Abstract
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.
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