Circulation. 2003;107:682-685
Published online before print February 3, 2003, doi: 10.1161/01.CIR.0000055187.67365.81
Published online before print February 3, 2003, doi: 10.1161/01.CIR.0000055187.67365.81
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(Circulation. 2003;107:682.)
© 2003 American Heart Association, Inc.
Brief Rapid Communications |
Cardioprotective Effect of Diazoxide Is Mediated by Activation of Sarcolemmal but Not Mitochondrial ATP-Sensitive Potassium Channels in Mice
From the Department of Pharmacology (M.S., T. Saito, T. Sato, M.T., H.N.) and the Department of Cellular and Molecular Medicine (T.M., S.S.), Graduate School of Medicine, Chiba University, Chiba, Japan.
Correspondence to Haruaki Nakaya, MD, Department of Pharmacology, Graduate School of Medicine, Chiba University, Inohana 1-8-1, Chuo-ku, Chiba 260-8670, Japan. E-mail nakaya{at}med.m.chiba-u.ac.jp
Background— We recently demonstrated that the sarcolemmal ATP-sensitive potassium (sarcKATP) channel plays a key role in cardioprotection against ischemia/reperfusion injuries in Kir6.2-knockout (KO) mice. In the present study, we evaluated the effects of diazoxide, a mitochondrial ATP-sensitive potassium (mitoKATP) channel opener, on ischemia-induced myocardial stunning in sarcKATP channel-deficient mice.
Methods and Results— Langendorff-perfused hearts of wild-type (WT) and KO mice were subjected to global ischemia/reperfusion. Diazoxide improved the recovery of contractile function in WT hearts but not in KO hearts. Treatment with HMR1098 (a sarcKATP channel blocker) but not 5-hydroxydecanoate (a mitoKATP channel blocker) abolished the cardioprotective effect of diazoxide in WT hearts. In coronary-perfused WT ventricular muscle preparations, action potential shortening during ischemia was accelerated in the presence of diazoxide.
Conclusions— Diazoxide enhances action potential shortening during ischemia by activating sarcKATP channels and provides cardioprotection in mouse hearts.
Key Words: potassium • ischemia • reperfusion • ion channels
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