Abstract

Simultaneous measurements of peptic activity were made in the stomach wall and in gastric secretions collected after 2 hours of pylorus ligation. These measurements allowed interpretation of alterations of pepsin secretion in terms of residual stored pepsinogen. Two mechanisms were differentiated as having an influence on pepsinogen secretion: a ‘release mechanism,’ whereby pepsinogen was retained in the cell and a ‘synthesis mechanism,’ whereby inadequate synthesis of enzyme resulted in depression of pepsinogen secretion. Thus the injection of 5% dextrose, in this case acting as a hypotonic solution caused inhibition of the release mechanism, similar to that seen with atropine, whereas adrenalectomy reduced the synthesis of pepsinogen which resulted in a diminished output of enzyme, without affecting the release mechanism. Isotonic saline injections stimulated the secretion of, and as a result increased the synthesis of pepsinogen. Adrenalectomy reduced gastric secretion of acid as well as pepsinogen; effects that were grossly exaggerated by salt withdrawal, which also resulted in an excessive secretion of sodium into the stomach. ACTH given for 1–3 weeks, by contrast with the adrenal insufficiency state, did not stimulate gastric secretion, emphasizing again the trophic or permissive rather than stimulant role of the adrenal cortex in gastric secretory mechanisms.

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