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Am J Physiol Renal Physiol 262: F939-F942, 1992;
0363-6127/92 $5.00
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AJP - Renal Physiology, Vol 262, Issue 6 939-F942, Copyright © 1992 by American Physiological Society


ARTICLES

Inhibition of renal nitric oxide synthesis with NG-monomethyl-L-arginine and NG-nitro-L-arginine

P. A. Naess, K. A. Kirkeboen, G. Christensen and F. Kiil
Institute for Experimental Medical Research, University of Oslo, Ullevaal Hospital, Norway.

In barbiturate-anesthetized dogs, the effects of intrarenal infusion of the two selective inhibitors of nitric oxide synthesis, NG-monomethyl-L-arginine (L-NMMA) and NG-nitro-L-arginine (NO-Arg), were compared. Basal renal blood flow (RBF) was reduced by 15 +/- 2% after L-NMMA at 0.28 mumol/ml, by 20 +/- 3% after NO-Arg at 0.07 mumol/ml, and by 31 +/- 5% after NO-Arg at 0.56 mumol/ml. Endothelium-dependent vasodilation induced by intrarenal infusion of acetylcholine was unaltered after L-NMMA, reduced by 24 +/- 3% after NO-Arg at 0.07 mumol/ml, and reduced by 59 +/- 13% after NO-Arg at 0.56 mumol/ml. Endothelium-independent vasodilation induced by intrarenal infusion of atrial natriuretic factor was not reduced after L-NMMA and NO-Arg. This study shows that NO-Arg is more potent than L-NMMA in inhibiting basal renal nitric oxide synthesis. In contrast to L-NMMA, NO-Arg exerted an inhibitory effect on acetylcholine-induced renal vasodilation. Our findings indicate that one-third of the basal RBF and more than one-half of the increase in RBF during acetylcholine infusion are dependent on nitric oxide synthesis.


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