Role of nitric oxide in kidney and liver (as distance organ) function in bilateral renal ischemia-reperfusion: Effect of L-Arginine and NG-nitro-L-Arginine methyl ester

Abstract

BACKGROUND: Renal ischemia-reperfusion (RIR) is a major cause of renal dysfunction that acts through different mechanisms. We investigated the role of L-Arginine as an endogenous nitric oxide (NO) precursor and NG-nitro-L-Arginine methyl ester (L-NAME) as an NO inhibitor on kidney and liver function in RIR model. MATERIALS AND METHODS: Fifty-eight Wistar rats were randomly assigned to four groups. Groups 1 (sham-operated, n = 13) received a single dose of saline (4 ml/kg, i.p.) and 2 (Ischemia Isch, n = 14) received a single dose of saline (4 ml/kg, i.p.). Groups 3 (Isch + L-NAME, n = 15) received a single dose of L-NAME (20 mg/kg, i.p.) and 4 (Isch + L-Arginine n = 16) received a single dose of L-Arginine (300 mg/kg, i.p.), After 2 h, renal failure was induced by clamping both renal pedicles for 45 min, followed by 24-h reperfusion in Groups 2-4. Finally, blood samples were obtained, and kidney tissue samples were subjected for pathology investigations. RESULTS: The body weight decreased, and the serum levels of blood urea nitrogen (BUN) and creatinine (Cr), and kidney tissue damage score (KTDS) increased significantly in the Isch and Isch + L-NAME groups compared with the sham group while L-Arginine improved weight reduction (P < 0.05), and it reduced the serum levels of BUN and Cr, and KTDS when compared with the Isch and Isch + L-NAME groups. Kidney weight increased significantly in all groups compared with the sham group. L-Arginine reduced the liver tissue level of malondialdehyde and increased alkaline phosphatase. CONCLUSION: L-Arginine as an NO precursor can improve kidney function against RIR. It also improves oxidative stress in liver tissue.