Multiple mechanisms of bronchoconstrictive responses to endothelin-1.
Multiple mechanisms of bronchoconstrictive responses to endothelin-1.
复制标题
对内皮素 1 的支气管收缩反应的多种机制。
DOI：
10.1097/00005344-199100177-00061
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发表时间：
1991
影响因子：
3
通讯作者：
Hasegawa,S
中科院分区：
文献类型：
--
作者：
Nomura,A;Ninomiya,H;Saotome,M;Ohse,H;Ishii,Y;Uchida,Y;Hirata,F;Hasegawa,S
本文研究了内皮素-1（ET-1）引起豚鼠气管平滑肌支气管收缩的机制。ET-1呈剂量依赖性收缩气管。联合应用FPL 55712（白三烯拮抗剂）、苯海拉明（组胺拮抗剂）和吲哚美辛（环氧化酶抑制剂）可使ET-1的量效曲线右移，并抑制最大收缩。氮卓斯汀一种抗过敏剂，产生了基本上相似的结果。目前的数据表明，ET-1不仅通过对气管平滑肌的直接作用来收缩气道平滑肌，还通过在肌肉以外的细胞中产生各种化学介质介导的间接作用来收缩气道平滑肌。
We investigated the mechanism of the endothelin-1 (ET-1 (-induced bronchoconstriction of guinea pig tracheal smooth muscles. ET-1 contracted the tracheas in a dose-dependent manner. A combination of FPL55712 (leukotriene antagonist), diphenhydramine (histamine antagonist), and indomethacin (cyelooxygenase inhibitor) shifted the dose-response curve of ET-1 to the right and suppressed the maximal constriction. Azelastine. an antiallergic agent, exerted essentially similar results. The present data suggest that ET-1 constricts the airway smooth muscles not only by direct action on the tracheal smooth muscles but also by indirect action mediated through production of various chemical mediators in cells other than muscles.