title: Neurotensin inhibition of gastric exocrine secretions in the cat.
abstract: The gastric exocrine inhibitory activities of neurotensin were characterized in conscious cats prepared with gastric fistulae. Neurotensin was a potent inhibitor of pentagastrin-stimulated pepsin secretion (ID50, approx. 0.3 mumol . kg-1 . h-1) but was approximately 60 times less potent against acid secretion. Neurotensin did not significantly reduce submaximal histamine-stimulated acid or pepsin secretions. the total 2 h acid and pepsin outputs in response to insulin-hypoglycaemia were not reduced by neurotensin, although the peak 15-min outputs were reduced. The reduction in peak secretion was possibly related to neurotensin antagonism of the ability of insulin to lower blood glucose concentrations. Neurotensin alone was not hyperglycaemic when given as an intravenous infusion. Two C-terminal fragments of neurotensin, the dodecapeptide and nonapeptide, inhibited pentagastrin-stimulated pepsin secretion, but were less potent than neurotensin. The observations with the C-terminal fragments indicate that the major determinants of gastric exocrine inhibitory activity of neurotensin reside in its C-terminal; this agrees with observations on other biological activities of neurotensin. The reduced potency of the dodecapeptide indicates the importance of the N-terminal pyroglutamyl residue for full gastric exocrine inhibitory activity.
mesh_terms: D000818:Animals; D002415:Cats; D004305:Dose-Response Relationship, Drug; D005744:Gastric Acid / Q000378:metabolism*; D006632:Histamine / Q000494:pharmacology; D007003:Hypoglycemia / Q000378:metabolism; D007328:Insulin / Q000494:pharmacology; D009496:Neurotensin / Q000494:pharmacology*; D010418:Pentagastrin / Q000494:pharmacology; D010434:Pepsin A / Q000378:metabolism*; D013004:Somatostatin / Q000494:pharmacology
chemical_list: D007328:Insulin; D009496:Neurotensin; D013004:Somatostatin; D006632:Histamine; D010434:Pepsin A; D010418:Pentagastrin