D'Orleans-Juste P, De Nucci G, Vane J R
William Harvey Research Institute, St. Bartholomew's Hospital Medical College, London, U.K.
Eur J Pharmacol. 1989 Jun 20;165(2-3):289-95. doi: 10.1016/0014-2999(89)90723-1.
Spirally cut strips of arteries and veins were prepared from the rabbit or the dog and superfused in cascade. Venous strips were more sensitive to endothelin-1 (ET-1) than arterial ones and, in particular, the rabbit jugular and the rabbit mesenteric veins were contracted by as little as 0.5-2.5 pmol of ET-1 in a reproducible and dose-dependent way. The calcium agonist Bay K 8644 had a different profile of activity on the vascular strips, being more potent on the rabbit mesenteric artery than on the rabbit jugular or mesenteric veins. Nicardipine (10(-7) M) did not affect the ET-1-induced vascular contractions but abolished the contractile activity of Bay K 8644. Contractions induced by ET-1 were not affected by the kininase II inhibitor captopril in the rabbit jugular veins but were potentiated by methylene blue in both veins of the rabbit. Our results indicate that ET-1 potently contracts venous and arterial isolated vessels via the activation of specific receptors or channels that differ from the dihydropyridine-sensitive calcium channels. The fact that ET-1 is more active on venous than on arterial smooth muscle may have important pathophysiological implications.
从兔或犬身上获取螺旋状切割的动脉和静脉条带，并进行级联灌流。静脉条带比动脉条带对内皮素 -1（ET -1）更敏感，特别是兔颈静脉和兔肠系膜静脉，低至0.5 - 2.5皮摩尔的ET -1就能以可重复且剂量依赖的方式使其收缩。钙激动剂Bay K 8644对血管条带的活性表现不同，对兔肠系膜动脉的作用比对兔颈静脉或肠系膜静脉更强。尼卡地平（10⁻⁷ M）不影响ET -1诱导的血管收缩，但可消除Bay K 8644的收缩活性。兔颈静脉中，激肽酶II抑制剂卡托普利不影响ET -1诱导的血管收缩，但亚甲蓝可增强兔两条静脉中ET -1诱导的收缩。我们的结果表明，ET -1通过激活不同于二氢吡啶敏感钙通道的特定受体或通道，有效地使离体的静脉和动脉血管收缩。ET -1在静脉平滑肌上比在动脉平滑肌上更具活性这一事实可能具有重要的病理生理学意义。
