Hypertension reigns as a leading cause of cardiovascular morbidity and mortality worldwide. Excessive reactive oxygen species (ROS) has emerged as a central common pathway by which disparate influences may induce and exacerbate hypertension. Potential sources of excessive ROS in hypertension include NADPH oxidase, mitochondria, xanthine oxidase, endothelium-derived NO synthase (eNOS), cyclooxygenase 1 and 2, cytochrome P450 epoxygenase and transition metals. While a significant body of epidemiological and clinical data suggests that antioxidant rich diets reduce blood pressure and cardiovascular risk, randomized trials and population studies using natural antioxidants have yielded disappointing results. The reasons behind this lack of efficacy are not completely clear, but likely include a combination of 1) ineffective dosing regimens 2) the potential pro-oxidant capacity of some of these agents 3) selection of subjects less likely to benefit from antioxidant therapy (too healthy or too sick), 4) inefficiency of non-specific quenching of prevalent ROS versus prevention of excessive ROS production. Commonly used antioxidants include Vitamins A, C and E, L-arginine, flavanoids, and mitochondria targeted agents, Coenzyme Q10, acetyl-L-carnitine and alpha-lipoic acid. Various reasons, including incomplete knowledge of the mechanisms of action of these agents, lack of target specificity, and potential inter-individual differences in therapeutic efficacy preclude us from recommending any specific natural antioxidant for antihypertensive therapy at this time. This review focuses on recent literature regarding above mentioned issues evaluating naturally occurring antioxidants with respect to their impact on hypertension.
Keywords: Hypertension, Antioxidants, Oxidative Stress