Nongenomic, ER-mediated activation of endothelial nitric oxide synthase: how does it work? What does it mean?
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).
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D000818:Animals; D002318:Cardiovascular Diseases / Q000201:enzymology / Q000517:prevention & control; D004721:Endoplasmic Reticulum / Q000201:enzymology*; D004789:Enzyme Activation / Q000502:physiology; D004967:Estrogens / Q000627:therapeutic use; D005260:Female; D018841:HSP90 Heat-Shock Proteins / Q000378:metabolism; D020249:Hormone Replacement Therapy; D006801:Humans; D008297:Male; D019001:Nitric Oxide Synthase / Q000378:metabolism*; D052250:Nitric Oxide Synthase Type III; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D010766:Phosphorylation / Q000187:drug effects; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism; D021122:Protein Subunits; D011960:Receptors, Estrogen / Q000378:metabolism; D015398:Signal Transduction
D004967:Estrogens; D018841:HSP90 Heat-Shock Proteins; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III; D019869:Phosphatidylinositol 3-Kinases; D017346:Protein Serine-Threonine Kinases; D021122:Protein Subunits; D011960:Receptors, Estrogen; C496314:NOS3 protein, human