Cardioprotective effect of diazoxide is mediated by activation of sarcolemmal but not mitochondrial ATP-sensitive potassium channels in mice

Dirk J. Duncker*, Pieter D. Verdouw

*Corresponding author for this work

Research output: Contribution to journalComment/Letter to the editorAcademicpeer-review

2 Citations (Scopus)
1 Downloads (Pure)

Abstract

To the Editor:

Recently, Suzuki et al reported that attenuation of myocardial stunning by diazoxide in mice was mediated through activation of sarcolemmal rather than mitochondrial K+ATP channels. Although the authors used an elegant approach by combining both pharmacological tools (utilizing the mitochondrial K+ATP-channel inhibitor 5-hydroxydecanoate and the sarcolemmal K+ATP channel inhibitor HMR-1098) and molecular tools (sarcolemmal K+ATP channel [Kir6.2]-deficient mice), interpretation of the results is difficult.

Thus, the authors claim to have investigated the protective effects of pretreatment with diazoxide against myocardial stunning, produced by 20 minutes of no-flow global ischemia in isolated buffer-perfused hearts. However, stunning is defined as reversible myocardial dysfunction that persists after a brief period of ischemia despite full reperfusion. In isolated buffer-perfused rodent hearts, 20 minutes of ischemia already results in significant cardiac necrosis. [...]
Original languageAmerican English
Pages (from-to)e44
JournalCirculation
Volume108
Issue number6
DOIs
Publication statusPublished - 12 Aug 2003

Bibliographical note

Includes a response by M. Suzuki et al.

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