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Am J Physiol Renal Physiol 253: F1283-F1289, 1987;
0363-6127/87 $5.00
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AJP - Renal Physiology, Vol 253, Issue 6 1283-F1289, Copyright © 1987 by American Physiological Society

ARTICLES

Platelet-activating factor mediates endotoxin-induced acute renal insufficiency in rats

J. Wang and M. J. Dunn
Department of Medicine, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106.

Platelet-activating factor (PAF) may contribute to the renal functional impairment of endotoxemia. We therefore examined 1) the effects of two specific PAF-receptor antagonists, L-653,150 and L-652,731, on endotoxin-induced acute renal insufficiency and 2) the renal hemodynamic actions of PAF in anesthetized postpartum Wistar rats. An intravenous injection of endotoxin at 150 micrograms/kg reduced glomerular filtration rate (GFR), renal plasma flow (RPF), and filtration fraction (FF) without a change in mean arterial pressure. L-653,150, 50 mg/kg orally, attenuated the endotoxin-induced fall in GFR, RPF, and FF. An intravenous injection of L-652,731, 0.3 mg/kg, followed by an infusion at 16 micrograms.kg-1. min-1 prevented the endotoxin-elicited reduction in GFR, RPF, and FF. L-652,731 also reversed the endotoxin-induced renal functional impairment. PAF, infused at 16 ng.kg-1.min-1 into the suprarenal aorta, reduced GFR, RPF, and FF without a significant change in renal arterial pressure. L-652,731 prevented the PAF-induced changes. In contrast, meclofenamate worsened the renal hemodynamic effects of PAF. We conclude that PAF may play an important role in mediating the endotoxin-induced acute hemodynamic renal insufficiency in rats with normotensive endotoxemia.


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Role of Platelet-Activating Factor in Cardiovascular Pathophysiology
Physiol Rev, October 1, 2000; 80(4): 1669 - 1699.
[Abstract] [Full Text] [PDF]


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