| Keywords |
Hypertension ; Hydrogen peroxide ; Nitric oxide ; Vasodilation |
| Abstract |
Hypertension is an independent risk factor for coronary artery disease and associated with endothelial dysfunction. Endothelium-derived relaxation factors (EDRF) including nitric oxide (NO) are reduced bioavailability in hypertension and cause increased agonist-induced vasoconstriction. Recently studies, regular exercise has been shown to improve endothelium function via various mechanical change as a shear stress and cell signal transduction in hypertensive animal model and in patients with hypertension. In addition, hydrogen peroxide (H2O2) and adiponectin independently lead to vasodilation and increasing endothelium nitric oxide synthase. H2O2 activates K+ channel either by direct regulation of the channels or increase of endothelial nitric oxide synthease (eNOS). Hypodiponectinemia is associated with impaired endothelium-dependent vasodilation, which indicate reduced vasodilation. This review summarizes the current information on the improvement of NO bioavailability by regular exercise in hypertensive animal models and hypertensive patient. |