作者: Ching-Chia Chang Chien , Ming-Jai Su
DOI: 10.1186/S12929-015-0149-8
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摘要: 5-hydroxytryptamine (5-HT)-induced coronary artery responses have both vasoconstriction and vasorelaxation components. The vasoconstrictive effects of 5-HT been well studied while the mechanism(s) how causes relaxation arteries has less investigated. In isolated rat hearts, 5-HT-induced flow increases are partially resistant to nitric oxide synthase inhibitor Nω-Nitro-L-arginine methyl ester (L-NAME) blocked by 5-HT7 receptor antagonists. present study, we investigated role in hearts absence L-NAME, also evaluated involvement endothelium-derived hyperpolarizing factor (EDHF) L-NAME-treated with inhibitors arachidonic acid metabolism blockers Ca2+-activated K+ channels. agonist 5-carboxamidotryptamine induced increases, these were selective antagonist SB269970; SB269970-treated decreases, which effect was 5-HT2A blocker R96544. phospholipase A2 quinacrine cytochrome P450 SKF525A, but not inhibited cyclooxygenase indomethacin. As channel blockers, TRAM-34 (intermediate-conductance blocker) UCL1684 (small-conductance blocker), large-conductance on various: penitrem A paxilline did significantly affect tetraethylammonium suppressed elicited 5-HT. found that mediated activation L-NAME. Metabolites P450s, small-conductance channel, intermediate-conductance involved resemble mechanisms EDHF-induced vasorelaxation. needs further investigation.