Mechano- or chemostimulation of the proximal duodenum inhibits gastric motility in rats; both vagal and spinal reflex pathways are involved. Electrical stimulation of vagal efferent fibers releases VIP, an enteric neurotransmitter that inhibits gastric smooth muscle, and produces a VIP-dependent inhibition of gastric motility. The role of VIP in duodenal-induced reflex inhibition of gastric motility has been investigated using a polyclonal antibody (VIPab). Methods: Inhibition of proximal gastric motility (PGM) was measured manometrically in urethane-anesthetized rats in response to mechanostimulation (distension), chemostimulation (acid) of the proximal duodenum, or intravenous injection of CCK-8 (1- 100 pmol) before and after treatment with KLHab (2 mg; control) or VIPab (1 or 2 mg). Results: 1. Distension of the proximal duodenum (0.1-1.0 ml) produced a dose-dependent inhibition of PGM which was unaltered by administration of either dose of VIPab or KLHab. 2. Perfusion of HCl (100 umol over 10 min) inhibited PGM by 2.15 ± 0.35 cmH2O which was unaltered by KLHab (2.15 ± 0.6 CmH2O ) or VIPab (2.2 + 0.4 cmH2O). Intravenous administration of CCK-8 (1-100 pmol) produced a dose dependent inhibition of PGM, which was unaltered by VIPab. Administration of either dose of VIPab, but not KLHab, abolished exogenous VIP-induced inhibition of PGM. Conclusions: Although the vagal efferent inhibitory pathway has been shown to be involved in duodenal-induced inhibition of gastric motility, no evidence for a role for VIP was obtained using immunoneutralization.
|Original language||English (US)|
|State||Published - Mar 20 1998|
ASJC Scopus subject areas
- Agricultural and Biological Sciences (miscellaneous)
- Biochemistry, Genetics and Molecular Biology(all)
- Cell Biology