Fadillioglu Ersin, Erdogan Hasan, Polat Alaadin, Emre Memet Hanifi
Department of Physiology, Faculty of Medicine, Inonu University, TR-44069 Malatya, Turkey.
Kidney Blood Press Res. 2002;25(4):211-6. doi: 10.1159/000066341.
Nitric 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.
一氧化氮（NO）在高血压的发病机制中起作用。当NO生成减少时，血管平滑肌的舒张功能受损，导致血管外周阻力增加。Nω-硝基-L-精氨酸甲酯（L-NAME）是NO生成的抑制剂之一。本研究的目的是探讨L-NAME诱导的高血压大鼠肾组织的氧化-抗氧化系统。将大鼠分为三组：对照组和分别用100或500 mg/l L-NAME处理15天的研究组。在诱导高血压后，研究肾组织中过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GSH-Px）和超氧化物歧化酶（SOD）的活性，以及丙二醛（MDA）和NO的水平。两个L-NAME组的动脉血压均升高。500 mg L-NAME组的CAT活性高于对照组。500 mg L-NAME组的GSH-Px活性低于100 mg组。500 mg L-NAME组的NO水平低于对照组。两个L-NAME组的MDA水平均低于对照组。总之，口服L-NAME可诱导高血压。500 mg L-NAME组中，CAT活性增加与GSH-Px活性降低相互代偿。两个研究组均因NO受抑制而免受脂质过氧化作用。
