Tachykinin-mediated increase in motility acts independently of vasoactive intestinal polypeptide release in the canine ileum.

Tachykinins induce motor activity in the canine ileum, and their mechanism of excitation may include inhibition of the release of a nonadrenergic, noncholinergic inhibitor, for which vasoactive intestinal polypeptide (VIP) is a candidate. Both substance P and neurokinin A produced a dose-dependent increase in ileal contractility with no significant change in VIP output. The highly selective NK1 agonist [Sar9, Met(O2)11]substance P and the highly selective NK2 agonist [Nle10]neurokinin A (4-10) also increased motor activity in the absence of any change in VIP released. These data suggest that the tachykinins produce motor activity in the canine ileum via a mechanism that does not involve changes in VIP output but may involve excitation through both NK1 and NK2 receptors.