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Am J Physiol Heart Circ Physiol 276: H926-H934, 1999;
0363-6135/99 $5.00
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Vol. 276, Issue 3, H926-H934, March 1999

Estrogen increases Ca2+ efflux from female porcine coronary arterial smooth muscle

Y. S. Prakash, A. A. Togaibayeva, M. S. Kannan, V. M. Miller, L. A. Fitzpatrick, and G. C. Sieck

Departments of Anesthesiology, Physiology and Biophysics, Surgery, and Endocrinology, Mayo Foundation, Rochester 55905; and Departments of Veterinary PathoBiology and Pediatrics, University of Minnesota, St. Paul, Minnesota 55108

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. 17beta -Estradiol (E2beta ), but not 17alpha -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, E2beta still decreased [Ca2+]i. The response was blocked by extracellular lanthanum. These data indicate that E2beta decreases [Ca2+]i in coronary artery smooth muscle by affecting Ca2+ efflux via a receptor-mediated mechanism.

vasodilation; endothelin; receptor; calcium adenosine 5'-triphosphatase


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