Abstract
INTRODUCTION: Diazoxide maintains myocyte volume and contractility during stress via an unknown mechanism. The mechanism of action may involve an undefined mitochondrial adenosine triphosphate-sensitive potassium (mKATP) channel and is dependent upon the KATP channel subunit SUR1. KATP channel openers have been shown to inhibit succinate dehydrogenase (SDH) and a gene for a portion of SDH has been found in the SUR intron. Thus, diazoxide may be cardioprotective via inhibition of SDH, which may form part of a KATP channel. This study investigated the role of inhibition of SDH in the cardioprotection provided by diazoxide and its relationship to the SUR1 subunit.
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