Cholinergic stimulation and suppression of gastrin release in gastric fistula dogs.

Publisher Website
Google Scholar
Abstract
Urecholine effects on gastrin release and on gastric acid were studied in 7 gastric fistula dogs, 4 with intact vagi and 3 others with fundic, highly selective vagotomy (HSV). In the intact dogs, infusion of 20 .mu.g/kg .cntdot. h i.v. caused a fall in serum gastrin, but 120 .mu.g/kg .cntdot. h slowly raised serum gastrin concentrations. In HSV dogs both doses caused prompt and much larger increases in serum gastrin to 2-3 times basal. Gastric secretion of acid was the same at 120 .mu.g/kg .cntdot. h for both groups. Vagal stimulation by deoxyglucose and hormonal stimulation by bombesin [isolated from frog skin] caused more gastrin release in HSV than in dogs with intact vagi. This increase was reversed by background doses of urecholine 10-40 .mu.g/kg .cntdot. h whether the fundic vagus was intact or cut. The lowest doses of urecholine caused an insufficient change in acid secretion to account for the gastrin suppression. Higher doses of urecholine background caused more gastric secretion, but without more suppression of gastrin. The vagus has a dual action on gastrin release (suppression and stimulation), and the suppression depends on the intactness of the fundic vagus. In the vagotomized animals, the suppression could be reproduced by doses of urecholine subthreshold for acid secretion. Both effects appear cholinergic, the former evident at low doses and the latter at higher doses.