TY - JOUR
T1 - Role of cholecystokinin in canine pancreatic exocrine response to bombesin stimulation
AU - Nealon, William H.
AU - Beauchamp, R. Daniel
AU - Townsend, Courtney M.
AU - Thompson, James C.
N1 - Funding Information:
From the Department of Surgery, The Unwersity of Texas MedIcal Branch, Galveston, Texas Supported In part by grants from the National institutes of Health (RO 1 DK 1524 1, PO 1 DK 35608, RCDA CA 00854) and Grant PDT-220 from the American Cancer Society, New York, New York Requests for reprints should be addressed to James C Thompson, MD, Department of Surgery, The Uwersity of Texas Medical Branch, Galveston, Texas 77550 Presented at the 27th Annual Meeting of the Society for Surgery of the Alimentary Tract, San Francisco, California, May 20-21, 1986
PY - 1987/1
Y1 - 1987/1
N2 - The role of cholecystokinin in bombesin-stimulated pancreatic secretion in dogs was examined by the use of a specific cholecystokinin antagonist, proglumide. The primary component of bombesin-stimulated pancreatic secretion at the lowest tested dose was due to cholecystokinin, with only 25 percent of bombesin-stimulated protein output preserved during proglumide infusion. Maximal stimulation of cholecystokinin release was achieved by even the lowest dose of bombesin, whereas dose-related increases in bombesin-stimulated protein secretion were observed. This increase in exocrine secretion is probably explained by increased direct bombesin stimulation. Our findings suggest that the maximal dose of bombesin is lower for cholecystokinin release than its effective dose for enzyme secretion. We conclude that, in all probability, postprandial release of bombesin (or its analogue, gastrin-releasing peptide) affects pancreatic function primarily through release of cholecystokinin.
AB - The role of cholecystokinin in bombesin-stimulated pancreatic secretion in dogs was examined by the use of a specific cholecystokinin antagonist, proglumide. The primary component of bombesin-stimulated pancreatic secretion at the lowest tested dose was due to cholecystokinin, with only 25 percent of bombesin-stimulated protein output preserved during proglumide infusion. Maximal stimulation of cholecystokinin release was achieved by even the lowest dose of bombesin, whereas dose-related increases in bombesin-stimulated protein secretion were observed. This increase in exocrine secretion is probably explained by increased direct bombesin stimulation. Our findings suggest that the maximal dose of bombesin is lower for cholecystokinin release than its effective dose for enzyme secretion. We conclude that, in all probability, postprandial release of bombesin (or its analogue, gastrin-releasing peptide) affects pancreatic function primarily through release of cholecystokinin.
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U2 - 10.1016/0002-9610(87)90208-X
DO - 10.1016/0002-9610(87)90208-X
M3 - Article
C2 - 3799899
AN - SCOPUS:0023104033
SN - 0002-9610
VL - 153
SP - 96
EP - 101
JO - The American Journal of Surgery
JF - The American Journal of Surgery
IS - 1
ER -