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pubmed-article:17481584pubmed:abstractTextTo 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 Ca(2+)- and voltage-dependent and were inhibited by 0.1 microM 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(+).lld:pubmed
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pubmed-article:17481584pubmed:dateRevised2007-12-3lld:pubmed
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pubmed-article:17481584pubmed:year2007lld:pubmed
pubmed-article:17481584pubmed:articleTitleHypoxia increases BK channel activity in the inner mitochondrial membrane.lld:pubmed
pubmed-article:17481584pubmed:affiliationDepartment of Pediatrics (Section of Respiratory Medicine), University of California San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0735, USA.lld:pubmed
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