EFFECT OF L364-718 ON INTERDIGESTIVE PANCREATIC EXOCRINE SECRETION AND GASTRODUODENAL MOTILITY IN CONSCIOUS SHEEP

Citation
T. Onaga et al., EFFECT OF L364-718 ON INTERDIGESTIVE PANCREATIC EXOCRINE SECRETION AND GASTRODUODENAL MOTILITY IN CONSCIOUS SHEEP, Regulatory peptides, 68(2), 1997, pp. 139-146
Citations number
34
Categorie Soggetti
Endocrynology & Metabolism",Physiology
Journal title
ISSN journal
01670115
Volume
68
Issue
2
Year of publication
1997
Pages
139 - 146
Database
ISI
SICI code
0167-0115(1997)68:2<139:EOLOIP>2.0.ZU;2-J
Abstract
The present study examined roles of endogenous cholecystokinin (CCK) a nd CCK-A receptors in the regulation of pancreatic exocrine secretion and gastroduodenal motility in conscious sheep during interdigestive p eriod. Interdigestive exocrine secretion of ovine pancreas changed cyc lically corresponding with cycle of duodenal migrating myoelectric com plexes (MMC). During second phase of the duodenal MMC, intravenous inj ection of L364 718 at 2.45 mu mol kg(-1) inhibited exogenous CCK-8-ind uced pancreatic exocrine secretion. Intravenous infusion of the antago nist at 2.45 mu mol kg(-1)/5 min for 5 min also inhibited significantl y the pancreatic enzyme secretion without CCK-stimulation to half of t hat in the control, but not the fluid and bicarbonate secretion. Atrop ine infusion (i.v.) at 72.0 nmol kg(-1)/5 min significantly inhibited not only enzyme but also fluid and bicarbonate secretion. Correspondin g to the inhibition of the exocrine secretion, L364 718 induced premat ure phase III in duodenal electromyogram (EMG) in three of the five sh eep. Omasal EMG was inhibited slightly but significantly by L364 718, however, neither regular ruminal contractions nor abomasal EMG were al tered by L364 718. In contrast, the atropine infusion inhibited only a mplitude of ruminal contractions. These results suggest that endogenou s CCK contributes to the regulation of interdigestive pancreatic exocr ine secretion, omasal contractions and duodenal MMC in the ovine gastr ointestinal tract via CCK-A receptors. (C) 1997 Elsevier Science B.V.