Non-genomic effects of estrogen and the vessel wall

Abstract

Estrogen, like other steroids, is now believed to possess rapid membrane effects independent of the classical gene activation pathway of steroid action. The presence of membrane estrogen receptors has been demonstrated in different cell types, but not yet in vascular tissue. In vivo, estrogen administration rapidly promotes acetylcholine-induced vasodilation of the coronary and peripheral vascular beds of postmenopausal women. Estrogen also causes relaxation of precontracted isolated arterial segments and perfused organ preparations, within minutes of administration of the hormone. These rapid vasomotor effects of estrogen may be related to blockade of the cell membrane voltage-dependent calcium channels, resulting in inhibition of extracellular Ca2+ mobilization and flux. Recently, estradiol has been shown to rapidly affect cyclic nucleotide turnover in vascular segments, smooth muscle, and epithelial cell cultures, suggesting the possibility of a "cross-talk" between membrane-mediated events and nuclear receptor activation.