Vasopressin release induced by intracranial injection of tachykinins is due to activation of central neurokinin-3 receptors.

The present study investigated the effect on vasopressin release of the intracerebroventricular injection of tachykinins in rats. The selective neurokinin (NK)-3 receptor agonists [MePhe7]neurokinin B and [Asp5,6MePhe8]substance P(5-11) evoked vasopressin release. Also eledoisin, physalaemin and kassinin, which show good affinity for central NK-3 receptors, released vasopressin. On the other hand, neurokinin A, substance P and the selective NK-1 agonist [Pro9,Met(O2)11]substance P were devoid of activity. At doses releasing vasopressin, central injection of NK-3 selective agonists and of the natural tachykinins never produced hypotension. Present results indicate that activation of central NK-3 receptors is involved in vasopressin release induced by tachykinins, and rule out the possibility that the effect might be consequent to hypotension due to passage of tachykinins into the peripheral circulation.