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"Conversación cruzada" entre el péptido opioide y la señalización del receptor adrenérgico en el corazón de rata

S Pepe¹, R P Xiao, C Hohl

¹Laboratory of Cardiovascular Science, Gerontology Research Center, National Institute on Aging, Baltimore, Md 21224, USA.

|April 15, 1997

Resumen

Los receptores de péptidos opioides (OPR) interactúan con los receptores beta-adrenérgicos (beta-AR) en el corazón. La estimulación Delta-OPR inhibe los efectos beta1-AR mediante la reducción de la cAMP, mediada por una proteína G (i/o) sensible al PTX.

Área de la Ciencia:

Fisiología cardiovascular fisiología cardiovascular.
Farmacología Molecular Farmacología Molecular
Neurocardiología Neurocardiología

Sus antecedentes:

Las células cardíacas poseen tanto catecolaminas como receptores de péptidos opioides (OPR).
Los péptidos opioides se liberan con las catecolaminas de las terminales nerviosas cardíacas.
Investigar la influencia de la OPR en los efectos de la estimulación del receptor beta-adrenérgico (beta-AR) es crucial.

Objetivo del estudio:

Para determinar si la estimulación de la OPR afecta la estimulación beta-AR en corazones de rata aislados.
Para dilucidar el mecanismo de interacción, centrándose en los subtipos beta-AR y la modulación de la cAMP.
Para explorar el papel de las proteínas G (i/o) en este diálogo cruzado.

Principales métodos:

Modelo de corazón de rata isovolumico y aislado.
Estimulación con norepinefrina (NE), leucina-encefalina (LE, agonista de la delta-OPR) y forskolina.
Medición de la presión sistólica ventricular izquierda (LVSP) y los niveles de cAMP.
Uso del antagonista de la OPR naloxona y la toxina de la tos ferina (PTX) para estudios mecanicistas.
Evaluación de los efectos de los agonistas beta2-AR (Zinterol).

Principales resultados:

La norepinefrina (NE) aumentó el LVSP y el cAMP.
La leucina-encefalina (LE) inhibió los aumentos inducidos por NE en LVSP y cAMP.
Los efectos de LE fueron revertidos por la naloxona, lo que indica la participación de OPR.
LE no afectó a las respuestas inotrópicas independientes del CAMP mediadas por agonistas beta2-AR.
El pretratamiento de la toxina de la tos ferina (PTX) eliminó los efectos inhibidores de LE, implicando a las proteínas G.

Conclusiones:

Existe una conversación cruzada potente e inhibidora entre las vías de señalización delta-OPR y beta1-AR.
Esta interacción está mediada por una proteína G (i/o) sensible a PTX.
El mecanismo implica la inhibición de la adenilil ciclasa, reduciendo los niveles de cAMP en el corazón de la rata.

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