In women, the risk of coronary heart disease increases significantly after menopause. Estrogen therapy, however, reduces the risk of cardiovascular disease in healthy postmenopausal women. Estrogen enhances endothelial function of the coronary arteries, and this may contribute to the cardioprotective effects of the female hormone.
The precise mechanisms that mediate the beneficial effects of estrogen on arterial endothelial function are incompletely understood. What is known is that the long-term effects of estrogen occur through activation of estrogen receptors and subsequent modulation of gene expression. Moreover, estrogen has also been shown to effect endothelium-dependent function via its effects on expression of endothelial nitric oxide synthase.
A New Study
Conclusions and Discussion
Based on the above findings, the researchers conclude that NO-mediated dilation is preserved in ERáKO mice through compensatory activation of ER-á independent pathways. Further study is needed to determine whether modulation of endothelium-dependent, NO-mediated vasodilation in coronary arteries occurs through an ER-â pathway.
Source: November 2003 edition of the American Journal of Physiology—Heart and Circulatory Physiology.
Donna Krupa | APS
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