Cholecystokinin in the regulation of intestinal motility and pancreatic secretion in dogs

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Abstract
Peptidal (CR-1409) and nonpeptidal (L-364,718) cholecystokinin (CCK) receptor antagonists were used to determine the possible involvement of CCK in the fasted and fed intestinal motility patterns and the related alterations in pancreatic secretion. Dogs were implanted with electrodes along the small bowel and with chronic pancreatic fistulas. In fasted dogs, the typical migrating motor complex (MMC) cycles and accompanying fluctuations in pancreatic secretion were recorded. Neither of the CCK antagonists affected these motor and secretory components of the MMC. Feeding interrupted the MMC and increased spike activity at all levels of the small bowel, and this was accompanied by a significant increase in pancreatic secretion and in plasma hormone [gastrin, CCK, and pancreatic polypeptide (PP)] levels. Both CCK antagonists significantly reduced the postprandial spike activity but failed to restore the fasted pattern. Exogenous gastrin and CCK, as well as bombesin, induced fedlike motility patterns accompanied by marked pancreatic protein secretion. These effects were completely reversed to the fasted patterns during intravenous infusion of CCK antagonists. In contrast, cholinergic stimulation (bethanechol) induced a fedlike pattern that was more resistant to CCK antagonists. We conclude that CCK does not play a major role in the fasted motility pattern and related fluctuations in pancreatic secretion but may be partly involved (by itself and by released PP) in the induction of the fed motility pattern and the postprandial stimulation of the exocrine pancreas.

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