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La inhibición de la enzima convertidora de angiotensina aumenta la liberación del activador de plasminógeno del tipo
Mias Pretorius1, David Rosenbaum, Douglas E Vaughan
1Department of Anesthesiology, Vanderbilt University Medical Center, Nashville, Tenn 37232-6602, USA.
Circulation
|February 5, 2003
Resumen
La inhibición de la enzima convertidora de angiotensina (ECA) aumenta la liberación del activador de plasminógeno de tipo tisular (t-PA). Esto ocurre a través de la bradicinina endógena, que mejora la liberación endotelial de t-PA en los fumadores.
Área de la Ciencia:
- Investigación Cardiovascular Investigación Cardiovascular Investigación Cardiovascular Investigación Cardiovascular Investigación Cardiovascular
- Farmacología Farmacología.
- La función endotelial es la función endotelial.
Sus antecedentes:
- La inhibición de la enzima convertidora de angiotensina (ECA) mejora la respuesta a la bradicinina exógena.
- El mecanismo preciso por el cual los inhibidores de la ECA influyen en la función endotelial requiere una mayor aclaración.
Objetivo del estudio:
- Para probar la hipótesis de que la inhibición de la ECA aumenta la liberación del activador de plasminógeno (t-PA) del tipo de tejido endotelial a través de la bradicinina endógena.
- Para investigar el papel de la bradicinina en la mediación de los efectos de los inhibidores de la ECA en la liberación de t-PA.
Principales métodos:
- La administración intra-arterial de enalaprilato en 24 fumadores.
- Medición del flujo sanguíneo del antebrazo (FBF) y la liberación neta de t-PA.
- Infusión de bradicinina y metacolina antes y durante el enalaprilato.
- El uso de antagonistas de los receptores de bradicinina HOE 140 o vehículo.
Principales resultados:
- Enalaprilat aumentó significativamente la liberación neta de t-PA en reposo, un efecto eliminado por HOE 140.
- La inhibición de la ECA potenciaba las respuestas FBF y t-PA a la bradicinina exógena.
- La potenciación de la liberación de t-PA por el enalaprilato fue significativamente mayor que la potenciación de FBF.
Conclusiones:
- La inhibición de la ECA aumenta la liberación de t-PA endotelial constitutivo.
- Este efecto está mediado por la bradicinina endógena.
- La bradicinina juega un papel crucial en la mediación de la liberación de t-PA inducida por los inhibidores de la ECA.
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