Abstract

Hypertension is a major public health problem worldwide, affecting more than 50 million Americans. It is a major risk factor for target organ damage resulting in coronary artery disease, heart failure, stroke, and kidney disease. Large epidemiological surveys have shown that more women, primarily elderly women, than men have hypertension.1 Therefore, in addition to age2 and race,3 gender seems to influence significantly the natural history of hypertension and probably the selection of antihypertensive agents and the response to treatment. Gender and age differences in blood pressure have been suggested to be associated with the sex hormones. Among these, estrogen is proposed to be responsible for the lower blood pressure in premenopausal young women. The cardioprotective effects of estrogen, though controversial in postmenopausal women,4,5 have been suggested by multiple studies in experimental animals and in humans, and the loss of endogenous estrogen with aging contributes to the rapid increase in the incidence of coronary artery disease after menopause. Estrogen improves lipoprotein profiles, has vasodilatory effects on the endothelium, and inhibits vascular smooth muscle cell growth and constriction. However, the time course of the maximal decrease in blood pressure does not coincide with the maximal rise in hormone levels, suggesting that the relationship between blood pressure and endogenous levels of hormones is complex and is probably affected by other factors.6 Alternatively, it was found that menopause was accompanied by a steeper rise of systolic pressure with age and by an increase in the absolute level of diastolic pressure, which was independent of age.7 One recent study demonstrated that aging was accompanied by a greater increase in sympathetic traffic in women than in men, independent of menopausal status.8 These results parallel epidemiological data indicating a higher prevalence of hypertension in elderly women …

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