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Platelet-activating factor is a renal vasodilator in the anesthetized rat
R K Handa1, J W Strandhoy, V M Buckalew
1Department of Medicine/Nephrology, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, North Carolina 27103.
The American Journal of Physiology
|June 11, 1990
Summary
Platelet-activating factor (PAF) increases renal blood flow in rats via a receptor-mediated pathway. This effect on kidney function is independent of the nervous system and other signaling molecules.
Area of Science:
- Nephrology
- Pharmacology
- Physiology
Background:
- Platelet-activating factor (PAF) is a potent lipid mediator with known vasoactive properties.
- Understanding the specific effects of PAF on renal hemodynamics is crucial for comprehending its role in kidney function.
Purpose of the Study:
- To investigate the renal hemodynamic effects of platelet-activating factor (PAF).
- To determine the mechanisms underlying PAF-induced renal vasodilation and systemic hypotension.
Main Methods:
- Administration of C16-PAF (0.5-10 ng/kg) as a bolus into the renal artery of anesthetized Wistar rats.
- Evaluation of renal blood flow and systemic blood pressure.
- Testing the involvement of renal innervation, eicosanoid synthesis (indomethacin, dexamethasone), dopamine receptors (haloperidol), and PAF receptors (L-659,989).
Main Results:
- Intrarenal PAF administration caused a dose-dependent increase in renal blood flow (6-15%).
- PAF-induced renal vasodilation and systemic hypotension were abolished by a PAF-receptor antagonist.
- These effects were independent of renal innervation, eicosanoid synthesis, and dopamine receptors.
Conclusions:
- Platelet-activating factor (PAF) mediates renal vasodilation in the rat kidney through a specific PAF-receptor pathway.
- The observed renal effects of PAF do not involve the sympathetic nervous system or the release of vasodilatory arachidonic acid metabolites or dopamine.