The cardioprotective effects of 17β-estradiol (E2) in women are hypothesized to be partially mediated by its metabolites, 2-hydroxyestradiol (2-HOE) and 2-methoxyestradiol (2-MeOH). Therefore, the purpose of our study was to determine the acute effects of E2, 2-HOE, and 2-MeOH to inhibit coronary arterial constriction. Right coronary arteries were dissected out of hearts obtained from breeding sows, cut into 4 mm rings, and suspended in organ baths. Incubation of the rings with E2, 2-HOE, and 2-MeOH (10 μmol/L) for 60 min attenuated a subsequent KCl-induced contraction by ~ 50%; the protein synthesis inhibitor, cycloheximide, and the estrogen receptor antagonists, ICI 182,780 and tamoxifen, did not effect the attenuation. Moreover, E2, 2-HOE, and 2-MeOH antagonized the contraction induced by the vasospasm agonist, endothelin-1 (0.1μmol/L) by ~ 36%; when the L-type Ca2+ channel blocker, nifedipine, was added at the conclusion of the experiment no additional contractile attenuation was present. Our results suggest that E2, 2-HOE, and 2-MeOH demonstrate a similar nongenomic inhibition of agonist-induced extracellular Ca2+-dependent contractions.
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