McLeod J D, Piper P J
Department of Pharmacology, Hunterian Institute, Royal College of Surgeons, Lincoln's Inn Fields, London, U.K.
Eur J Pharmacol. 1992 Feb 25;212(1):67-72. doi: 10.1016/0014-2999(92)90073-d.
The coronary vascular endothelium of the guinea-pig isolated perfused heart was removed by treatment with 3-[(3-cholamidopropyl)-dimethylammonio]-1-propanesulfonate (CHAPS), a zwitterionic detergent. After CHAPS treatment of the heart the vasoconstrictor responses of leukotriene (LT) C4, LTD4 and angiotensin II (AII) were significantly attenuated whereas the vascular actions of U46619, a thromboxane (Tx) A2 mimetic, and endothelin-1 (ET-1) were unaltered. The endothelium-dependent vasoconstrictor response of LTC4 and LTD4 could not be attributed to the release of TxA2, platelet-activating factor or AII since indomethacin, WEB 2086 and captopril had no effect on LT actions. However, in the presence of cromakalim, a potassium channel activator, the vasoconstrictor effects induced by LTC4, LTD4 and AII were significantly attenuated to a greater extent than the responses of U46619 and ET-1. The results suggest that in the coronary vasculature of the guinea-pig isolated heart the vasoconstrictor responses of LTC4, LTD4 and AII are endothelium-dependent and may involve a cromakalim-sensitive mechanism.
用两性离子去污剂3-[(3-胆酰胺丙基)-二甲基铵]-1-丙烷磺酸盐（CHAPS）处理豚鼠离体灌流心脏，去除其冠状血管内皮。用CHAPS处理心脏后，白三烯（LT）C4、LTD4和血管紧张素II（AII）的血管收缩反应明显减弱，而血栓素（Tx）A2模拟物U46619和内皮素-1（ET-1）的血管作用未改变。LTC4和LTD4的内皮依赖性血管收缩反应不能归因于TxA2、血小板活化因子或AII的释放，因为吲哚美辛、WEB 2086和卡托普利对LT的作用没有影响。然而，在钾通道激活剂克罗卡林存在的情况下，LTC4、LTD4和AII诱导的血管收缩作用比U46619和ET-1的反应更明显减弱。结果表明，在豚鼠离体心脏的冠状血管系统中，LTC4、LTD4和AII的血管收缩反应是内皮依赖性的，可能涉及一种对克罗卡林敏感的机制。
