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Uvnas,1 in the 1940's was the first to note a decreasing response to repeated stimulation with crude gastrin extracts, but this effect was thought to be due to a contaminating inhibitory factor. The inhibition of gastric acid secretion by extracts containing gastrin was first demonstrated clearly by Gillespie and Grossman2 in 1963 and confirmed by Gregory and Tracy3 (1964) using a highly purified preparation. The mechanism of this dual action of gastrin, also possessed by the synthetic pentapeptide has not been adequately explained. The ability of a substance to act in a stimulatory capacity in small doses and to inhibit when given in larger amounts is, however, well recognized, eg, acetylcholine and nicotine. In the case of gastrin, this dual action has been thought of little importance in the physiologic mechanisms responsible for controlling its release and activity in the normal state.Most studies2,4-9 on gastrin

The method of assaying gastric secretogogues, first described by Ghosh and Schild1 was modified by Lai2 for the assay of gastrin in extracts of gastric antrum and other tissues. This technique was subsequently employed by Sircus3 and by Moore and his colleagues4 for the detection of gastrin-like activity in the serum and gastric juice of patients with the Zollinger-Ellison syndrome. The last-named authors reported a high incidence of positive results and emphasized the reliability of the method in the preoperative diagnosis of such patients. Ellison and Wilson,5 however, were unable, in several instances, to detect a gastric secretogogue in the serum of patients with proven ulcerogenic tumors of the pancreas.In establishing the bioassay method for gastrin in our laboratory, it was considered necessary to re-evaluate the factors affecting its sensitivity, range, and reliability, using the now available synthetic gastrin pentapeptide. This report is based