Natural estrogens such as 17β-estradiol are endogenous vasodilators and have been implicated in the gender differences of hypertension. These hormones activate estrogen receptors ERα and ERβ, which mediate part of estrogendependent vasodilation. In addition, a novel G protein-coupled estrogen-binding receptor termed GPER/GPR30 has been identified that is expressed in the cardiovascular system. Using knock-out animals or drugs selectively targeting GPER/GPR30, a significant role for this receptor as a mediator of acute estrogen-dependent vasodilation involving nitric oxide (NO) and blood pressure-lowering activity has been demonstrated. The accumulating evidence that GPER/GPR30 is responsible for control of vascular tone indicates that this receptor may represent a novel drug target for pharmacologic treatment of hypertension in postmenopausal women and possibly also men.
Keywords: Blood pressure, endothelium, hormone therapy, hypertension, menopause, nitric oxide, vasodilation
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