The vagus and neurotensin release in duodenal ulcer--clinical and experimental studies

Although meal-stimulated neurotensin release from the small intestine is inhibited by cholinergic blockade, it is uncertain whether this cholinergic mechanism involves the vagus. This study examines the role of the vagus in neurotensin release by first determining the effect of vagotomy on meal-stimulated plasma neurotensin in man and second, the effect on plasma neurotensin of electrical stimulation of the vagus in sheep. Six volunteers were studied 6-8 weeks after truncal vagotomy and pyloroplasty. Basal plasma neurotensin at 32(15-67) pmol/l (median, range) was greater than in normal controls at 17 (9-52) pmol/l (P less than 0.05). Following a standard meal, plasma neurotensin rose significantly (P less than 0.05), but similarly in both post-vagotomy and control groups to maxima of 74 (43-76) pmol/l and 52 (35-65) pmol/l, respectively. Basal plasma neurotensin in the six sheep was below the detection limit of the assay and remained undetectable during electrical stimulation of the vagus. Significant rises in plasma pancreatic polypeptide and gastrin confirmed the efficacy of the electrical stimulation. It is concluded that although the vagus might have a tonic inhibitory effect on basal plasma neurotensin, meal-stimulated neurotensin release is vagally independent. The inhibitory cholinergic influence on meal-stimulated release is most likely therefore to be mediated by cholinergic nerves of the enteric nervous system.