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We have studied the effects of 17-alpha-estradiol, a non-estrogenic steroid, on pig coronary arteries contracted by K+, Ca2+ or serotonin. Experiments were performed on helicoidal strips and rings of left circumflex coronary arteries from freshly slaughtered white pigs and on helicoidal strips of rat thoracic aorta. The strips and rings were suspended inside a water-jacketed muscle chamber in an oxygenated Krebs solution at 37 degrees C. From the initial K(+)-evoked contraction, 17-alpha-estradiol caused a relaxation with an IC50 (15 microM) which was in the range of the IC50s obtained for nitroglycerin (1.3 microM) and nicorandil (50 microM). Contractions evoked by Ca2+ were inhibited by 17-alpha-estradiol, but full blockade could not be achieved. Serotonin-evoked contractions were also blocked by 17-alpha-estradiol with an IC50 of 2.1 microM; 17-beta-estradiol also inhibited the serotonin-evoked contractions. In the presence of 100 microM of the nitric oxide synthase inhibitor N-nitro-L-arginine methyl ester, the relaxing properties of 17-alpha-estradiol in pig coronary arteries and rat thoracic aorta were unaffected, suggesting that endothelial NO release was unrelated to these effects. 17-alpha-Estradiol also relaxed denuded pig coronary artery strips, suggesting that other endothelial-derived relaxing factors were not involved in its vascular effects. The results are compatible with the idea that 17-alpha-estradiol causes relaxation of coronary vessels by acting directly on the cell membrane of smooth muscle cells; these effects seem to be unrelated to the genomic physiological effects of estrogens.(ABSTRACT TRUNCATED AT 250 WORDS)
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