Shoji T, Goto K
R&D Division, Eisai Co., Ltd., Tokyo, Japan.
Eur J Pharmacol. 1991 Feb 14;193(3):371-4. doi: 10.1016/0014-2999(91)90154-i.
Endothelin-1 (ET-1) potentiated both the fast and the slow components of the twitches of the isolated field-stimulated rat vas deferens, whereas Bay k 8644 potentiated only the fast component. Nicardipine tended to decrease the potentiation. ET-1, but not Bay k 8644, caused membrane depolarization and resting tension elevation, which were suppressed by nicardipine. The excitatory junction potentials (EJPs) were augmented by Bay k 8644 and the effect was not changed by nicardipine. ET-1, however, apparently did not augment the EJPs, because of the accompanying depolarization. These results indicate a difference in mechanism of the potentiating effects of ET-1 and Bay k 8644.
内皮素-1（ET-1）增强了离体电场刺激大鼠输精管收缩的快速和慢速成分，而Bay k 8644仅增强了快速成分。尼卡地平倾向于降低这种增强作用。ET-1可引起膜去极化和静息张力升高，但Bay k 8644不会，而尼卡地平可抑制ET-1的这些作用。Bay k 8644可增强兴奋性接头电位（EJP），且该作用不受尼卡地平影响。然而，由于伴随的去极化作用，ET-1显然并未增强EJP。这些结果表明ET-1和Bay k 8644增强作用的机制存在差异。
