Ischaemic preconditioning and a mitochondrial KATP channel opener both produce cardioprotection accompanied by F1F0-ATPase inhibition in early ischaemia.
Basic Res Cardiol
; 98(4): 250-8, 2003 Jul.
Article
en En
| MEDLINE
| ID: mdl-12835954
ABSTRACT
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 (F(1)F(0)-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 (31)P 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 F(1)F(0)-ATPase, although involvement of the energy state in protection could not be proved.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Cardiotónicos
/
Daño por Reperfusión Miocárdica
/
Canales de Potasio
/
Precondicionamiento Isquémico Miocárdico
/
Diazóxido
Límite:
Animals
Idioma:
En
Revista:
Basic Res Cardiol
Año:
2003
Tipo del documento:
Article
País de afiliación:
Finlandia