IT is a matter of debate whether histamine in the gastric mucosa acts as a local chemical mediator for other gastric stimulants1–5, and the isolated bullfrog mucosa provides a convenient model for investigation of the question. The preparation responds to gastric stimulants such as pentagastrin, acetylcholine and histamine; the secretory rate can be monitored easily and there are no complicating factors such as changes in blood flow. Nevertheless, conflicting reports have appeared: Davidson et al.6 found no changes in histamine content after addition of a gastrin-like pentapeptide, while Kasbekar et al.7 showed that pentagastrin and acetylcholine increased the efflux of labelled histamine. I have now used a more direct approach and found that histamine is released in response to pentagastrin and acetylcholine for which it seems to be a common mediator.