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Background: Ischemia/reperfusion-induced acute renal failure causes excretory functional disorders of nephrones. Ischemia/reperfusion injury increases iNOS expression in the renal tissue. Inhibition of iNOS expression and its activity can ameliorate ischemia/reperfusion-induced renal injury. The aim of this study was to determine the role of iNOS on progression of renal functional disturbances over the immediate post-ischemic reperfusion period. Materials and Methods: In this experimental study, renal hemodynamic and excretory functions were evaluated in male Sprague-Dawley rats. First, a 30-min control clearance period was taken. Then following bilateral renal artery clamping for 30 minutes, four consecutive 30-min clearance periods were taken during reperfusion, while saline or L-NIL as a selective iNOS inhibitor was infused. In plasma and urine samples, Cr and sodium concentration levels were measured. Results: Renal ischemia for 30 minutes decreased glomerular filtration rate and urine osmolality during reperfusion and increased urine flow and sodium excretion. L-NIL did not change the glomerular filtration rate and urine osmolality prior to ischemia but it improved them during reperfusion and there were progressive increases in urine flow. Additionally, L-NIL lowered ischemia-induced rises in sodium excretion. Conclusion: iNOS had a considerable role in the development of disorders in hemodynamic and excretory renal functions during early hours after ischemia.

Keywords: Glomerular filteration, iNOS enzyme, Ischemia, L-NIL, Reperfusion

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