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El antagonismo agudo y crónico del receptor de angiotensina-1 invierte la disfunción endotelial en la aterosclerosis
A Prasad1, T Tupas-Habib, W H Schenke
1Cardiology Branch, Office of Biostatistics Research, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Circulation
|May 24, 2000
Resumen
La inhibición del receptor de angiotensina-1 (AT(1) con losartan mejoró la disfunción endotelial en pacientes con aterosclerosis al mejorar la disponibilidad de óxido nítrico. Esto sugiere que el bloqueo del receptor AT(1) puede ofrecer beneficios terapéuticos para la aterosclerosis.
Área de la Ciencia:
- Medicina Cardiovascular La medicina cardiovascular es una especialidad de la salud.
- Farmacología Farmacología.
- Biología Vascular Biología Vascular
Sus antecedentes:
- El sistema renina-angiotensina juega un papel en la aterogénesis promoviendo la disfunción endotelial.
- El bloqueo del receptor de angiotensina-1 (AT(1) se investiga por su potencial para mejorar la función endotelial.
Objetivo del estudio:
- Para determinar si la inhibición del receptor AT(1) mejora la disfunción endotelial en pacientes con aterosclerosis.
- Evaluar el impacto del losartán en las respuestas microvasculares y la vasodilatación.
Principales métodos:
- Las respuestas microvasculares a los agentes vasoactivos se estudiaron en pacientes con aterosclerosis y controles antes y después del losartán intraarterial.
- La vasodilatación de la arteria braquial mediada por el flujo se evaluó mediante ultrasonido después de 8 semanas de terapia oral con losartan.
- Se midieron los niveles séricos de óxido nítrico.
Principales resultados:
- El losartán intraarterial inhibió la vasoconstricción mediada por angiotensina II y aumentó la vasodilatación inducida por acetilcolina en pacientes.
- El tratamiento con losartan oral mejoró la dilatación de la arteria braquial mediada por el flujo y aumentó los niveles séricos de óxido nítrico.
- Las respuestas a la hiperemia reactiva fueron mejoradas, mientras que las respuestas a la nitroprusida de sodio y a la nitroglicerina se mantuvieron sin cambios.
Conclusiones:
- La inhibición del receptor AT(1) invierte la disfunción endotelial en pacientes con aterosclerosis.
- La mejora de la disponibilidad de óxido nítrico es un mecanismo clave para los beneficios observados.
- El bloqueo del receptor AT(1) puede tener un potencial terapéutico a largo plazo para la aterosclerosis.
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