Abstract
The HDL-raising effect of estrogen replacement is mediated by an increase in HDL-apolipoprotein A-I production and not by a decrease in the clearance rate. Large-scale clinical trials have shown that medroxyprogesterone acetate removes most of the HDL-raising effects of concomitant estrogen treatment. Testosterone decreases HDL levels in both men and women. Lipoprotein (a) levels are reduced by estrogen replacement, but are not affected by medroxyprogesterone. The acute systemic administration of estrogen to postmenopausal women improves the endothelium-dependent vasodilation of coronary arteries and forearm resistance vessels. Usual doses of oral estrogen replacement therapy improve the endothelium-dependent and endothelium-independent vasodilator responses in the forearm in women who have risk factors for atherosclerosis. These effects may be mediated by an antioxidant action of estrogen.
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