作者: Babaei Hossein , Y A Azarmi
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摘要: Objectives: The vasorelaxant effect of estrogens on blood vessels is one the important cardiovascular protective mechanisms estrogen. present experiments were designed to study 17β-estradiol (E2) in human saphenous veins (HSV). Methods: HSV obtained from patients undergoing coronary artery bypass graft surgery Tabriz Madani Heart Center. role K + channels and endothelium derived hyperpolarizing factor (EDHF) effects E2 studied by incubating tissues with blockers: glibenclamid (3µM), 4-aminopyridin (1mm), tetraethyl ammonium (TEA, at lower higher concentration: 1mm 10mM), BaCl2 (30µM) combination charybdotoxin apamin. In order assess inhibitory TEA (10mM) relaxant E2, responses elicited denuded vein rings. Results: 1mm, (selective inhibitor large-conductance, BKCa, Ca 2+ activated channels), 4- aminopyridin voltage dependent channels) ATP did not affect PGF2α-induced contractions. concentration, an small-conductance (SKCa) intermediate-conductance (IKCa) channels, significantly inhibited E2-induced vasorelaxation. This was endothelium-dependent abolished denuding. intact tissues, pretreatment either a apamin (inhibitors EDHF), or BaCl2, reduced relaxation produced E2. Conclusion: data suggest that maybe mediated EDHF which involves