Inhibition of nitric oxide synthase does not influence urinary nitrite plus nitrate excretion after renal ischemic injury

Abstract

Background and aims: Whether renal nitric oxide production caused by ischemia/reperfusion (I/R) influences the urinary excretion of nitric oxide (NO) metabolites (nitrite and nitrate) is far from being elucidated. In the present study, we evaluated the role of NO synthase inhibition using N ^G-nitro-L-arginine methyl ester (L-NAME) in a model of experimental renal I/R injury. Methods: Male Wistar rats were used in our experiments, and renal I/R injury was achieved after a 30-min occlusion of the bilateral renal artery followed by a 60-min period of reperfusion. Renal function including nitrite plus nitrate excretion and hemodynamics in reperfused kidneys were measured in the presence and absence of L-NAME. Results: Intravenous application of L-NAME (5 mg/kg body weight) resulted in a marked reduction of urine flow, renal plasma flow (0.7±0.3 ml/min), and the glomerular filtration rate (0.1±0.01 ml/min), but a significant increase in NO excretion (FENOx, 67.9±10.5%). In addition we found after L-NAME injection a significant increase of the fractional excretion of sodium (FENa, 49.3±7.7%) and lithium (FELi, 70.2±1.6%), as well as the renal vascular resistance compared with animals with renal I/R but non-treated with L-NAME (P<0.001). Furthermore, we observed a high correlation between FENOx and FELi (r²=0.80, P<0.01). Conclusion: Our results suggest that renal excretion of NO derivatives is not influenced by NO production during renal I/R injury, although NO contributes to the tubular transport capacity in the ischemia/reperfused kidney.