The role of adrenal medulla in endogenous dopaminergic inhibition of aldosterone secretion

Evidence has accumulated that aldosterone secretion is under endogenous dopaminergic inhibition. To examine potential sources of the dopamine thus inhibitorily acting in the adrenal zona glomerulosa, the responsiveness of aldosterone, plasma renin activity, prolactin, and plasma catecholamines to haloperidol, a dopaminergic antagonist, was studied in rats 6 weeks after unilateral adrenalectomy (Group B), 6 weeks after unilateral adrenal demedullation followed by contralateral adrenalectomy 5 days later (Group C), and in controls without any pretreatment (Group A). In Group C, there were increases in basal levels of norepinephrine (P less than 0.01), prolactin (P less than 0.02), and aldosterone (P less than 0.01). Basal plasma renin activity was also increased (P less than 0.05), epinephrine concentrations were decreased. Two hours after haloperidol 1 mg/kg b.wt. i.p., aldosterone levels were increased in Groups A + B (P less than 0.01) but unresponsive in Group C. Haloperidol-induced stimulation of prolactin and norepinephrine was not impaired by the surgical procedures. Epinephrine levels were increased by haloperidol only in groups A + B (P less than 0.002). In none of the groups were plasma renin activity or dopamine levels influenced by haloperidol. It is concluded that dopaminergic inhibition of aldosterone production is brought about neither by circulating dopamine nor by potential dopaminergic nerves accompanying arterial blood supply of the adrenal cortex but by dopamine originating directly in adrenal medulla.