[Effect of estrogens on vascular proliferation]

Therapie. 1999 May-Jun;54(3):333-7.
[Article in French]


Studies on the effect of oestrogen on the circulatory apparatus have shown changes in vascular reactivity and structural alterations of blood vessels that participate in vascular growth and remodelling, whether physiological or pathological (atherosclerosis, ischaemia, restenosis). Direct vascular effects of oestradiol are mediated by functional steroid receptors, ER alpha and ER beta. ER alpha is predominantly found in arterial smooth muscle cells. During the menstrual cycle and pregnancy, endometrial vascular growth is required to allow embryo implantation and the development of the blood supply for fetal growth; oestradiol, in association with progesterone, promotes the growth of endometrial arteries, via ER and unknown mechanisms which probably involve the production of growth factors; oestradiol also induces endometrial angiogenesis, via the production of vascular endothelial growth factor (VEGF) by epithelial cells and fibroblasts. Oestradiol inhibits the proliferation of smooth muscle cells in the arterial wall (except in the genital tract), explaining in part the protective role of oestrogen against restenosis and chronic graft rejection. Further studies are required to determine the molecular mechanisms of these actions and the respective role of ER alpha and ER beta.

Publication types

  • English Abstract

MeSH terms

  • Animals
  • Blood Vessels / cytology
  • Blood Vessels / drug effects
  • Blood Vessels / physiology*
  • Cell Division / drug effects
  • Cell Division / physiology
  • Endothelium, Vascular / cytology
  • Endothelium, Vascular / drug effects
  • Endothelium, Vascular / physiology
  • Estradiol / pharmacology
  • Estradiol / physiology*
  • Female
  • Humans
  • Muscle, Smooth, Vascular / cytology
  • Muscle, Smooth, Vascular / drug effects
  • Muscle, Smooth, Vascular / physiology
  • Pregnancy
  • Receptors, Estrogen / physiology*
  • Vascular Diseases / physiopathology


  • Receptors, Estrogen
  • Estradiol