Affiliation:
1. Department of Cellular and Integrative Physiology, Indiana University, School of Medicine, Fort Wayne, Indiana 46805
Abstract
We tested the hypothesis that the ability of coronary arteries to withstand functional damage from superoxide (O[Formula: see text]) is altered by exposure of the arteries to a physiological concentration of β-estradiol. Female porcine coronary arterial rings were incubated in an O2-CO2incubator, under normoxic conditions, at 37°C for 22–24 h. Arteries were then placed in baths containing a physiological salt solution at 37°C with 95% O2-5% CO2for isometric force recordings. In rings from 14 female pigs, vasorelaxation to A-23187 and diethylamine-NONOate (DEA-NONOate) was determined with and without prior 15-min exposure to 400 μM pyrogallol. Sensitivity (−logM ED50) and maximum relaxation to A-23187, but not DEA-NONOate, were significantly impaired by exposure to pyrogallol (pyrogallol treated: 7.39 ± 0.09, 82 ± 5%; control: 7.76 ± 0.11, 99 ± 1%, means ± SE; P < 0.01 and P < 0.05, respectively). This effect was attenuated by concurrent exposure to equimolar ascorbate. Arterial rings from 12 separate female pigs were incubated for 22–24 h with or without 1 nM β-estradiol before pyrogallol exposure. β-Estradiol significantly enhanced arterial sensitivity to A-23187 and prevented pyrogallol impairment without affecting DEA-NONOate responses. Therefore, superoxide-mediated endothelial damage and impaired endothelium-dependent relaxation of coronary arteries are prevented by overnight exposure of the arteries to a physiological concentration of β-estradiol.
Publisher
American Physiological Society
Subject
Physiology (medical),Physiology
Cited by
6 articles.
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