Platelet-activating factor is a renal vasodilator in the anesthetized rat.

In view of the potent vasoactive properties of platelet-activating factor (PAF), we investigated the renal hemodynamic effects of this lipid. C16-PAF (0.5-10 ng/kg) given as a bolus into the renal arterial circulation of pentobarbital sodium-anesthetized male Wistar rats produced a dose-dependent increase in renal blood flow (6-15%), before causing systemic hypotension. The PAF-induced renal vasodilation and systemic hypotension was independent of renal innervation, unaltered by eicosanoid synthesis inhibition with indomethacin or dexamethasone, unchanged by the nonselective dopamine-receptor antagonist haloperidol, but was abolished by the PAF-receptor antagonist, L-659,989. Non-hypotensive intrarenal PAF infusion at 0.5 ng.min-1.kg-1 caused an increase in renal blood flow. Thus PAF can cause renal vasodilation in the rat kidney that is PAF-receptor mediated and does not involve the sympathetic nervous system or the release of vasodilatory arachidonic acid metabolites or dopamine.