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Effect of L‑arginine and L‑NAME on Kidney Tissue Damage in Rats after 24 h of Bilateral Ureteral Obstruction
Abstract
Background: Bilateral ureteral obstruction (BUO) affects renal function adversely. Previous investigations have implied that nitric oxide (NO) improves renal function in obstructive
nephropathy. The aim of the current study was to investigate the role of NO precursor, L‑arginine, and NO blocker agent, L‑NAME on kidney tissue damage in rats after 24 h of BUO.
Methods: Forty Wistar rats (18 male, 22 female) were divided into four groups as follows; group 1: Sham or negative control group that received saline 3 days prior to the sham operation, group 2: Vehicle or positive control group that received saline 3 days prior to BUO, and groups 3 and 4: L‑arginine and L‑NAME groups that were treated same as group 2 except L‑arginine (300 mg/kg) and L‑NAME (4 mg/kg) instead of saline, respectively. Twenty‑four hours after obstruction, the
serum levels of blood urea nitrogen (BUN), creatinine (Cr), nitrite, and malondialdehyde (MDA) as well as kidney tissue levels of nitrite and MDA were measured and histopathological studies were done on left kidney.
Results: The serum levels of BUN and Cr and kidney and body weights increased and the tissue levels of MDA and nitrite decreased significantly in all BUO groups (P < 0.05). However,
the tissue damage score was significantly lower in the L‑arginine treated group in comparison to the vehicle and L‑NAME groups (P < 0.05). As expected, the serum level of nitrite significantly
increased in the L‑arginine group (P < 0.05).
Conclusions: Endogenous NO donor; L‑arginine, may protect the kidney tissue against BUO. However, this renoprotective role of L‑arginine did not attenuate the increased kidney function
markers (BUN and Cr) induced by obstruction.
Keywords: Bilateral ureteral obstruction, kidney tissue damage, L‑arginine, nitric oxide
nephropathy. The aim of the current study was to investigate the role of NO precursor, L‑arginine, and NO blocker agent, L‑NAME on kidney tissue damage in rats after 24 h of BUO.
Methods: Forty Wistar rats (18 male, 22 female) were divided into four groups as follows; group 1: Sham or negative control group that received saline 3 days prior to the sham operation, group 2: Vehicle or positive control group that received saline 3 days prior to BUO, and groups 3 and 4: L‑arginine and L‑NAME groups that were treated same as group 2 except L‑arginine (300 mg/kg) and L‑NAME (4 mg/kg) instead of saline, respectively. Twenty‑four hours after obstruction, the
serum levels of blood urea nitrogen (BUN), creatinine (Cr), nitrite, and malondialdehyde (MDA) as well as kidney tissue levels of nitrite and MDA were measured and histopathological studies were done on left kidney.
Results: The serum levels of BUN and Cr and kidney and body weights increased and the tissue levels of MDA and nitrite decreased significantly in all BUO groups (P < 0.05). However,
the tissue damage score was significantly lower in the L‑arginine treated group in comparison to the vehicle and L‑NAME groups (P < 0.05). As expected, the serum level of nitrite significantly
increased in the L‑arginine group (P < 0.05).
Conclusions: Endogenous NO donor; L‑arginine, may protect the kidney tissue against BUO. However, this renoprotective role of L‑arginine did not attenuate the increased kidney function
markers (BUN and Cr) induced by obstruction.
Keywords: Bilateral ureteral obstruction, kidney tissue damage, L‑arginine, nitric oxide