Volume 12, Issue 4 (2-2010)                   J Arak Uni Med Sci 2010, 12(4): 51-60 | Back to browse issues page

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Gholampour F, Shid Moosavi S M, Owji S M, Haji zadeh S. The role of inducible nitric oxide synthase (iNOS) in ischemia/reperfusion-induced acute renal failure in anaesthetized rats. J Arak Uni Med Sci. 2010; 12 (4) :51-60
URL: http://amuj.arakmu.ac.ir/article-1-185-en.html
1.PhD PhD of physiology , gholampourf@yahoo.com
Abstract:   (15067 Views)
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.
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Type of Study: Original Atricle | Subject: Orology
Received: 2009/02/28

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