育亨宾和rauwolscine抑制5-hydroxytryptamine-induced大冠状动脉的收缩小腿通过5 HT2受体的封锁。
文章的细节
-
引用
复制到剪贴板 -
Kaumann AJ
育亨宾和rauwolscine抑制5-hydroxytryptamine-induced大冠状动脉的收缩小腿通过5 HT2受体的封锁。
Naunyn Schmiedebergs拱杂志。1983年6月,323 (2):149 - 54。
- PubMed ID
-
6136920 (在PubMed]
- 文摘
-
5 -羟色胺(5 HT)全身收缩了冠状动脉cocaine-treated条牛大。1。阿尔法2-adrenoceptor阻滞剂rauwolscine和育亨宾引起了竞争性5 HT-induced收缩。估计平衡离解常数KB(日志mol / l)育亨宾rauwolscine分别为7.1和7.3。育亨宾的亲和力的受体介导反应5 HT似乎10倍高于突触后α1-adrenoceptors但低于突触后血管α2-adrenoceptors 10倍。2。(-)去甲肾上腺素和α- 2-adrenoceptor-selective受体激动剂B-HT 920造成最大收缩只占20%和2%,分别为最大5 HT的效果。无论是60 mumol / l B-HT 920还是1 mumol / l引起哌唑嗪5 HT的效果。3所示。Ketanserin竞争对手(KB = 9.2(日志mol / l)的影响5 HT。 Combinations of rauwolscine or yohimbine with ketanserin antagonized the 5 HT effects as expected from competition of the 4 drugs for a single class of receptor. 4. The evidence is consistent with an interaction of 5 HT, ketanserin, rauwolscine and yohimbine with 5 HT2 receptors. alpha-Adrenoceptors only play a minor role in large coronary arteries and appear not to be involved in the 5 HT-induced contractions. A possible clinical involvement of 5 HT in coronary artery spasm is discussed.