ESTROGEN AND POSTMENOPAUSAL ESTROGEN PROGESTIN THERAPY - EFFECT ON ENDOTHELIUM-DEPENDENT PROSTACYCLIN, NITRIC-OXIDE AND ENDOTHELIN-1 PRODUCTION/

It is well documented that postmenopausal estrogen/progestin therapy ( HRT) protects women against cardiovascular disorders. However, the mec hanism(s) by which this protection is mediated remains largely unresol ved, because beneficial effects of estrogen on the blood lipid profile account for only 20-30% of the overall protection. Growing evidence s uggests that estrogen has direct effects on the blood vessel wall indi cating that vascular endothelium may play a key role in mediating thes e effects by producing vasoactive factors, such as prostacyclin (PGI(2 )), nitric oxide (NO) and endothelin-1 (ET-1). In vitro estrogen stimu lates endothelial PGI(2) and NO production; whereas ET-1 production is not affected. Moreover, in vivo studies indicate that estrogen and HR T increase PGI(2) and NO production, whereas ET-1 production decreases . These effects are evidently mediated through estrogen receptors in e ndothelial cells. Thus, estrogen and HRT lead to the dominance of vaso dilatory and antiaggregatory agents released by the endothelial cells. This may be an important new mechanism in the cardiovascular protecti on mediated by estrogen and HRT. (C) 1998 Elsevier Science Ireland Ltd .