Acute estrogen administration relaxes vascular smooth muscle by decreasing intracellular Ca2+ concentration ([Ca2+](i)). In the present study, we examined the hypothesis that this reduction in [Ca2+](i) is mediated in part by enhanced Ca2+ efflux. Coronary artery smooth muscle cells were isolated from gonad-intact, sexually mature female pigs. The [Ca2+](i) response to endothelin-1 was measured using fluo 3 and confocal microscopy. 17β-Estradiol (E2β), but not 17α-estradiol or triamcinolone acetonide, caused a concentration-dependent (IC50 = 10 nM) decrease in the [Ca2+](i) response to endothelin-1. This decrease was blocked by the specific estrogen receptor antagonist ICI-182780. Under conditions in which Ca2+ influx and sarcoplasmic reticulum Ca2+ reuptake were blocked, E2β still decreased [Ca2+](i). The response was blocked by extracellular lanthanum. These data indicate that E2β decreases [Ca2+](i) in coronary artery smooth muscle by affecting Ca2+ efflux via a receptor-mediated mechanism.
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|Issue number||3 45-3|
|State||Published - Mar 1999|
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