Endothelial Dysfunction in Postmenopausal Women and Hypertension

The endothelium is a major regulator of homeostasis and exerts a number of vasoprotective effects, such as vasodilation, inhibition of inflammatory responses and suppression of smooth muscle cell growth. Dysfunction of the endothelium thus causes reduction or abolition of these vasoprotective effects. Factors that lead to endothelial dysfunction (ED) include a reduction in nitric oxide (NO) production, increased oxidative stress and a decrease in NO bioavailability, whereas endothelium-derived contracting factors are increased. This imbalance leads to an impairment of endothelium-dependent vasodilation, which represents the functional characteristic of ED. Moreover, ED also comprises a specific state of ‘endothelial activation’, which is characterized by a proinflammatory, proliferative and procoagulatory milieu that favors all stages of atherogenesis [1,2]. Hence, ED it is considered a systemic disorder and a key variable in the pathogenesis of atherosclerosis and its complications. Current evidence suggests that endothelial status is not determined solely by the individual risk-factor burden but, rather, may be regarded as an integrated index of all atherogenic and atheroprotective factors present in an individual. ED reflects a vascular phenotype prone to atherogenesis, and may therefore serve as a marker of the inherent atherosclerotic risk in an individual. In line with this hypothesis, dysfunction of either the coronary or peripheral vascular endothelium was shown to constitute an independent predictor of cardiovascular events, providing valuable prognostic information additional to that derived from conventional risk-factor assessment [3].