To explore the regulatory roles of CNS on the renal function, clonidine, a specific presynaptic α-adrenoceptor agonist, was administered into a lateral ventricle of the brain (icv) and the changes of renal function were studies in urethane-anesthetized rabbits. 5μg/kg icv elicited no significant changes in renal function. However, 15μg/kg induced marked natriuresis and kaliuresis for 20 min. Neither RPF nor GFR changed significantly. The fractional sodium reabsorption was significantly reduced, indicating that the renal action was of the tubular origin. Changes of systemic blood pressure were not contributory to the renal action. Yohimbine, a specific antagonist for presynaptic α-adrenoceptor, when given icv in doses of 100μg/kg 20 min prior to clonidine, completely abolished the renal action of icv clonidine. Yohimbine icv did not produce any significant changes in renal function. Intravenous clonidine, 15μg/kg, elicited antidiuresis and decrement of renal function immediately after administration, followed by a slight tendency toward natriuresis, but no natriuresis corresponding to those seen after the icv clonidine were observed, indicating that in the renal action of icv clonidine no direct action is involved. These observations indicate that the central sympathetic tone plays a role in the regulation of renal function in the rabbit.