Carbon monoxide inhibits inward rectifier potassium channels in cardiomyocytes

Shenghui Liang, Quanyi Wang, Weiwei Zhang, Hailin Zhang, Shengjiang Tan, Asif Ahmed and Yuchun Gu ()
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Shenghui Liang: Laboratory of Molecular Pharmacology, Institute of Molecular Medicine, Peking University
Quanyi Wang: Laboratory of Molecular Pharmacology, Institute of Molecular Medicine, Peking University
Weiwei Zhang: Laboratory of Molecular Pharmacology, Institute of Molecular Medicine, Peking University
Hailin Zhang: Hebei Medical University
Shengjiang Tan: MRC Laboratory of Molecular Biology, Hills Road
Asif Ahmed: Vascular Medicine Unit, Aston Medical School, Aston University
Yuchun Gu: Laboratory of Molecular Pharmacology, Institute of Molecular Medicine, Peking University

Nature Communications, 2014, vol. 5, issue 1, 1-7

Abstract: Abstract Reperfusion-induced ventricular fibrillation (VF) severely threatens the lives of post-myocardial infarction patients. Carbon monoxide (CO)—produced by haem oxygenase in cardiomyocytes—has been reported to prevent VF through an unknown mechanism of action. Here, we report that CO prolongs action potential duration (APD) by inhibiting a subset of inward-rectifying potassium (Kir) channels. We show that CO blocks Kir2.2 and Kir2.3 but not Kir2.1 channels in both cardiomyocytes and HEK-293 cells transfected with Kir. CO directly inhibits Kir2.3 by interfering with its interaction with the second messenger phosphatidylinositol (4,5)-bisphosphate (PIP2). As the inhibition of Kir2.2 and Kir2.3 by CO prolongs APD in myocytes, cardiac Kir2.2 and Kir2.3 are promising targets for the prevention of reperfusion-induced VF.

Date: 2014
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DOI: 10.1038/ncomms5676

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