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Introduction: Ischemia/reperfusion (IR) injury involves a complex interrelated sequence of events. High levels of nitric oxide (NO) are generated with inducible form of nitric oxide synthase (iNOS) leading to the renal IR injury and glutathione (GSH) depletion. The present study was designed to investigate the effect of L-Nil (N6- (1-Iminoethyl)-L- lysine.hydrochloride), a selective inhibitor of iNOS, in prevention of renal GSH depletion and IR injury. Methods: Ischemia was induced by 40-min clamping of the renal arteries followed by 6 h reperfusion. Rats were randomly assigned to four groups: Sham operated, Sham- L-Nil, IR and IR- L-Nil. In the IR groups, rats were administered saline or L-Nil (3 mg/kg iv bolus followed by infusion of 1 mg/kg/h) 15 min prior ischemia. Other groups underwent surgery protocol but did not undergo renal arteries occlusion and were maintained under anesthesia for the duration of the experiment (40 min + 6 h). Renal function was assessed by plasma creatinine (Cr), Blood Urea Nitrogen (BUN), and aspartate aminotransferase (AST) measurements. Fractional excretion of Na+ (FENa+), urinary N-acetyl-ß-D-glucosaminidase (NAG) activity and renal GSH level were also measured. Results: We found that L-Nil significantly reduced the IR mediated increases in Cr, BUN, AST, FENa+, NOx and urine NAG activity. Conclusion: These results emphasize the multifactorial nature of renal IR injury and the need for a multidrug therapy in the future.

Keywords: Kidney, Ischemia-reperfusion, Nitric oxide synthase, Rat, L-Nil.

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