Genomic and nongenomic effects of estrogen in the vasculature.
Estrogen has both rapid vasodilatory effects and longer-term effects on the vasculature. The longer-term effects of estrogen are produced, at least in part, by changes in vascular cell gene and protein expression that are mediated by the ligand-activated transcription factors, estrogen receptor (ER)-alpha and ER-beta. The rapid vasodilatory effects of estrogen do not require changes in gene expression and are produced by estrogen-stimulated increases in endothelial cell nitric oxide synthase activity. This results in nitric oxide-mediated increases in cyclic guanosine monophosphate in vascular smooth muscle cells, which mediate vasodilatation. This article briefly reviews recent progress in this field of vascular biology.
Mendelsohn
Michael E
ME
Tufts University School of Medicine, Molecular Cardiology Research Institute, Tufts-New England Medical Center, Boston, Massachusetts 02111, USA. mmendelsohn@lifespan.org
D000818:Animals; D002319:Cardiovascular System / Q000187:drug effects / Q000378:metabolism*; D003324:Coronary Artery Disease / Q000517:prevention & control; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism; D004967:Estrogens / Q000494:pharmacology; D005260:Female; D005786:Gene Expression Regulation; D006801:Humans; D019001:Nitric Oxide Synthase / Q000187:drug effects / Q000378:metabolism*; D052250:Nitric Oxide Synthase Type III; D011960:Receptors, Estrogen / Q000187:drug effects / Q000235:genetics* / Q000378:metabolism*
D004967:Estrogens; D011960:Receptors, Estrogen; C496314:NOS3 protein, human; D019001:Nitric Oxide Synthase; D052250:Nitric Oxide Synthase Type III