Dopamine when given icv induces antidiuresis along with transient natriuretic tendency, and it has been suggested that both subtypes of central dopamine receptors may influence renal function differentially. This study was undertaken to delineate the role of central D2 receptors employing domperidone (DOM), a selective D2 antagonist. DOM icv elicited antidiuresis and antinatriuresis in doses ranging from 15 to 135μg/kg. GFR and RPF as well as sodium excretion decreased. Systemic blood pressure increased slightly. Intravenous DOM did not elicit significant changes in sodium excretion. Denervation of the kidney abolished the hemodynamic change induced by icv DOM, but sodium excretion decreased on both innervated and denervated kidneys. No diuretic tendency was uncovered by the denervation. Dopamine, 150μg/kg icv, produced antidiuresis along with decreases in hemodynamics. These effects were not affected by DOM-pretreatment, and no natriuretic tendency was unveiled. Bromocriptine, a D2 receptor agonist, 200μg/kg icv, elicited marked diuresis and natriuresis, which were completely abolished by DOM-pretreatment. Apomorphine, another prototype of D2 agonist, 150μg/kg icv, produced diuresis and natrituresis with increases in renal hemdoynamics, followed by decreases in all parameters. DOM-pretreatment did not affect the renal hemodynamic effects, wherease the increases in urine flow and sodium excretion were markedly reduced by DOM, Present study suggests that central 200μg/kg receptors mediate natriuretic and diuretic influence to the kidney, possibly through mediation of natriuretic humoral factor, and provide further evidence supporting the hypothesis that central 200μg/kg receptors mediate antidiuretic influence via nerve pathway, whereas natriuresis are brought about through mediation of central 200μg/kg receptors.kg$ receptors.