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El óxido nítrico activa directamente los canales de potasio dependientes del calcio en el músculo liso vascular
V M Bolotina1, S Najibi, J J Palacino
1Robert Dawson Evans Department of Clinical Research, Boston University Medical Center, Massachusetts 02118.
Nature
|April 28, 1994
Resumen
El óxido nítrico (NO) activa directamente los canales de potasio dependientes del calcio (K + Ca) sin GMP cíclico. Este hallazgo revela un nuevo mecanismo para la relajación del músculo liso mediada por NO, independiente de las vías tradicionales.
Área de la Ciencia:
- Fisiología Fisiología Fisiología.
- Biología Molecular Biología Molecular
- Investigación Cardiovascular Investigación Cardiovascular Investigación Cardiovascular Investigación Cardiovascular Investigación Cardiovascular
Sus antecedentes:
- El óxido nítrico (NO) es un factor relajante derivado del endotelio (EDRF) clave que media la relajación del músculo liso.
- El mecanismo establecido implica la activación de la guanylato ciclasa, la producción de GMP cíclico (cGMP) y la posterior señalización intracelular.
- Se cree que la proteína quinasa dependiente de cGMP activa los canales de potasio, lo que contribuye a la relajación.
Objetivo del estudio:
- Investigar un posible mecanismo directo de acción del óxido nítrico en los canales iónicos.
- Para determinar si el óxido nítrico puede activar los canales de potasio dependientes del calcio (K + Ca) independientemente de la vía cGMP.
- Para dilucidar el papel de la interacción directa del canal NO-K+Ca en la relajación del músculo liso vascular.
Principales métodos:
- Electrofisiología de la pinza de parche para estudiar los canales K + dependientes de Ca2 + (K + Ca) en parches de membrana libres de células.
- Aplicación de óxido nítrico exógeno y EDRF nativo a las grabaciones de canales.
- Inhibición farmacológica de la guanylato ciclasa mediante el uso de azul de metileno.
- Evaluación de la relajación vascular en la aorta del conejo con óxido nítrico y inhibidores específicos de los canales K+Ca (caribdotoxina).
Principales resultados:
- Tanto el óxido nítrico exógeno como el EDRF nativo activaron directamente canales individuales de K+Ca en parches libres de células.
- Esta activación del canal directo se produjo independientemente de la producción cíclica de GMP (cGMP).
- La relajación de la aorta del conejo inducida por el óxido nítrico persistió incluso cuando se inhibió la guanylata ciclasa.
- Esta relajación persistente fue abolida por la caribdotoxina, un inhibidor específico de los canales K + Ca, lo que confirma la participación de estos canales.
Conclusiones:
- El óxido nítrico ejerce una acción novedosa y directa sobre los canales K+ dependientes de Ca2+ .
- Esta vía directa contribuye a la relajación del músculo liso vascular, evitando la cascada de señalización clásica de cGMP.
- Los hallazgos amplían nuestra comprensión de las múltiples funciones del óxido nítrico en la fisiología cardiovascular.
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