Nongenomic, ER-mediated activation of endothelial nitric oxide synthase: how does it work? What does it mean?
- PMID: 11090536
- DOI: 10.1161/01.res.87.11.956
Nongenomic, ER-mediated activation of endothelial nitric oxide synthase: how does it work? What does it mean?
Abstract
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).
Comment on
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Membrane estrogen receptor engagement activates endothelial nitric oxide synthase via the PI3-kinase-Akt pathway in human endothelial cells.Circ Res. 2000 Oct 13;87(8):677-82. doi: 10.1161/01.res.87.8.677. Circ Res. 2000. PMID: 11029403
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