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La adenosina inicia la apertura de los canales de potasio mitocondriales sensibles al ATP: un paso clave en el
1Institute of Molecular Cardiobiology, Johns Hopkins University, Baltimore, MD 21205, USA.
Circulation
|August 16, 2000
Resumen
La adenosina prima los canales mitocondriales K (((ATP) para la cardioprotección a través de la proteína quinasa C. Esto explica cómo la adenosina inicia el precondicionamiento isquémico, vinculando elementos clave en la cascada.
Área de la Ciencia:
- Fisiología cardiovascular fisiología cardiovascular.
- Biología mitocondrial Biología mitocondrial
- La señalización celular de las células.
Sus antecedentes:
- La adenosina inicia el precondicionamiento isquémico, un fenómeno protector contra las lesiones cardíacas.
- Los canales mitocondriales de potasio (K(ATP)) sensibles al ATP están implicados como efectores clave en el precondicionamiento.
- El vínculo mecánico preciso entre la adenosina y los canales mitocondriales K (((ATP) aún no se había aclarado.
Objetivo del estudio:
- Determinar las interacciones mecánicas entre los canales de adenosina y K (ATP) mitocondriales en el contexto del precondicionamiento isquémico.
- Para investigar el papel de la proteína quinasa C en la mediación de los efectos de la adenosina en los canales mitocondriales K (ATP).
Principales métodos:
- La actividad del canal mitocondrial K (((ATP) se cuantificó en los miocitos ventriculares de conejo utilizando la oxidación de flavoproteínas inducida por diazóxido.
- Los efectos de la adenosina en la actividad del canal se evaluaron en presencia y ausencia de antagonistas de los receptores y inhibidores de la quinasa.
- Los efectos cardioprotectores se evaluaron en un modelo de isquemia simulada, con intervenciones bloqueadas por bloqueadores específicos de los canales K ((ATP).
Principales resultados:
- La adenosina (100 μmol / L) aumentó la actividad del canal mitocondrial K (((ATP) y redujo la latencia hasta la apertura.
- Estos efectos fueron eliminados por el antagonista del receptor de adenosina 8-(p-sulfofenil) -teofilina y el inhibidor de la proteína quinasa C polimyxin B.
- La adenosina mitigó la lesión celular inducida por isquemia simulada, un efecto bloqueado por el bloqueador de los canales mitocondriales K (((ATP) 5-hidroxidecanoato pero no HMR1098.
Conclusiones:
- La activación del receptor de adenosina inicia la apertura de los canales mitocondriales K (((ATP) de una manera dependiente de la proteína quinasa C.
- Estos hallazgos establecen un vínculo directo entre la señalización de la adenosina y la función del canal mitocondrial K (((ATP) en la cardioprotección.
- El estudio aclara los eventos moleculares clave en la cascada de precondicionamiento isquémico.
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