Cardiovascular protection by postmenopausal estrogen replacement therapy: possible mechanisms of the estrogen action.
Estrogen replacement therapy reduces the cardiovascular risk in postmenopausal women, but the mechanism has yet to be evaluated. There is growing evidence that estradiol administration results in direct vasodilatory effects on vessel walls. The biochemical mechanisms have been investigated in human arteries and veins with respect to different mediators and cell systems. Whereas estradiol had no direct effect on the prostaglandin system we found a endothelin-mediated stimulation of prostacyclin production in endothelial cell cultures. In experiments with the NO/cGMP-system estradiol activity could be demonstrated. In addition estradiol provoked an increase in the intracellular Ca2+ concentration. These results indicate that several mechanisms may be involved in the vasodilating effect of estradiol.
Mück
A O
AO
Department of Obstetrics and Gynaecology, Tübingen, Germany.
Seeger
H
H
Korte
K
K
Lippert
T H
TH
D002118:Calcium / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000517:prevention & control*; D002478:Cells, Cultured; D006152:Cyclic GMP / Q000096:biosynthesis; D016232:Endothelins / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000502:physiology; D011464:Epoprostenol / Q000096:biosynthesis; D004958:Estradiol / Q000494:pharmacology*; D015914:Estrogen Replacement Therapy; D005260:Female; D006801:Humans; D014469:Umbilical Arteries; D014471:Umbilical Veins; D014664:Vasodilation / Q000187:drug effects*
D016232:Endothelins; D004958:Estradiol; D011464:Epoprostenol; D006152:Cyclic GMP; D002118:Calcium