Abstract
We have previously shown that endothelin-1 (ET-1) stimulates corticosterone and aldosterone secretion by the frog adrenal gland through activation of ET A receptors. In the present study, we have investigated the transduction pathways involved in the corticotropic action of ET-1. Exposure of frog adrenal explants to ET-1 provoked a time- and dose-dependent increase in inositol phosphate production and a parallel decrease in membrane polyphosphoinositide content. Incubation of adrenal explants with ET-1 also induced a dose-related increase of cAMP formation. The selective ET A receptor antagonist BQ-485 totally abolished the stimulatory effects of ET-1 on both inositol phosphate and cAMP production. In contrast, the selective ET B receptor agonist IRL 1620 did not significantly modify polyphosphoinositide hydrolysis or cAMP formation. Administration of the phospholipase C inhibitor U-73122 or the protein kinase A inhibitor H-89 to perifused frog adrenal slices significantly reduced the stimulatory effect of ET-1 on corticosterone and aldosterone secretion. Concomitant administration of the two inhibitors almost completely suppressed the corticotropic effect of ET-1. Taken together, these data indicate that, in the frog adrenal gland, the stimulatory effect of ET-1 on corticosteroid secretion is mediated through activation of both the phospholipase C and the adenylyl cyclase transduction pathways.
Published Version
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