Rat kidneys were isolated and perfused with a modified Krebs-Henseleit buffer containing 4% albumin. Perfusate recirculated except during L-platelet activating factor (L-PAF), angiotensin II (ang II), and norepinephrine (NE) infusions. L-PAF caused a dose-dependent decrease in renovascular resistance (RVR): −6 ± 3% at 10−9M, −12 ± 6% at 10−8M, −18 ± 3% at 10−7M and −20 ± 7% at 10−6M. L-PAF increased immunoreactive PGE (iPGE) and thromboxane (iTXB) release into the venous effluent from 2.4 ± 0.2 to 3.9 ± 0.4 ng/min (p<0.05) and from 2.1 ± 0.4 to 3.5 ± 0.5 ng/min (p<0.05), respectively. Vasodilation by L-PAF (10−7M) in the presence of indomethacin (INDO) (5 μM) was enhanced compared to the non-INDO response (RVR change: L-PAF = −18 ± 3% vs. L-PAF + INDO = −26 ± 3%;p<0.05). As a control for specificity, the structural isomer D-PAF was infused at 10−9M, 10−8M, and 10−7M. None of these concentrations changed renal vascular resistance. To study the vascular receptor responsible for L-PAF-induced vasodilation, dose-response curves to NE and ang II were established with and without L-PAF (10−7M). The NE dose-response curve was unchanged by L-PAF, whereas the ang II dose-response curve was shifted to the right by one order of magnitude. In kidneys pretreated with INDO (5 μM), the L-PAF-induced shift of the ang II dose-response relation was increased to 2–3 orders of magnitude. Renin release was unchanged at 10−9M, 10−8M, and 10−7M L-PAF, but rose threefold at 10−6M concomitant with maximal vasodilation. We conclude that L-PAF is a potent vasodilator of the rat renal vasculature, specifically antagonizing ang-II-induced vasoconstriction. L-PAF also releases prostaglandins, which antagonize the vasodilation. Renin release is increased at a high dose of L-PAF and may be an indirect effect secondary to decreased perfusion pressure.