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Estrogen receptor-a disruption and vasodilation in coronary arteries

Bethesda, MD 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
Accordingly, a new study tests the hypothesis that estrogen modulates nitric oxide (NO)-dependent vasodilation of coronary arteries through its action on estrogen receptor- (ER-) to increase protein levels of endothelial nitric oxide synthase (eNOS) and Cu/Zn superoxide dismutase (SOD-1). The authors of the study, entitled "Regulation of Nitric Oxide-Dependent Vasodilatation in Coronary Arteries of Estrogen Receptor--Deficient Mice," are Judy M. Muller-Delp, Kathryn E. Nichol, Texas A&M University, College Station, TX; and Dennis B. Lubahn, Brian J. Philips, Elmer M. Price, Edward M. Curran and M. Harold Laughlin, all of the University of Missouri, Columbia, MO. Their findings appear in the November 2003 edition of the American Journal of Physiology--Heart and Circulatory Physiology, one of 14 journals published each month by the American Physiological Society (APS).

Methodology
The investigators followed the primary procedures outlined below:

Animals: A total of 43 ER knockout (ERKO) mice and 36 wild-type (WT) female mice were used for the study of coronary artery vasomotor reactivity experiments. A total of 19 ERKO and 18 W
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Contact: Donna Krupa
djkrupa1@aol.com
703-527-7357
American Physiological Society
12-Nov-2003


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