Genomic and nongenomic effects of estrogen in the vasculature

Am J Cardiol. 2002 Jul 3;90(1A):3F-6F. doi: 10.1016/s0002-9149(02)02418-9.

Abstract

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.

Publication types

  • Review

MeSH terms

  • Animals
  • Cardiovascular System / drug effects
  • Cardiovascular System / metabolism*
  • Coronary Artery Disease / prevention & control
  • Disease Models, Animal
  • Endothelium, Vascular / drug effects
  • Endothelium, Vascular / metabolism
  • Estrogens / pharmacology
  • Female
  • Gene Expression Regulation
  • Humans
  • Nitric Oxide Synthase / drug effects
  • Nitric Oxide Synthase / metabolism*
  • Nitric Oxide Synthase Type III
  • Receptors, Estrogen / drug effects
  • Receptors, Estrogen / genetics*
  • Receptors, Estrogen / metabolism*

Substances

  • Estrogens
  • Receptors, Estrogen
  • NOS3 protein, human
  • Nitric Oxide Synthase
  • Nitric Oxide Synthase Type III