Caracterização farmacologica dos receptores de endotelina na circulação portal de figado isolado de cão

AUTOR(ES)

Heryck Jose Stella

DATA DE PUBLICAÇÃO

1997

RESUMO

Endothelins constitute a family of vasoactive mediators, capable of producing potent and long-lasting pressor responses in several vascular territories. Endothelin-1 has been implicated in the regulation of resistance to portal blood flow, particularly in the presence of cirrhosis and portal hypertension. However, the receptor subtypes mediating this phenomenon have not been clearly elucidated. In this study we attempted to characterize the endothelin receptor population in the portal circulation. Portal vascular responses to endothelin-1 (ETA/ETB agonist), IRL 1620 (ETB agonist) and noradrenaline were investigated using the isolated, perfused canine liver. The effects of a selective ETA receptor antagonist, FR 139317, and the selective ETB receptor antagonist, BQ -788, on portal vascular responses to the agonists were investigated, in addition, the modulation of these responses by prostaglandins and nitric oxide were also assessed. Endothelin-1 and IRL 1620 produced a dose-dependent increase in portal inflow resistance. This effect was significantly attenuated by treatment with FR 139317 and BQ-788. Blockade of prostaglandin and nitric oxide synthesis with indomethacin and L-NAME, respectively, potentiated the endothelin-1-, but not IRL 1620-induced portal vascular responses. We conclude that there is a mixed population of endothelin receptors in the portal circulation of the canine liver. Endothelin-1-induced portal vasoconstriction is mediated by ETA and ETB receptors. The effects induced via ETA receptors is modulated by prostaglandins and nitric oxide. ETB receptor activation might play an important role in resistance to portal blood flow in disease states such as portal hypertension, a condition associated with increased circulating levels of endothelin-1 and endothelin-3

ASSUNTO(S)

hipertensão portal fluxo sanguineo oxido nitrico endotelinas

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