Central and peripheral effects of clonidine on the adrenal medullary function in spontaneously hypertensive rats.

The sites of action of clonidine-induced adrenal suppressant effect were investigated in spontaneously hypertensive rats. For analysis of the adrenal medullary function, efferent adrenal nerve discharges and adrenal venous catecholamine secretion rates were determined. Five to 10 min after i.v. administration of clonidine (3-100 micrograms/kg), there was a decrease in both sympathetic adrenal nerve activity and adrenal catecholamine secretion rates along with the decrease in arterial blood pressure and heart rate. After acute splanchnicotomy, clonidine (50 micrograms/kg i.v.) produced a significant decrease in catecholamine secretion rates from the denervated adrenal medulla during electrical stimulation of the splanchnic nerve. Furthermore, i.c.v. administration of clonidine (1-10 micrograms) decreased adrenal nerve activity. These findings indicate that both the adrenal medulla and the spinal clonidine-induced adrenal suppressant effect. The fact that the clonidine-induced decrease in adrenal catecholamine secretion rates was approximately parallel to the decrease in preganglionic adrenal nerve discharges in nerve intact spontaneously hypertensive rats suggests that the central action of clonidine is important in the adrenal suppressant effect relative to its peripheral action.