Modulation by opioid peptides of mechanosensory pathways supplying the guinea-pig inferior mesenteric ganglion

1. Radioimmunological techniques were used in isolated guinea-pig inferior mesenteric ganglion (IMG)-colon preparations to determine whether opioid peptides and neurotensin^8-13 (NT^8-13), the C-terminal region of NT^1-13 recognized by neurotensin receptors, modulate distension-induced release of substance P (SP)- and vasoactive intestinal polypeptide (VIP)-like immunoreactive (LI) material. 2. Colonic distension significantly increased the amount of SP- and VIP-LI material released in the ganglionic superfusate. A low-Ca²⁺ (0.1 mM), high-Mg²⁺ (15 mM) solution blocked their release. 3. In vivo capsaicin pretreatment abolished release of SP-LI material during colonic distension but had no significant effect on distension-induced release of VIP-LI material. 4. The addition of (Leu⁵]enkephalin, [Met⁵]enkephalin, PL017 (a μ-receptor agonist) and DPDPE (a δ-receptor agonist) to the ganglion side of a two-compartment chamber blocked distension-induced release of SP-LI material. The addition of naloxone and ICI-174,864 (a δ-receptor antagonist) to the ganglion compartment reversed the inhibitory effect of the μ- and δ-receptor agonists. 5. Addition of [Leu⁵]enkephalin and [Met⁵]enkephalin to the ganglion compartment had no significant effect on release of VIP-LI material during colonic distension. 6. Addition of NT^8-13 to the ganglion compartment significantly increased in the amount of SP-LI material released during colonic distension but had no affect on distension-induced release of VIP-LI material. 7. The results suggest the hypothesis that under in vivo conditions, enkephalinergic nerves decrease and neurotensinergic nerves increase the release of SP from peripheral branches of primary afferent sensory nerves.