Bodelsson G, Stjernquist M
Department of Obstetrics and Gynecology at Malmö, University of Lund, General Hospital, Sweden.
Eur J Pharmacol. 1993 Nov 16;249(3):299-305. doi: 10.1016/0014-2999(93)90526-n.
The mechanisms of endothelin-1-induced contractile response in the human umbilical artery were investigated in vitro. Autoradiography revealed 125I-endothelin-1 binding sites in the smooth muscle layer of the vessel wall. Endothelin-1 and sarafotoxin S6b induced concentration-dependent contractions while endothelin-3 was virtually without contractile effect. The endothelin ETA receptor antagonist BQ 123 did not affect the contraction to endothelin-1 but antagonized the contraction to sarafotoxin S6b. The contraction to endothelin-1 and sarafotoxin S6b was diminished by both verapamil and nicardipine. It can be concluded that endothelin-1 is a vasoconstrictor in the human umbilical artery, probably acting via more than one contraction-mediating receptor. The 125I-endothelin-1 binding sites demonstrated in the smooth muscle layer of the vessel may correspond to receptors mediating the contractile effect. The mechanisms of action seems to involve activation of Ca2+ channels. The present study does not give any evidence for interaction of endothelin-1 with other endothelium-derived vasoactive agents in this vessel.
我们在体外研究了内皮素-1诱导人脐动脉收缩反应的机制。放射自显影显示在血管壁的平滑肌层中有125I-内皮素-1结合位点。内皮素-1和铃蟾毒素S6b诱导浓度依赖性收缩，而内皮素-3几乎没有收缩作用。内皮素ETA受体拮抗剂BQ 123不影响对内皮素-1的收缩反应，但拮抗对铃蟾毒素S6b的收缩反应。维拉帕米和尼卡地平均可减弱对内皮素-1和铃蟾毒素S6b的收缩反应。可以得出结论，内皮素-1是人脐动脉中的血管收缩剂，可能通过不止一种收缩介导受体起作用。在血管平滑肌层中显示的125I-内皮素-1结合位点可能对应于介导收缩作用的受体。作用机制似乎涉及钙通道的激活。本研究没有提供内皮素-1与该血管中其他内皮衍生血管活性物质相互作用的任何证据。
