AJP - Gastrointestinal and Liver Physiology, Vol 257, Issue 6 944-G949, Copyright © 1989 by American Physiological Society
Role of endogenous cholecystokinin on vagally stimulated pancreatic secretion in dogs
C. K. Kim, K. Y. Lee, T. Wang, G. Sun, T. M. Chang and W. Y. Chey
University of Rochester School of Medicine and Dentistry, Isaac Gordon Center for Digestive Disease and Nutrition, Department of Medicine, Genesee Hospital, Rochester, New York 14607.
Pancreatic exocrine secretion was evoked by electrical stimulation of the
vagus nerves (EVS) in dogs to determine whether a gut hormone was
responsible for the pancreatic stimulatory activity. In 39 dogs, pancreatic
juice was continuously collected to measure volume, bicarbonate, and
amylase output, while portal and femoral venous plasma concentrations of
gastrin, cholecystokinin (CCK), vasoactive intestinal polypeptide (VIP),
and pancreatic polypeptide (PP) were determined by radioimmunoassay. EVS
produced a significant increase in the pancreatic secretion. Although
concentrations of all four peptides significantly increased in plasma, only
CCK at the concentration in venous circulation was bioactive in dispersed
rat pancreatic acini preparations. This bioactivity of CCK was completely
blocked by CR 1409, a CCK-receptor antagonist. The pancreatic secretion by
EVS was reduced significantly by intravenous MK-329 (formerly L364,718) to
as low as 22% of control values and was completely suppressed by
intravenous atropine. The increment in plasma CCK by EVS was also
significantly suppressed by atropine. The present study indicates that
increased pancreatic secretion by EVS is in part mediated by endogenous
CCK.
