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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.

Keywords: Ischemia, reperfusion, angiotensin II receptor type 1, Losartan, Sodium excretion

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