.
Siemen, Detlef
Parvez, Suhel
Cheng, Yu
Xue, Jin
Zhou, Dan
Sun, Xiaolu
Jonas, Elizabeth A.
Haddad, Gabriel G.
机构
[1] Univ Calif San Diego, Dept Pediat, Sect Resp Med, La Jolla, CA 92093 USA
[2] Univ Calif San Diego, Dept Neurosci, La Jolla, CA 92093 USA
[3] Rady Childrens Hosp, San Diego, CA 92123 USA
[4] Univ Magdeburg, Dept Neurol, D-39120 Magdeburg, Germany
[5] Yale Univ, Sch Med, Dept Internal Med, New Haven, CT 06520 USA
关键词
BK channels; hypoxia; mitoplast;
D O I
10.1016/j.bbrc.2007.04.110
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:311 / 316
页数:6
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