The isolated, perfused, canine stomach was used to investigate the effect of three neurotransmitters—nor-epinephrine, acetylcholine (or its analogue carbamyl-choline), and VIP (vasoactive intestinal peptide)—on gastric glucagon release. Norepinephrine at the two concentrations tested (3.10−6 and 7.10−7 M) did not influence gastric glucagon release. In contrast, acetylcholine or carbamylcholine (5.10−6 M) as well as VIP (46–60 ng/ml) unequivocally stimulated gastric glucagon release, an effect apparently independent of the changes in blood flow. These results are in sharp contrast with the previously reported lack of effect of an electric stimulation of the vagus nerves on the release of glucagon from the dog stomach. An absence of innervation of the canine gastric A-cell would probably best explain this situation.

This content is only available via PDF.