Oxidative stress in hypertension : Association with antihypertensive treatment.

There is growing evidence that oxidative stress contributes to the pathogenesis of hypertension. Our aim was to measure oxidative stress in hypertensive subjects, and assess the potential confounding influences of antihypertensive therapy. Serum malondialdehyde and antioxidant levels were estimated in patients at the time of presentation and also after a antihypertensive therapy for 3 months. During the period of study no antioxidant/s was given to the patients and control subjects. Mean blood pressure values were altered in the hypertensive patients following antihypertensive therapy from their respective values observed at the time of presentation. Serum malondialdehyde levels were significantly higher in the hypertensive patients in comparison to control cases. The antioxidant activity of enzymes super oxide dismutase, glutathione and non enzymatic antioxidant levels of vitamins E and C were significantly lower in patients compared to controls. After 3 months of antihypertensive treatment all the above parameters showed reversal in the respective levels of serum malondialdehyde and antioxidant activity. Antihypertensive medications lower the blood pressure and thereby results in reduced oxidative stress which indicates that oxidative stress is not the cause, but rather a consequence, of hypertension.

Oxidative stress in patients with essential hypertension.

BACKGROUND: Free oxygen radicals react with membrane lipids to form lipid hydroperoxides, a destructive process known as lipid peroxidation. Lipid hydroperoxides decompose to form a variety of products including malondialdehyde, which is used as an indicator of the oxidative damage of cells and tissues. Endogenous antioxidant enzymes such as superoxide dismutase counteract the oxidative damage from oxidative stress. There is increasing evidence that free radicals are involved in the pathogenesis of hypertension by altering endothelial function. We evaluated the oxidative stress and endogenous enzymatic antioxidant status in patients with essential hypertension before and 3 months after treatment with antihypertensives. METHODS: Fifty patients with essential hypertension attending the outpatient services of the Department of Medicine, Institute of Medical Sciences, Banaras Hindu University and 20 age- and sex-matched healthy controls were studied. The serum malondialdehyde and superoxide dismutase levels were measured in patients at the time of presentation and after 3 months of antihypertensive treatment. No antioxidants were given to the patients during the period of the study. RESULTS: The mean (SD) serum malondialdehyde level was found to be significantly higher (0.33 [0.07] mmol/L) in patients with hypertension compared with controls (0.21 [0.05] mmol/L; p < 0.001). This showed a significant decrease following antihypertensive therapy (0.23 [0.06] mmol/L; p < 0.001) compared with pre-treatment values. The serum superoxide dismutase activity was significantly lower in patients (6.93 [1.35] mg protein/ml of serum) compared with controls (20.12 [3.65] mg protein/ml serum; p < 0.001) at the time of presentation and, compared with the pre-treatment values, increased significantly after 3 months of treatment (10.66 [2.91] mg protein/ml of serum; p < 0.001). CONCLUSION: Our study shows that essential hypertension is associated with increased oxidative stress and reduced antioxidant status. Adequate control of blood pressure with antihypertensive therapy decreases oxidative stress and improves the antioxidant status in these patients.

Antithrombin III activity in cerebrovascular accidents.

Cerebrovascular accidents are commonly due to occlusive or haemorrhagic lesions. The present prospective study was planned to find out role of antithrombin in possible etiopathological process, which might predispose an individual for stroke. METHOD: Biological activity of antithrombin III was done by the method as described by Innerfield et al (1976). Immunological estimation of an antithrombin III was done by single radial immunodiffusion by the technique of Mancini et al modified by Fahey and Mckelvey. RESULTS: The biological and immunological activity of antithrombin III was measured in 98 patient of occlusive and 56 patients of haemorrhagic strokes. Significant depression in biological as well as immunological activity (p<0.001) was observed in occlusive stroke. In haemorrhagic stroke both, biological and immunological activity was increased. In follow up study, there was progressive normalization of both, biological as well as of immunological activity in both group. CONCLUSION: Decrease of antithrombin III in occlusive and increase in haemorrhagic stroke indicates that these changes have at least an additive role in the pathogenesis of stroke.