The effects of PGI2 and PGE2, given in the same doses were compared as to renal hemodynamics and functions and renin release. The same experimental conditions were used for both compounds and experiments were carried out in pentobarbital anesthetized dogs. Adrenergic influences were excluded by renal denervation. Given intrarenally at doses at 0.1 microgram/min and 1 microgram/min, PGE2 caused significant increase in RBF, UF and UNaV, but had no effect on BP and GFR. Intrarenal infusion of PGI2 at a rate of 1 microgram/min resulted in a significant increase of RBF and in a marked fall of BP, but only little change in GFR, UF and UNaV. With a dose of 0.1 microgram/min, the parameters remained the same. Intravenous infusion of PGI2 (1 microgram/min) caused a significant fall in BP with no change in the other parameters. Both PGI2 and PGE2 had a similar effect on intrarenal hemodynamics, i.e., caused a progressively greater proportional vasodilation from superficial to deep cortex. Given intrarenally in a dose of 1 microgram/min, PGI2 and PGE2 increased renin release. But with a dose of 0.1 microgram/min and 1 microgram/min, i.v., renin secretion was not influenced. The effect of PGI2 on systemic blood pressure was more potent than that of PGE2, however, with regard to renal vasodilating action and tubular effects, PGE2 was the more potent. Present data indicate that PGI2 and PGE2 stimulate renin secretion through a direct action on the juxtaglomerular cells.