Journal
BASIC RESEARCH IN CARDIOLOGY
Volume 98, Issue 4, Pages 250-258Publisher
SPRINGER HEIDELBERG
DOI: 10.1007/s00395-003-0413-z
Keywords
ischaemia; preconditioning; K-ATP channel; ATP synthase diazoxide
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Ischaemic preconditioning gives powerful protection against prolonged ischaemia affecting several intracellular regulatory and messenger pathways, although their mutual importance is far from established. Protective, preconditioning-like effects have been reported for K-ATP channel openers, and most of the evidence points to the mitochondrial K-ATP channels. We show here that the K-ATP channel opener diazoxide, which acts selectively on the mitochondrial channel, causes potentiation of ischaemic inhibition of mitochondrial ATP synthase (F1F0-ATPase) along with cardioprotection. These effects are comparable with that of ischaemic preconditioning. The administration of diazoxide did not affect the cellular energy state as monitored with P-31 NMR. The actions of both diazoxide and ischaemic preconditioning were prevented by 5-hydroxydecanoate, a specific inhibitor of the mitochondrial K-ATP channel. Thus mitochondrial K-ATP channel opening and ischaemic preconditioning must share common mechanisms of action involving mitochondrial F1F0-ATPase, although involvement of the energy state in protection could not be proved.
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