Effects of Atropine and of Antral Acidification on Gastrin Release and Acid Secretion in Response to Insulin and Feeding in Dogs

Abstract

In 5 dogs with innervated antral and Pavlov pouches, insulin, 0.5 U per kg intravenously, caused significant increases in serum gastrin concentrations from basal values of 94 pg per ml to peak values of 216 pg per ml when the antral pH was maintained at neutrality. Acidification of the antrum to pH 1 completely abolished the increase in serum gastrin in response to insulin but decreased acid secretion by only 60%. Prior administration of atropine sulfate, 0.1 mg per kg subcutaneously, completely suppressed acid secretion in 4 of 4 dogs but failed to inhibit the increase in serum gastrin in 2 of 4. A higher dose of atropine, 0.2 mg per kg, abolished the increase in serum gastrin in these 2 dogs. These studies show that insulin is an effective stimulant of gastrin release when the antral pH is maintained at neutrality, that part of the acid secretory response to insulin is not dependent upon increase in serum gastrin levels, and that higher doses of atropine are necessary to suppress gastrin release than to suppress acid secretion. In 2 dogs with Pavlov pouches and gastric fistulae, prior administration of atropine sulfate, 0.15 mg per kg, abolished the acid response to a beef liver meal but did not prevent the increase in serum gastrin. Again, atropine was more effective in suppressing acid secretion than in blocking gastrin release, and gastrin release by feeding was more resistant to blocking by atropine than was gastrin release by insulin.