ABSTRACT: Hypertension and related oxidative stress are involved in the pathogenesis of any renal diseases. Angiotensin-converting enzyme
inhibitors have multi-directional renoprotective effects. In this study, we aimed to investigate whether lisinopril treatment
has any biochemical alterations on renal tissue in l-NAME (Nε-nitro-l-arginine methyl ester) induced hypertension model. Twenty-eight Sprague–Dawley rats were included in this study and divided
into four equal groups (n=7): control group, l-NAME treated group (75mg/kg/day), l-NAME plus lisinopril treated group and only lisinopril treated group (10mg/kg/day). l-NAME and lisinopril were continued for 6weeks. Systolic blood pressures were measured by using tail cuff method. In biochemical
analysis, malondialdehyde (MDA, an index of lipid peroxidation) levels, the activities of superoxide dismutase (SOD), catalase
(CAT), and glutathione peroxidase (GSH-Px) in renal tissues were used as markers of oxidative stress-induced renal impairment.
Microalbumin and N-acetyl-β-d-glucosaminidase (NAG) in urine were determined as markers of renal tubular damage related to hypertension. Chronic l-NAME administration resulted in a significant depletion of serum nitric oxide (NO). When compared with control group, serum
creatinine, microalbumin, urine NAG, renal tissue MDA level, and CAT activities were significantly high, while renal tissue
SOD and GSH-Px activities low in l-NAME group. In the l-NAME plus lisinopril treated group, serum creatinine, microalbumin and urine NAG, renal MDA level and CAT activity decreased,
whereas SOD, GSH-Px activities in renal tissue and serum NO levels were increased. Thus, lisinopril treatment reversed these
effects. There were not any significant difference between l-NAME plus lisinopril treated group and control group concerning serum creatinine, renal tissue MDA level and SOD, GSH-Px,
CAT activities. These results suggest that lisinopril could diminish biochemical alterations in l-NAME induced hypertensive renal damage that occurs by oxidative stress.
l-NAME–Experimental hypertension–Lisinopril–Oxidative stress
Molecular and Cellular Biochemistry 04/2012; 352(1):247-253. · 2.06 Impact Factor