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Am J Physiol Renal Physiol 267: F374-F379, 1994;
0363-6127/94 $5.00
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AJP - Renal Physiology, Vol 267, Issue 3 374-F379, Copyright © 1994 by American Physiological Society

ARTICLES

Role of nitric oxide (EDRF) in radiocontrast acute renal failure in rats

D. Schwartz, M. Blum, G. Peer, Y. Wollman, A. Maree, I. Serban, I. Grosskopf, S. Cabili, Y. Levo and A. Iaina
Department of Nephrology, Ichilov Hospital, Tel-Aviv Sourasky Medical Center, Israel.

This study was undertaken to examine the possible role of endothelium-derived relaxing factor (EDRF), identified as nitric oxide (NO), in the pathogenesis of radiocontrast-induced acute renal failure in rats. Normal and salt-depleted rats were monitored for 60 min or 24 h after radiocontrast administration. The administration of L-arginine to normal rats abolished the immediate decrease in p-aminohippurate clearance (CPAH) and attenuated the decrease in inulin clearance (CIn). The administration of NO synthase inhibitor to the salt-depleted animals resulted in a significantly more pronounced decrease in CPAH compared with both the control and the L-arginine-treated animals. The recovery of CIn 24 h after radiocontrast administration to the salt-depleted rats was significantly better in the L-arginine-treated rats than in either the control or inhibitor-treated groups. The administration of radiocontrast material resulted in a significant decrease in urinary guanosine 3',5'-cyclic monophosphate as well as NO2 + NO3 excretion. This decrease was significantly attenuated by L-arginine. Our results 1) suggest that NO plays a major role in the pathogenesis of radiocontrast-induced acute renal failure and 2) suggest a novel therapeutic approach, i.e., the use of L-arginine in this form of acute renal failure.


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