Gerritsen M E, Lederis K
Pharmacology. 1979;18(2):72-9. doi: 10.1159/000137233.
Urotensin I (UI) was found to elicit dose-related relaxation responses in isolated helical strips of the rat tail artery. The responses were not prevented by adrenergic, cholingergic or histaminergic blocking agents. Competitive and non-competitive components of antagonism were observed to noradrenaline-, 5-hydroxytryptamine-, and arginine vasopressin-induced contractions. Atropine caused a direct relaxation of the isolated vascular tissues, as well as a significant potentiation of UI responses.
在大鼠尾动脉离体螺旋条中,发现尾加压素I(UI)可引发剂量相关的舒张反应。肾上腺素能、胆碱能或组胺能阻断剂不能阻止这些反应。观察到去甲肾上腺素、5-羟色胺和精氨酸血管加压素诱导的收缩存在竞争性和非竞争性拮抗成分。阿托品可使离体血管组织直接舒张,还可显著增强UI反应。