Oxytocin causes endothelium-dependent relaxations of canine basilar arteries by activating V1-vasopressinergic receptors.

Experiments were designed to study the effects of oxytocin on canine basilar and femoral arteries and to compare these with the effects of vasopressin. Rings of the arteries were suspended in physiological salt solution for isometric tension recording. Oxytocin and vasopressin caused endothelium-dependent relaxation of basilar arteries contracted with prostaglandin F2 alpha. Vasopressin was more potent than oxytocin. In the femoral artery, the two hormones caused endothelium-independent contractions with the same order of potency. The relaxations of the basilar artery occurred at lower concentrations of each substance than the contractions of the femoral artery. The relaxations in response to both agonists were inhibited competitively, and the contractions noncompetitively, by the V1-vasopressinergic antagonist d(CH2)5Tyr(Me)AVP; the antagonist did not affect endothelium-dependent relaxations in response to bradykinin. Thus, both oxytocin and vasopressin cause endothelium-dependent relaxation of the basilar artery by activating V1-vasopressinergic receptors; the contractions of femoral arteries that they cause also may be mediated in part by V1-vasopressinergic receptors.