Protective effects of estrogen on the cardiovascular system.
Estrogen has direct and indirect effects on the cardiovascular system that are mediated by the estrogen receptors ER-alpha and ER-beta. The direct effects of estrogen occur through rapid nongenomic and longer-term genomic pathways. The rapid effects of estrogen are mediated by ERs and result in the activation of endothelial nitric oxide synthase, leading to arterial vasodilation. Longer-term effects involve changes in gene and protein expression, modulating the response to injury and atherosclerosis. Estrogen also indirectly influences serum lipoprotein and triglyceride profiles, and the expression of coagulant and fibrinolytic proteins. Advanced atherosclerosis and certain progestins, however, may attenuate some of the protective effects of estrogen.
Mendelsohn
Michael E
ME
Tufts University School of Medicine, Molecular Cardiology Research Institute, Tufts-New England Medical Center, Boston, Massachusetts 02111, USA.
D000818:Animals; D002318:Cardiovascular Diseases / Q000209:etiology / Q000517:prevention & control*; D002319:Cardiovascular System / Q000187:drug effects*; D015914:Estrogen Replacement Therapy; D004967:Estrogens / Q000494:pharmacology*; D005260:Female; D006801:Humans; D006937:Hypercholesterolemia / Q000150:complications / Q000517:prevention & control; D051379:Mice; D018345:Mice, Knockout; D019001:Nitric Oxide Synthase / Q000378:metabolism; D011960:Receptors, Estrogen / Q000187:drug effects / Q000502:physiology; D012307:Risk Factors; D014664:Vasodilation / Q000187:drug effects
D004967:Estrogens; D011960:Receptors, Estrogen; D019001:Nitric Oxide Synthase