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Abstract
The present study in the dog evaluates neurotensin as a potential hormone, mediating the inhibition of gastric acid secretion by duodenal acidification. Histamine-stimulated acid output was determined before and during duodenal acidification. Portal vein blood was obtained and assayed for carboxy-terminal neurotensin-like immunoreactivity (NTLI). Duodenal perfusion with 15 mmol HCl for 30 min significantly inhibited histamine-stimulated acid output to 67% of control output. This inhibition was not associated with any change in the peripheral plasma NTLI, but the portal plasma NTLI was significantly elevated from 27 to 78 pM. The effect of duodenal acidification on liver extract meal-stimulated acid secretion was determined in a second group of dogs without portal vein catheter. Duodenal perfusion with 15 mmol HCl for 30 min significantly inhibited meal-stimulated acid secretion to 37% of control output. Intravenous infusion of synthetic neurotensin to a plasma level of 130 pM was required to inhibit meal-stimulated acid output significantly. In summary, NTLI is elevated in portal, but not peripheral, plasma after duodenal acidification. The associated inhibition of acid secretion is not due to hormonal action of neurotensin.