ABSTRACT
Numerous in vitro experiments and several clinical studies indicate that estrogens exert various positive effects on the vasculature. By modulating the synthesis of nitric oxide (NO), prostacyclin and endothelin, and blocking calcium channels, estrogens beneficially affect the vasotonus. Atherogenesis, which is considered an inflammatory, fibroproliferative process, may be delayed by estrogens via downregulation of inflammatory markers such as cell-adhesion molecules and chemokines. The delay is further based on inhibition of smooth muscle cell proliferation and downregulation of angiotensin receptor gene expression as well as by its antioxidative property. In addition, estrogens may stabilize the atherosclerotic plaque by reducing the expression of matrix metalloproteinases. The thrombogenic potency of the ruptured plaque may also be reduced by estrogens downregulating the synthesis of plasminogen activator inhibitor-1 (PAI-1). In addition, clinical studies suggest that other nonendothelial-derived vasoactive surrogate markers, such as serotonin and urodilatin, may be positively influenced by estrogens.
