Nitric oxide and asymmetric dimethyl arginine (ADMA) levels in an experimental hydronephrotic kidney caused by unilateral partial ureteral obstruction

Abstract

Aim Our aim is to measure asymmetric dimethyl arginine and nitric oxide levels in rats with induced unilateral acute ureteral obstruction to research the effects on the kidney.Material and Methods The study included 21 adolescent (average age 6 weeks) Sprague-Dawley male rats weighing between 240-290g divided at random into 3 groups. Group-1: Control group (n=6): underwent no procedures. Group-2: Sham group (n=6): underwent the same procedures as the experimental group without ureter and psoas muscle dissection. Group-3: Group with induced partial unilateral ureteral obstruction (n=9). All rats were sacrificed after 12 weeks. Superoxide dismutase enzyme activity and nitrite and nitrate salt levels were measured in renal tissue. Plasma nitrite-nitrate and ADMA levels were examined.Results In the experimental group histopathological changes observed included renal pelvis dilatation, flattened papillae, sclerotic glomerulus and fibrosis. In the experimental group tissue SOD and blood ADMA levels were higher than the control and sham groups (p<0.05) while tissue NO and plasma NO values were lower than in the sham and control groups (p<0.05).Conclusion Oxidative stress and disruption of NO synthesis play an important role in renal function and histopathological changes after obstructive renal disease. To prevent renal complications developing after obstructive nephropathy we believe that a new strategy may be research on reducing ADMA.

Treatment with β-blocker nebivolol ameliorates oxidative stress and endothelial dysfunction in tenofovir-induced nephrotoxicity in rats

“…In addition to MAP restoration, TDF+NBV rats showed a significant increase in RBF and an important decrease in RVR. It is acknowledged that reduced NO production or availability is related to endothelial dysfunction, hypertension and progression of CKD ( 32 , 33 ). Renal NO is synthesized primarily by eNOS and nNOS.…”

“…Another mechanism involved with endothelial dysfunction includes the increase in plasma ADMA, an endogenous competitive inhibitor of NOS isoforms. Higher plasma ADMA levels are also linked to oxidative stress ( 32 , 34 ). Corroborating previous data ( 24 , 26 ), our results showed that tenofovir-treated animals exhibited augmented plasma ADMA concentration which was reversed with the administration of nebivolol.…”

Contrast-induced nephropathy in an animal model: Evaluation of novel biomarkers in blood and tissue samples

“…Based on the evidence provided by the present study it is concluded, that SDMA-ADMA are absolute indicators of renal dysfunction, their levels are directly affected by CM administration and the results are observed in real time. It has been reported that SDMA-ADMA are endogenous inhibitors of NO synthesis and elevated levels indicate renal damage, leading to renal hypoxia/ischemia [35]. It has also been reported that patients with chronic kidney disease (CKD) present high SDMA-ADMA levels [36], which are usually used as biomarkers of renal dysfunction in human [37].…”

Biomarkers of early kidney cells dysfunction in patients with membranous nephropathy

“…A large increase in plasma levels of malondialdehyde (MDA) was found in patients with focal segmental glomerulosclerosis; it occurs early and could play an important role in the pathogenesis of glomerulosclerosis. Attenuation of antioxidant system is also present in patients with nephrotic syndrome, lupus nephritis, IgA nephropathy, and other glomerular diseases [13][14][15][16][17].…”