Estradiol is known to exert a protective effect against the development of atherosclerosis, but the mechanism by which this protection is mediated is unclear. Since animal studies strongly suggest that production of endothelium-derived relaxing factor is enhanced by estradiol, we The incidence of cardiovascular disease, the leading cause of mortality in western societies, is higher in men than in premenopausal women but increases in postmenopausal women. An abundance of epidemiological data supports a role for estrogens in this atheroprotective effect, prompting recommendations for their widespread use in postmenopausal replacement therapy (1, 2). However, the mechanism whereby this protection is mediated remains obscure. It is traditionally thought to be due to potentially favorable changes in blood lipids and lipoproteins (1), but a number of human (3) as well as animal studies strongly suggest a direct effect on the vascular system (4-6) and more specifically that basal endotheliumderived relaxing factor is enhanced in estradiol-treated females compared with oophorectomized controls (7-11).The endothelium-derived relaxing factor has been identified as nitric oxide (NO) or a closely related compound derived from the amino acid L-arginine, able to induce stimulation of the soluble guanylate cyclase enzyme contained in vascular smooth muscle cells (12)(13)(14) Because the molecular mechanisms of the endotheliumderived relaxing factor-enhanced activity observed in estradiol-treated animals has not yet been precisely elucidated, we sought to determine the effects of estradiol on NO production and simultaneously on NOS mRNA, protein, and activity in a well-characterized culture system of endothelial cells. MATERIALS AND METHODSCell Culture and Materials. Bovine aortic endothelial cells (BAEC) were obtained and grown as described (25,26)
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