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Non-invasive Assessment of Microvascular and Endothelial Function
Published on: January 29, 2013
La vasoconstricción a la endotelina-1 endógena se incrementa en la circulación periférica de pacientes con
S Taddei1, A Virdis, L Ghiadoni
1Department of Internal Medicine, University of Pisa, Pisa, Italy.
Circulation
|October 20, 1999
Resumen
La endotelina-1 (ET-1) juega un papel en la hipertensión esencial. El bloqueo de los receptores ET-1 con TAK-044 causó una mayor vasodilatación en pacientes hipertensos, vinculada a la reducción de la liberación de óxido nítrico (NO).
Área de la Ciencia:
- Fisiología cardiovascular fisiología cardiovascular.
- Farmacología Farmacología.
Sus antecedentes:
- La endotelina (ET)-1 está implicada en enfermedades cardiovasculares como la hipertensión esencial.
- El papel de ET-1 en la regulación del tono vascular en la hipertensión requiere una mayor aclaración.
Objetivo del estudio:
- Evaluar el papel de ET-1 en el control del tono vascular en la hipertensión esencial.
- Para evaluar la respuesta vascular del antebrazo a un antagonista del receptor ET(A) /ET(B (TAK-044) en pacientes hipertensos frente a controles sanos.
Principales métodos:
- Se utilizó la pletismografía venosa con estirómetro para medir los cambios en el flujo sanguíneo del antebrazo.
- Se administraron infusiones intrabraquiales de TAK-044, nitroprussida de sodio, N (((G) -monometil-L-arginina (L-NMMA) y norepinefrina.
- Los niveles plasmáticos de ET-1 se midieron mediante radioinmunoensayo.
Principales resultados:
- TAK-044 indujo una vasodilatación significativamente mayor en pacientes hipertensos en comparación con sujetos normotensos (P<0,01).
- La vasoconstricción en respuesta a la L-NMMA se redujo significativamente en pacientes hipertensos (P<0,01).
- Las respuestas vasculares al nitroprussida de sodio y la norepinefrina, y los niveles plasmáticos de ET-1, fueron similares entre los grupos.
Conclusiones:
- Los vasos del antebrazo de los pacientes hipertensivos esenciales exhiben una mayor vasodilatación al bloqueo del receptor ET-1.
- Esta mayor respuesta está asociada con una disminución en la liberación de óxido nítrico tónico (NO) en la hipertensión.
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