Effect of parietal cell vagotomy and cholinergic blockade on gastrin release in man induced by gastrin-releasing peptide.
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.
Sjövall
M
M
Department of Surgery, Sahlgren's Hospital, University of Gothenburg, Sweden.
Lindstedt
G
G
Olbe
L
L
Lundell
L
L
D001839:Bombesin; D004381:Duodenal Ulcer / Q000503:physiopathology*; D005260:Female; D019886:Gastrin-Releasing Peptide; D005755:Gastrins / Q000378:metabolism*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010276:Parasympatholytics; D010455:Peptides; D011759:Pyrrolidines; D014629:Vagotomy, Proximal Gastric
D005755:Gastrins; D010276:Parasympatholytics; D010455:Peptides; D011759:Pyrrolidines; D019886:Gastrin-Releasing Peptide; C004460:benzilonium bromide; D001839:Bombesin