Inhibition of meal-stimulated gastric acid secretion in man by exogenous and endogenous pancreatic glucagon.
The effect of intravenous infusion of glucagon (300 ng x kg(-1) x h(-1)), 1-arginine (0.6 g x kg(-1) x h(-1)) and of saline on meal-stimulated gastric acid secretion was studied in six healthy volunteers. Infusion of glucagon and 1-arginine enhanced plasma concentrations of pancreatic glucagon to 65--85 pmol/l, a level similar to that seen after a normal protein-rich meal. Both infusions significantly inhibited the acid response to the meal, most pronounced after 1-arginine. The difference in acid inhibition could not be ascribed either to differences in plasma glucagon concentrations or to differences in serum gastrin concentrations. The study supports the concept that pancreatic glucagon is a physiological inhibitor of gastric acid secretion.
D000328:Adult; D001120:Arginine / Q000494:pharmacology; D001786:Blood Glucose / Q000032:analysis; D005260:Female; D005502:Food; D005750:Gastric Juice / Q000378:metabolism*; D005755:Gastrins / Q000097:blood; D005934:Glucagon / Q000097:blood / Q000494:pharmacology*; D006801:Humans; D008297:Male; D012636:Secretory Rate / Q000187:drug effects; D012965:Sodium Chloride / Q000494:pharmacology
D001786:Blood Glucose; D005755:Gastrins; D012965:Sodium Chloride; D005934:Glucagon; D001120:Arginine