Abstract
INTRODUCTION: Hypertension is becoming an important medical and public health problem all over the world and is the most common disorder of ageing. There is a growing evidence of involvement of vascular oxidative stress in the development of hypertension from animal studies. However, studies on humans with hypertension, particularly in elderly are least and data remained controversial. Moreover, studies in elderly people with hypertension are scarce. AIM: To investigate the possible role of oxidative stress and antioxidant defense in the pathogenesis of hypertension in elderly. MATERIALS AND METHODS: A cross-sectional study was conducted on elderly males (n=60) with newly diagnosed hypertension and with normal blood pressure. Oxidative stress and antioxidant status were evaluated by assessing the following parameters: plasma Malondialdehyde (MDA), and antioxidants: Superoxide Dismutase (SOD) activity, reduced Glutathione (GSH), and vitamin C levels; and total Nitric Oxide concentration in plasma (NOx). Difference between groups was determined by using unpaired t-test/Mann-Whitney U test. Bivariate correlation and multiple regression analysis were used to determine the relationship between variables. RESULTS: A significant rise in plasma MDA (p-value=0.013) and lower levels of endogenous antioxidants: SOD (p-value≤0.001) and GSH (p-value≤0.001) were observed in elderly individuals with hypertension when compared to healthy controls. Though not significant, there was a mean decrease in plasma NOx in hypertensive subjects than normotensive ones. While vitamin C showed no significant difference between two groups. Decrease in GSH (β=-0.398; p-value=0.001) and SOD (β=-0.423; p-value≤0.001) were the significant determinants of hypertension in elderly individuals. CONCLUSION: Above findings indicate that elevation in oxidative stress and decrease in endogenous antioxidant level may be involved in the pathogenesis of hypertension. However, it remains unclear whether oxidative stress causes or augments hypertension.