Effect of parietal cell vagotomy and cholinergic blockade on gastrin release in man induced by gastrin-releasing peptide

Digestion. 1990;46(2):114-20. doi: 10.1159/000200340.

Abstract

The influence of cholinergic blockade as well as vagal denervation of the oxyntic gland mucosa on the gastrin response to gastrin-releasing peptide (GRP) have been studied in patients with duodenal ulcer disease. The gastric luminal content was neutralized during the experiments. GRP induced a substantial increase in gastrin levels with a peak response already after 15 min of infusion. Vagal denervation of the parietal cell area induced a significant increase in basal gastrin concentrations and a significant enhancement of the GRP response. Two different doses of benzilonium bromide were studied and neither influenced the basal concentrations of gastrin. A significantly increased gastrin response to GRP was, however, observed after administration of both a high and a very low dose of the anticholinergic drug. Our results delineate a vagal, noncholinergic inhibitory influence on the basal gastrin release. In addition a vagally dependent oxyntopyloric mechanism inhibits the gastrin release stimulated by GRP. This inhibitory mechanism may hypothetically be a cholinergic reflex mechanism.

Publication types

  • Clinical Trial
  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Bombesin*
  • Duodenal Ulcer / physiopathology*
  • Female
  • Gastrin-Releasing Peptide
  • Gastrins / metabolism*
  • Humans
  • Male
  • Middle Aged
  • Parasympatholytics*
  • Peptides*
  • Pyrrolidines*
  • Vagotomy, Proximal Gastric*

Substances

  • Gastrins
  • Parasympatholytics
  • Peptides
  • Pyrrolidines
  • Gastrin-Releasing Peptide
  • benzilonium bromide
  • Bombesin