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Circulation Research. 2000;87:956-960

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(Circulation Research. 2000;87:956.)
© 2000 American Heart Association, Inc.


Editorial

Nongenomic, ER-Mediated Activation of Endothelial Nitric Oxide Synthase:

How Does It Work? What Does It Mean?

Michael E. Mendelsohn

From the Molecular Cardiology Research Institute, New England Medical Center, Tufts University School of Medicine, Boston, Mass.

Correspondence to Michael E. Mendelsohn, MD, New England Medical Center, 750 Washington St, No. 80, Boston, MA 02111. E-mail mmendelsohn{at}lifespan.org

The administration of estrogens in animals tends to inhibit the development of atherosclerosis... [Therefore], attempts are being made in human males to prevent further progress of the disease in cases of angina or previous coronary thrombosis by long-range estrogen therapy. This work is in its infancy. It is hoped that, with further research, compounds might be found that eliminate the undesirable action of such hormones and yet retain its beneficial effects on arteries (Samuel A. Levine, 1958).1


Key Words: estrogen • receptor • endothelium • nitric oxide • caveolae




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