Abstract
Introduction: Renal ischemia reperfusion injury is one of the main causes of acute renal failure, which is
associated with high mortality. Tissue damage caused by ischemia-reperfusion occurs due to the release of oxygen
free radicals. Type I angiotensin receptor antagonists such as valsartan can be useful in the treatment of chronic
kidney disease and hypertension.
Objectives: We aimed to evaluate the protective effect of valsartan against renal ischemia reperfusion via
antioxidant property and nitric oxide (NO) signaling pathway.
Materials and Methods: Fifty male Wistar rats (220±10 g) were randomly divided into five groups as follows:
Group 1; healthy rats without ischemia-reperfusion (control group). Group 2; rats with ischemia reperfusion (IR)
(IR control group). Group 3; rats with IR which received 30 mg/kg valsartan orally. Group 4; rats with IR which
received 30 mg/kg valsartan together with 40 mg/kg L-NAME. Group 5; rats with IR which received 30 mg/kg
valsartan together with 40 mg/kg L-arginine. To induce ischemia-reperfusion, rats were anesthetized with thiopental
and underwent surgery. Then, we induced ischemia with blocking blood vessels for 45 minutes by clamping.
Biochemical parameters including urea and creatinine were measured using commercial kits. Oxidative stress
and inflammatory parameters were measured by ELISA method. Renal tissues were stained with hematoxylin and
eosin. Finally, the Kolmogorov-Smirnov test was used to determine the normal distribution of data.
Results: The findings of this study indicated that treatment with valsartan and valsartan plus L-arginine leads to
significant decrease in the serum levels of creatinine, urea, and albumin/creatinine, malondialdehyde (MDA),
interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) in contrast to IR control group which has
increased level of these parameters. On the other hand, treatment with valsartan and valsartan plus L-arginine lead
to increase in the serum levels of glutathione peroxidase (GPX), in contrast to ischemia reperfusion control group.
Conclusion: Our data revealed that valsartan as a type I angiotensin receptor antagonist could decrease oxidative
stress and inflammation due to renal ischemia reperfusion injury. Hence, valsartan could propose as a therapeutic
agent for kidney diseases such as renal ischemia-reperfusion injury regarded to these renoprotective effects.