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In dogs with innervated fundic pouches an intravenous infusion of (Gln4)-neurotensin, 60 pmol X kg-1 X min-1, reduced the pentagastrin-stimulated acid secretion to 40% of the control secretory rate. After vagal denervation of the fundic pouches the same dose of (Gln4)-neurotensin did not significantly change the secretion. These findings suggest that (Gln4)-neurotensin does not act directly on parietal cells but inhibits acid secretion at a presynaptic level.

The effects of two methylated analogs of prostaglandin E2 (PGE2), namely 16,16-dimethyl PGE2 and its methyl ester, on gastric acid and pepsin secretion have been studied in 5 ulcer patients. Both analogs produced significant inhibition of acid secretion in a dose-dependent fashion, but the effect was less pronounced than the inhibition found in a group of healthy volunteers, and it was necessary to give 140 mug of each analog to reach about the ED50. The mean values of pepsin output and pepsin concentration were decreased following administration of PGE2, but the individual results varied.

In dogs with Heidenhain pouches and oesophageal and gastric fistulae, sham feeding inhibited pentagastrin-stimulated Heidenhain pouch acid output. Resection of the antrum and the duodenalbulb reduced oin stomach was diverted through the gastric cannula. The present results are conid secretion at least partly by inducing a vagal release of an inhibitory hormone. The results suggest that this hormone is released from the antrum and the duodenal bulb.