Vascular effects of estrogens: Arterial protection versus venous thrombotic risk

Margarita P. Bracamonte, Virginia M Miller

Research output: Contribution to journalArticle

38 Citations (Scopus)

Abstract

Mechanisms by which estrogen reduces the risk of arterial disease, while simultaneously increasing the risk of venous thrombosis in postmenopausal women, are not clearly understood. In addition to providing beneficial arterial effects on the lipid profile, estrogen both increases production of nitric oxide and decreases production of endothelin-1 from arterial endothelium, decreases intracellular calcium in arterial smooth muscle and might favor fibrinolysis. All of these effects could act in concert to protect against development of arterial occlusive disease. However, comparable effects on venous endothelium and smooth muscle have not been studied systematically, and although blood elements such as platelets and leukocytes contain estrogen receptors, much remains to be learned about the effect that dose and duration of estrogen-treatment might have upon these cells. An integrative approach to understanding the actions of estrogen on the venous system and the interaction of blood elements with the vascular wall is necessary before new therapeutic interventions will provide arterial protection with no risk of venous thrombosis.

Original languageEnglish (US)
Pages (from-to)204-209
Number of pages6
JournalTrends in Endocrinology and Metabolism
Volume12
Issue number5
StatePublished - 2001

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Blood Vessels
Estrogens
Venous Thrombosis
Endothelium
Smooth Muscle
Arterial Occlusive Diseases
Endothelin-1
Fibrinolysis
Estrogen Receptors
Nitric Oxide
Leukocytes
Blood Platelets
Calcium
Lipids
Therapeutics

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

Vascular effects of estrogens : Arterial protection versus venous thrombotic risk. / Bracamonte, Margarita P.; Miller, Virginia M.

In: Trends in Endocrinology and Metabolism, Vol. 12, No. 5, 2001, p. 204-209.

Research output: Contribution to journalArticle

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