Ischaemic preconditioning and a mitochondrial KATP channel opener both produce cardioprotection accompanied by F1F0-ATPase inhibition in early ischaemia.

Autor: Ala-Rämi, Antti, Ylitalo, Kari V., Hassinen, Ilmo E.
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Zdroj: Basic Research in Cardiology; Jul2003, Vol. 98 Issue 4, p250-258, 9p
Abstrakt: 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 KATP channel openers, and most of the evidence points to the mitochondrial KATP channels. We show here that the KATP 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 31P NMR. The actions of both diazoxide and ischaemic preconditioning were prevented by 5-hydroxydecanoate, a specific inhibitor of the mitochondrial KATP channel. Thus mitochondrial KATP 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. [ABSTRACT FROM AUTHOR]
Databáze: Complementary Index
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