The inhibitory effect of duodenal exposure to
acid and hyperosmolal solutions on
pentagastrin-stimulated gastric acid secretion was studied in conscious rats equipped with chronic
gastric fistula and duodenal Thiry-Vella loop. The loop was challenged with saline, HCl or hyperosmolal
polyethylene glycol. Gastric acid secretion was measured in samples from the
gastric fistula. Gut
peptide concentrations were measured in duodenal perfusates collected each 30 min, and in plasma samples collected both during stimulated
acid secretion alone, and at the end of experiments in combination with
luminal challenges of the loops. During
pentagastrin-stimulated gastric acid secretion,
luminal perfusion of the duodenal loop with
acid caused inhibition of
acid secretion (P < 0.001) and a prominent release of
somatostatin both to the lumen (P < 0.001) and to the circulation (P < 0.05). Also,
neurotensin (P < 0.01) and
vasoactive intestinal peptide (P < 0.01) were released to the lumen, but not to the circulation. Upon perfusion of the duodenal loop with hyperosmolal
polyethylene glycol,
acid secretion was inhibited (P < 0.05) and
somatostatin alone was released to the
luminal side (P < 0.01). In conclusion, duodenal exposure to
acid inhibits
pentagastrin-stimulated gastric acid secretion and releases SOM to the circulation that may directly inhibit
acid secretion. Concomitantly,
somatostatin (SOM),
neurotensin and
vasoactive intestinal peptide are released to the lumen. Duodenal exposure to hyperosmolal
polyethylene glycol inhibits
acid secretion with a
luminal release of SOM only. Thus,
luminal acid and hyperosmolal solutions inhibit gastric acid secretion by separate mechanisms. After
acid or hyperosmolal challenge, the release of SOM to the circulation indicates gastric acid inhibition in an endocrine manner, while a
luminal release of gut
peptides indicates a local
peptide overflow that might be of importance via paracrine regulatory mechanisms in the intact animal.