Fadillioglu, EErdogan, HPolat, AEmre, MH2024-08-042024-08-0420021420-40961423-0143https://doi.org/10.1159/000066341https://hdl.handle.net/11616/929919th Meeting of the Balkan Clinical Laboratory Federation (BCLF) -- SEP 12-15, 2001 -- LOANNINA, GREECENitric oxide (NO) has a role in the etiopathogenesis of hypertension. Relaxation of vascular smooth muscles is failed when NO production is reduced leading to increased vascular peripheral resistance. N sup omega nitro-L-arginine methyl ester (L-NAME) is one of the inhibitors of NO production. The aim of this study was to investigate oxidant-antioxidant systems of renal tissue in rats with hypertension induced by L-NAME. Rats were divided into three groups: control group and study groups treated with 100 or 500 mg/l L-NAME in drinking water for 15 days. The activities of catalase (CAT), glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD), and the levels of malondialdehyde (MDA) and NO were studied in the renal tissue after hypertension induction. Arterial blood pressure was increased in both L-NAME groups. CAT activity of 500-mg L-NAME group was higher than control. GSH-Px activity of 500-mg L-NAME group was decreased compared with 100-mg ones. NO level was lower in 500-mg L-NAME group than control. MDA levels in both L-NAME groups were decreased compared with control. In conclusion, hypertension was induced with oral L-NAME treatment. Increased CAT activity was compensated with decreased GSH-Px activity in 500-mg L-NAME group. Both study groups were protected from lipid peroxidation with NO inhibition.eninfo:eu-repo/semantics/closedAccesshypertensionL-NAMEantioxidantslipid peroxidationkidneyConference Object2542112161242442210.1159/0000663412-s2.0-0012430647Q2WOS:000179597600003Q3