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La liberación de calcio inducida por la corriente de sodio del retículo sarcoplasmático cardíaco
1Department of Physiology, University of Nevada School of Medicine, Reno 89557-0046.
Science (New York, N.Y.)
|April 20, 1990
Resumen
El intercambio sodio-calcio en las células cardíacas desencadena la liberación de calcio de las reservas internas, independientemente de la entrada directa en el canal de calcio. Este mecanismo influye en la contracción del músculo cardíaco y en los efectos de las drogas.
Área de la Ciencia:
- Cardiología Cardiología.
- Fisiología celular Fisiología celular.
- Biología Molecular Biología Molecular
Sus antecedentes:
- La función cardíaca depende del manejo preciso del calcio dentro de los miocitos.
- El intercambio sodio-calcio (NCX) es un regulador clave del calcio intracelular.
- El papel preciso de NCX en el desencadenamiento de la liberación de calcio en el retículo sarcoplásmico no se entiende completamente.
Objetivo del estudio:
- Investigar el papel del intercambio sarcolemmal de sodio y calcio en la liberación de calcio del retículo sarcoplásmico cardíaco.
- Para dilucidar el mecanismo de la liberación de calcio inducida por la corriente de sodio en los miocitos cardíacos.
Principales métodos:
- Utilizó miocitos cardíacos aislados y sujetos a tensión.
- Investigada la liberación de calcio en ausencia de actividad del canal de calcio dependiente de voltaje.
- Se evaluó la dependencia de la liberación de calcio en la entrada de sodio y las concentraciones de calcio extracelular.
Principales resultados:
- La despolarización de la membrana indujo la liberación de calcio de las reservas sensibles a la ryanodina sin entrada en el canal de calcio.
- Esta liberación de calcio dependía de la entrada de sodio a través de los canales de sodio sensibles a la tetrodotoxina.
- La liberación de calcio también dependía del calcio extracelular, lo que indica una liberación desencadenante inducida por el calcio que implica el intercambio sodio-calcio.
Conclusiones:
- El intercambio sodio-calcio puede desencadenar la liberación de calcio desde el retículo sarcoplásmico.
- Este mecanismo puede contribuir a los efectos inotrópicos de los glucósidos cardíacos.
- También puede explicar los efectos de los medicamentos antiarrítmicos que interactúan con los canales de sodio cardíacos.
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