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La nifedipina aumenta indirectamente la expresión de la superóxido dismutasa en las células endoteliales a través de
Keisuke Fukuo1, Jin Yang, Osamu Yasuda
1Department of Geriatric Medicine, Osaka University Medical School, Suita, Osaka, Japan. fukuo@geriat.med.osaka-u.ac.jp
Circulation
|July 18, 2002
Resumen
Los antagonistas del calcio como la nifedipina mejoran la función endotelial al aumentar la superóxido dismutasa (SOD) en las células endoteliales (CE). Este efecto está mediado por las células musculares lisas vasculares (VSMC) que liberan el factor de crecimiento endotelial vascular (VEGF).
Área de la Ciencia:
- Investigaciones Cardiovasculares Investigación Cardiovascular Investigaciones Cardiovasculares
- Biología celular endotelial Biología celular endotelial
- Función de las células del músculo liso Función de las células del músculo liso
Sus antecedentes:
- Se sabe que los antagonistas del calcio mejoran la disfunción endotelial en enfermedades cardiovasculares.
- El receptor específico para los antagonistas del calcio en las células endoteliales sigue sin identificarse.
- Se supone que las células del músculo liso vascular (CMSV) median los efectos de los antagonistas del calcio en las células endoteliales (CE).
Objetivo del estudio:
- Investigar si los VSMCs median la modulación de la actividad de la superóxido dismutasa endotelial (SOD) y la expresión por el antagonista del calcio nifedipina.
- Para aclarar el papel del factor de crecimiento endotelial vascular (VEGF) en este proceso.
Principales métodos:
- Estudios de co-cultura de las CE y VSMC.
- El tratamiento con nifedipina, un antagonista del calcio.
- Medición de la actividad y expresión de SOD.
- Evaluación de la producción del factor de crecimiento endotelial vascular (VEGF).
- Uso del antagonista del receptor de bradicinina B2 (HOE-140) y el anticuerpo neutralizante del VEGF.
Principales resultados:
- La nifedipina aumentó la expresión y actividad de SOD en ECs cuando se cocultivaba con VSMCs, pero no cuando se cultivaba sola.
- La nifedipina estimuló la producción de VEGF de los VSMC, que fue bloqueada por HOE-140.
- El anticuerpo neutralizante del VEGF inhibió la regulación de la SOD inducida por nifedipina en ECs.
- El VEGF recombinante aumentó la expresión de SOD en ECs.
- El supernatante VSMC aumentó la producción de óxido nítrico (NO) en las EC, un efecto dependiente del SOD.
Conclusiones:
- El antagonista del calcio nifedipina regula indirectamente la expresión endotelial de SOD.
- Esta regulación ascendente está mediada por la estimulación de VEGF de VSMCs adyacentes.
- Estos hallazgos ofrecen información sobre los mecanismos beneficiosos de los antagonistas del calcio en las enfermedades cardiovasculares.
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