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La activación de los canales de potasio mitocondriales dependientes del ATP por el óxido nítrico
1Institute of Molecular Cardiobiology, Johns Hopkins University, Baltimore, MD 21205, USA.
Circulation
|February 2, 2000
Resumen
El óxido nítrico (NO) activa directamente los canales mitocondriales K ((+) (mitoK ((ATP)) dependientes del ATP. Este hallazgo revela un nuevo mecanismo para la cardioprotección inducida por NO y potencia los efectos diazoxídicos.
Área de la Ciencia:
- Fisiología cardiovascular fisiología cardiovascular.
- Biología mitocondrial Biología mitocondrial
- La señalización celular de las células.
Sus antecedentes:
- El óxido nítrico (NO) es un presunto mediador del precondicionamiento isquémico.
- Se ha propuesto que los canales K ((+) (mitoK ((ATP)) mitocondriales dependientes del ATP sean efectores en este proceso.
- La relación precisa entre los canales NO y mitoK (ATP) sigue sin estar clara.
Objetivo del estudio:
- Investigar el efecto directo del óxido nítrico (NO) en los canales mitocondriales K ((+) (mitoK ((ATP)) dependientes del ATP.
- Para aclarar los vínculos mecánicos entre la señalización de NO y la actividad del canal mitoK (ATP).
Principales métodos:
- El potencial redox mitocondrial se midió en los miocitos ventriculares de conejo como un indicador de la apertura del canal mitoK (ATP).
- NO donante S-nitroso-N-acetil-DL-penicillamina (SNAP) fue utilizado para evaluar los efectos de NO.
- Se emplearon bloqueadores de canales selectivos de mitoK (((ATP) y recolectores de NO para confirmar la especificidad.
Principales resultados:
- SNAP oxidó la matriz mitocondrial dependiendo de la dosis, lo que indica la activación del canal mitoK (((ATP).
- Los efectos de SNAP fueron bloqueados por un bloqueador específico del canal mitoK (ATP) y un recolector de NO.
- La SNAP potenciaba los efectos oxidativos del diazóxido, otro abridor de canales de mitoK (ATP).
Conclusiones:
- El óxido nítrico (NO) activa directamente los canales mitocondriales K ((+) (mitoK ((ATP)) dependientes del ATP.
- NO mejora la capacidad de apertura de canales del diazoxido.
- Estos hallazgos establecen un nuevo vínculo mecánico entre la cardioprotección mediada por NO y los canales de mitoK (ATP).
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