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Introduction: The acute response to renal ischemia-reperfusion injury involves attenuation of glomerular filtration rate, as well as reduced tubular function. The possible mediators involved in ischemia-reperfusion injury include vasoconstrictor agents including angiotensin II (Ang II). Inhibition of the angiotensin II receptor type 1 (AT1) diminishes the deleterious effects of ischemia-reperfusion on glomerular function. This study is done to investigate the effect of angiotensin II receptor type 1 antagonist on renal hemodynamic and tubular responses to ischemia-reperfusion injury in rat. Materials and Methods: In this experimental study, acute renal failure was induced by 30 minutes clamping of both renal arteries in male Sprague-Dawley rats. Renal hemodynamic and excretory function was followed for 120 minutes reperfusion, while saline or the selective AT1 receptor antagonist (Losartan) was infused. In plasma and urine samples, Cr level was measured. Also plasma and urine content of Sodium was measured. Data was analyzed using ANOVA and Duncan tests. Results: Renal ischemia for 30 minutes decreased glomerular filtration rate during reperfusion and increased urine flow and Sodium excretion up to three fold. Losartan (10 mg/kg i.v.) did not change glomerular filtration rate prior to ischemia but improved it during reperfusion and there were progressive increases in urine flow. Losartan caused a lowering of ischemia-induced rise in Sodium excretion. Conclusion: The ischemic challenge may cause release of angiotensin II, which acts on AT1 receptors to decrease perfusion.

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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.