Renovascular hypertension in rats: Temporal antioxidant adaptation

39-44Renovascular hypertension is a form of secondary hypertension, and reactive oxygen species play an important role in the pathophysiology of hypertension. Here, we tried to evaluate temporal changes in lipid peroxidation and antioxidant enzymes activity, in the course of renovascular hypertension. To induce renovascular hypertension, adult male Wistar rats were submitted to Goldblatt 2K1C surgery or sham-operated (sham). The blood pressure was directly assessed after 7, 14, 21 and 28 days. Lipid peroxidation, superoxide dismutase, catalase, glutathione peroxidase (GPx), and glutathione-S-transferase activities were evaluated in heart and kidneys. Mean blood pressure (mmHg) was higher by 20, 14, 23 and 22% (P -1/mg protein) was 47% higher in the hearts (90.12±17.63 in sham group and 132.53±12.43 in hypertensive group), 98% in right kidney (66.13±15.10 in sham group and 131.23±28.32 in hypertensive group), 98% in left kidney of the hypertensive group 7 days in relation to sham group 7 days (67.05±17.87 in sham group and 132.87±35.31 in hypertensive group, P <0.05). The main adaptive change promoted by hypertension includes an induction of GPx during hypertensive status development

Renovascular hypertension in rats: Temporal antioxidant adaptation

Renovascular hypertension is a form of secondary hypertension, and reactive oxygen species play an important role in the pathophysiology of hypertension. Here, we tried to evaluate temporal changes in lipid peroxidation and antioxidant enzymes activity, in the course of renovascular hypertension. To induce renovascular hypertension, adult male Wistar rats were submitted to Goldblatt 2K1C surgery or sham-operated (sham). The blood pressure was directly assessed after 7, 14, 21 and 28 days. Lipid peroxidation, superoxide dismutase, catalase, glutathione peroxidase (GPx), and glutathione-S-transferase activities were evaluated in heart and kidneys. Mean blood pressure (mmHg) was higher by 20, 14, 23 and 22% (P &lt;0.05), respectively in hypertensive groups 7, 14, 21 and 28 days, than in the control groups (108±7 in 7 days, 101±4 in 14 days, 109±7 in 21 days and 104±7 in 28 days in sham group; and 130±12 in 7 days, 116±4 in 14 days, 135±16 in 21 days and 127±6 in 28 days in hypertensive group). Lipid peroxidation, superoxide dismutase, catalase and glutathione S-transferase showed no significant changes. The GPx activity (nmoles.min-1/mg protein) was 47% higher in the hearts (90.12±17.63 in sham group and 132.53±12.43 in hypertensive group), 98% in right kidney (66.13±15.10 in sham group and 131.23±28.32 in hypertensive group), 98% in left kidney of the hypertensive group 7 days in relation to sham group 7 days (67.05±17.87 in sham group and 132.87±35.31 in hypertensive group, P &lt;0.05). The main adaptive change promoted by hypertension includes an induction of GPx during hypertensive status development

Enalapril effects on nitric oxide synthase inhibition-induced hypertension: hemodynamic and oxidative stress evaluations

This study examined the effects of enalapril treatment on L-NAME-induced hypertensive rats and oxidative profile in the heart. Four experimental groups were established: control (received water for three weeks); L-NAME (600 mg/L in drinking for three weeks); enalapril (20 mg/L in drinking two last weeks); L-NAME + enalapril, treated with L-NAME for one week, and L-NAME plus enalapril in the last two weeks. Arterial blood pressure, lipid peroxidation (TBARS and chemiluminescence-CL), and catalase, superoxide dismutase, glutathione peroxidase, and glutathione-S-transferase activities were evaluated. An increase by 47 % in the arterial blood pressure was observed in L-NAME-treated rats. Hypertension was reduced (9 %) with enalapril. Hypertension increased TBARS (177 %), CL (23 %), and glutathione peroxidase (31 %), this last, reducing by 11 % in L-NAME + enalapril group. Glutathione-Stransferase increased by 46 % in enalapril group. These results suggest that L-NAME administration increased arterial pressure and oxidative stress, indicating glutathione peroxidase as an important antioxidant in this model.Colegio de Farmacéuticos de la Provincia de Buenos Aire

Comparison of the effects of two antioxidant diets on oxidative stress markers in triathletes

Intense exercise generates an imbalance in the redox system. However, chronic exercise can yield antioxidant adaptations. A few studies with humans have investigated the effects of antioxidant diets on athletes. Therefore we compared the effects of two dietary interventions on oxidative stress in competitive triathletes. Thirteen male triathletes were selected and divided into 2 groups: one that had a regular antioxidant diet (RE-diet) and the other that had a high antioxidant diet (AO-diet). The diet period was 14 days and blood samples were collected before and after this period. The AO-diet provided twice the dietary reference intake (DRI) of α-tocopherol (30 mg), five times the DRI of ascorbic acid (450 mg), and twice the DRI of vitamin A (1800 g), while the RE-diet provided the DRI of α-tocopherol (15 mg), twice the DRI of ascorbic acid (180 mg) and the DRI of vitamin A (900 μg). The oxidative stress parameters evaluated were: thiobarbituric acid reactive substances (TBARS), total reactive antioxidant potential (TRAP), total sulfhydryl, carbonyl, superoxide dismutase (SOD) activity, hydrogen peroxide consumption and glutathione peroxidase (GPx) activity. We observed, after the diet period, an increase in sulfhydryl, TRAP, TBARS and SOD activity, and a decrease in carbonyl levels. However, no changes were found in hydrogen peroxide consumption or GPx activity. We concluded that antioxidant-enriched diets can improve the redox status of triathletes