Cardioprotective effect of estrogen and raloxifene

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Recent evidence suggests that the direct actions of estrogen on blood vessels contribute to the cardioprotective effects of estrogen. There are many kinds of direct effects of estrogen on blood vessels, such as estrogen-induced increases of vasodilatation and inhibition of the response of blood vessels to injury and the development of atherosclerosis.Although both estrogen and raloxifene activate NO synthesis in endothelial cells, the mechanism of inhibition of the response of blood vessels to injury by estrogen and raloxifene remains unclear. We identified that both estrogen and raloxifene decrease the apoptosis and act as a survival factor. Since blockage of Akt-BAD cascade by gene transfection and addition of inhibitor attenuated the decrement of apoptosis by estrogen and raloxifene, Akt-BAD cascade is involved in the inhibition of the response of blood vessels to injury by estrogen and raloxifene. Moreover, we identified that estrogen and raloxifene act as a survival factor thorough ERα, but not ERα Lastly, we examined the effect of surgical menopause on the function of vascular endothelium by brachial artery flow mediated dilatation. The function of vascular endothelium was significantly decreased after 1 week of surgical menopause.