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Abstract
Animal studies evaluating gender difference, the effects of gonadectomy and estrogen
replacement and clinical studies in post-menopausal women with and without estrogen
replacement therapy (ERT) proved that estrogen exerts significant benefits on the
cardiovascular system. Since effects on the plasma lipoprotein profile is responsible
for only approximately 25-40% of the cardiovascular protection exerted by estrogens,
it is postulated that direct effects of estrogen on the vascular wall must play an
important role. Indeed, experimental and clinical evidence accumulated over the past
decade, and reviewed briefly here, indicate that at least a part of cardiovascular
benefits of 17 beta-estradiol can be attributed to the direct effect of the ovarian
sex steroid hormone on vascular endothelial cells. Maintenance and upregulation of
endothelial nitric oxide production and suppression of EDCF generation by 17 beta-estradiol
may play an important role in preventing or reversing endothelial dysfunction, associated
with atherosclerosis, hypertension and other cardiovascular diseases. Stimulation
of angiogenesis (especially collateral vessel formation in ischemic tissues) by the
ovarian steroid hormone could be beneficial in coronary artery disease, peripheral
vascular disease, cerebral ischemia (stroke) and congestive heart failure. Despite
these indisputable beneficial effects, several key questions remain to be answered
in the future, including the better understanding of the apparently opposite effects
of estrogen on prevention of cardiovascular disease vs. treatment of existing disease.