Dopaminergic stimulation of cortisol secretion from bovine zfr cells occurs through nonspecific stimulation of adrenergic β-receptors

Abstract

Previous reports have suggested a possible dopaminergic inhibition of the actions of AII on aldosterone secretion via adenylate-cyclase inhibitory ‘D2’ receptors. Others suggest a possible stimulation of aldosterone secretion via a stimulatory ‘D1’ receptor/cAMP pathway. We have examined the actions of dopamine on basal and AII-stimulated cortisol secretion by cultured bovine zfr cells. Dopamine alone caused a dose-dependent increase in cortisol secretion at doses >105 M, and also enhanced steroidogenic output in response to submaximal (1010M) but not maximal (10-8M) stimulatory doses of AII. The stimulatory action of dopamine alone on cortisol secretion was not, however, reproduced by the ‘D1’ agonist fenoldopam, and was fully blocked by propranolol. Dopamine had neither a stimulatory effect on basal phosphoinositol production nor an inhibitory effect on AII-stimulated phosphoinositol production. Our findings are therefore inconsistent with the activation of a ‘D1’ or ‘D2’ class receptor, and suggest the stimulation of cortisol secretion occurred nonspecifically through a β-adrenergic receptor.