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Los betabloqueantes de tercera generación estimulan la liberación de óxido nítrico de las células endoteliales a
Leszek Kalinowski1, Lawrence W Dobrucki, Miroslawa Szczepanska-Konkel
1Department of Chemistry and Biochemistry, Ohio University, Athens, Ohio 45701, USA.
Circulation
|May 14, 2003
Resumen
El nebivolol y el carvedilol promueven la relajación de los vasos sanguíneos al estimular la liberación de óxido nítrico (NO). Esto ocurre a través de la activación extracelular del trifosfato de adenosina (ATP) y del purinoceptor P2Y en las células endoteliales microvasculares.
Área de la Ciencia:
- Farmacología Farmacología.
- Investigación cardiovascular Investigación cardiovascular Investigación cardiovascular Investigación cardiovascular Investigación cardiovascular
- Biología Molecular Biología Molecular
Sus antecedentes:
- El nebivolol y el carvedilol son betabloqueantes de tercera generación con propiedades vasodilatadoras únicas.
- Su mecanismo para los efectos microcirculadores, distinto de los betabloqueantes clásicos, sigue sin estar claro.
- El ATP extracelular es una molécula de señalización clave en las funciones celulares a través de los purinoceptores P2.
Objetivo del estudio:
- Investigar si el nebivolol y el carvedilol estimulan la liberación de óxido nítrico (NO) de las células endoteliales microvasculares.
- Determinar el papel del trifosfato de adenosina (ATP) extracelular en este proceso.
- Para aclarar la participación de los purinoceptores P2 en la vasodilatación inducida por los betabloqueantes.
Principales métodos:
- Medición de la contracción y relajación de la vasculatura glomerular renal.
- Cuantificación de la liberación de NO biológicamente activo de las células endoteliales glomerulares individuales (CEG).
- Evaluar los niveles extracelulares de ATP y bloquear los purinoceptores P2Y y la liberación de ATP.
Principales resultados:
- El nebivolol y el carvedilol estimulan la liberación de ATP y NO de las GEC de una manera dependiente de la concentración.
- La inhibición de la liberación de ATP o de los purinoceptores P2Y abolió la vasorelajación inducida por los betabloqueantes y la liberación de NO.
- Los niveles de liberación de NO para el nebivolol y el carvedilol fueron comparables.
Conclusiones:
- El nebivolol y el carvedilol inducen la relajación microvascular glomerular renal.
- Esta relajación está mediada por el eflujo de ATP.
- El proceso implica la estimulación de la liberación de NO dependiente del purinoceptor P2Y de las GEC.
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