Estrogen directly regulates vasomotor tone through both short-term and long-term effects on blood vessels. Long term administration of estrogen is associated with deceased plasma concentrations of renin, angiotensin converting enzyme, endothelin-1 and decreased vascular expression of the gene for angiotensin II receptor type, as well as an increased ratio of nitric oxide to endothelin-1 in the blood. The net effect of these changes due to estrogen is to promote vasodilation: wide blood vessels.
Renin is an enzyme released by the kidney. Renin acts to raise blood pressure by activating angiotensin. Angiotensin-converting enzyme causes the conversion of angiotensin I to angiotensin II. Angiotensin II causes contraction of the smooth muscle in the blood vessels which raises blood pressure.
Angiotensin ll acts on the adrenal cortex to release aldosterone, which causes the kidneys to increase sodium and water retention. Diminished urinary output causes increased blood volume. The greater the blood volume the harder the heart has to work to send blood to organs and cells.
Endothelin 1 is a molecule that causes changes in blood vessels and helps regulate blood pressure. Endothelin 1 is produced in a variety of tissues including endothelial and vascular smooth-muscle cells, neurons and the central nervous system, and endometrial cells.
Alterations in estrogen levels (receptor activity) has potential to effect any of these mechanisms and helps explain why the incidence of cardiovascular diseases is low in premenopausal women, rises in postmenopausal women and is reduced to premenopausal levels in postmenopausal women who receive estrogen therapy.
Source:
The Protective Effects of Estrogen on the Cardiovascular System
Michael Mendelsohn MD
Vol 340: 1901-1811 June 10,1999
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