The facts that PGE₂ produced diuresis in the rabbit when given into a lateral ventricle of the brain and that PGE_2α is abundantly found in the brain prompted us to investigate the effects of PGE_2α introduced directly into the ventricle on the renal function. PGE_2α given intraventriculary in doses of 10μg and 100μg elicited prompt diuresis, 10-fold increase of sodium excretion and two-fold increment of potassium excretion. Free water reabsorption also increased along with the increased osmolar clearance. Neither renal plasma flow nor glomerular filtration rate did change significantly. This, along with the fact that the percentage of reabsorbed sodium filtered decreased from 99.5 to 93.9, indicates the tubular site of the diuretic and natriuretic action. Atropine pretreatment did not influence the renal effects of intraventricular PGE_2α. Intravenously administered PGE_2α in doses of 30 to 100μg did not produce any significant change in renal function. Intraventricular PGE_2α had no effect on the systemic blood pressure, whereas intravenous administration brought about a transient hypotension. These observations suggest that PGE_2α induces diuresis and natriuresis via central mechanism, that the site of the action resides in renal tubules, and that the reabsorption of sodium is inhibited in the proximal tubule, possibly through mediation of certain humoral agent. Overall, it is suggested that PGE_2α might play a roll in regulating renal function through the center.