Accelerated mobilization and formation of histamine in the gastric mucosa evoked by vagal excitation.

1. The changes in the rate of histamine formation and in the histamine content of the parietal cell containing region of the gastric mucosa have been studied in rats under the influence of agents which evoke or abolish vagal excitation.2. The hypoglycaemia producing agents, insulin and 2-deoxyglucose (2-DG), raised the mucosal histamine-forming capacity (HFC) in a way similar to that previously observed on re-feeding, gastrin injection, and distension of the stomach wall.3. In cats, insulin injection elicited an elevation of mucosal HFC similar to the corresponding effect of insulin in rats.4. Hoechst 9980, which inhibits post-ganglionic cholinergic transmission, counteracted the elevation of mucosal HFC following vagal excitation, but did not inhibit changes produced by gastrin, thus indicating the absence of a cholinergic intermediary link between gastrin and changes in mucosal histamine.5. It is emphasized that although re-feeding, vagus excitation, gastrin and distension all produce similar changes in mucosal histamine, the clarification of the precise role of histamine as a natural stimulant for the parietal cells may require a fresh kind of approach.