Acute estrogen administration relaxes vascular smooth muscle by decreasing
intracellular Ca2+ concentration ([Ca2+](i)). In the present study, we exam
ined the hypothesis that this reduction in [Ca2+](i) is mediated in part by
enhanced Ca2+ efflux. Coronary artery smooth muscle cells were isolated fr
om gonad-intact, sexually mature female pigs. The [Ca2+](i) response to end
othelin-1 was measured using flue 3 and confocal microscopy. 17-Estradiol (
E(2)beta), but not 17 alpha-estradiol or triamcinolone acetonide, caused a
concentration-dependent (IC50 = 10 nM) decrease in the [Ca2+](i) response t
o endothelin-1. This decrease was blocked by the specific estrogen receptor
antagonist ICI-182780. Under conditions in which Ca2+ influx and sarcoplas
mic reticulum Ca2+ reuptake were blocked, E(2)beta still decreased [Ca2+](i
). The response was blocked by extracellular lanthanum. These data indicate
that E(2)beta decreases [Ca2+](i) in coronary artery smooth muscle by affe
cting Ca2+ efflux via a receptor-mediated mechanism.