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Cardiac mitochondrial ATP‐sensitive potassium channel is activated by nitric oxide in vitro
Author(s) -
Ljubkovic Marko,
Shi Yang,
Cheng Qunli,
Bosnjak Zeljko,
Jiang Ming Tao
Publication year - 2007
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2007.07.071
Subject(s) - glibenclamide , nitric oxide , potassium channel , mitochondrion , chemistry , membrane potential , molsidomine , atp sensitive potassium channel , pharmacology , inner mitochondrial membrane , microbiology and biotechnology , biophysics , biochemistry , biology , endocrinology , organic chemistry , diabetes mellitus
Previous observations on the activation of the mitochondrial ATP‐sensitive potassium channel (mitoK ATP ) by nitric oxide (NO) in myocardial preconditioning were based on indirect evidence. In this study, we have investigated the direct effect of NO on the rat cardiac mitoK ATP after reconstitution of the inner mitochondrial membranes into lipid bilayers. We found that the mitoK ATP was activated by exogenous NO donor S ‐nitroso‐ N ‐acetyl penicillamine or PAPA NONOate. This activation was inhibited by mitoK ATP blockers 5‐hydroxydecanoate or glibenclamide. Our observations confirm that NO can directly activate the cardiac mitoK ATP , which may underlie its contribution to myocardial preconditioning.