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.
No takes yet. Share an insight, caveat, or question.
Handa et al. (1990) studied this question.