[17-beta estradiol induces type III nitric oxide synthase expression in cultured endothelial cells].

It has been suggested that the low incidence of cardiovascular diseases in premenopausal women, compared with that in men of the same age, is related to the interaction between the nitric oxide (NO) pathway and estrogens. The aim of the present work was to characterize the mechanism by which 17-beta estradiol produces an increment in NO release in cultured endothelial cells. Treatment of cells with 17-beta estradiol significantly increased the amount of nitrites delivered into the culture medium, compared with that from cells without estrogenic treatment. This effect was blocked by the antagonist of estrogen receptors, tamoxifen. By Western blot, it was shown that 17-beta estradiol significantly increased the amount of eNOS in treated cells, compared with that from their respective control cells. Moreover, the acetylcholine-induced release of nitrites in cells treated with 17-beta estradiol was higher than nitrite production induced by the same dose of acetylcholine in control cells. In conclusion, our data underline the physiological role of 17-beta estradiol, which promotes the increase in eNOS expression, potentiating the effects of vascular agonists that release nitric oxide, suggesting a cardiovascular protective role by estrogens.