Physiological role and localization of cholecystokinin release in dogs

• Published in: The American journal of physiology Vol. 250; no. 4 Pt 1; p. G391
• Main Authors: Konturek, S J, Tasler, J, Bilski, J, de Jong, A J, Jansen, J B, Lamers, C B
• Format: Journal Article
• Language: English
• Published: United States 01.04.1986
• Subjects: Animals; Atropine - pharmacology; Cholecystokinin - metabolism; Cholecystokinin - pharmacology; Dogs; Food; Gastric Fistula - metabolism; Meat; Oleic Acid; Oleic Acids - metabolism; Pancreatic Fistula - metabolism; Pancreatic Polypeptide - metabolism; Perfusion; Sincalide - pharmacology; Somatostatin - pharmacology
• ISSN: 0002-9513
• DOI: 10.1152/ajpgi.1986.250.4.g391

In dogs with pancreatic fistulas, meat feeding and intestinal perfusion with a sodium oleate or amino acid mixture increased pancreatic protein secretion to approximately 110, 100, and 50%, respectively, of the response to cholecystokinin (CCK) at a dose of 85 pmol X kg-1 X h-1. Plasma CCK response increased in these studies to approximately 100, 180, and 40%, respectively, of the value obtained with exogenous CCK, suggesting that, in addition to CCK, other neurohormonal factors contribute to pancreatic enzyme secretion in response to endogenous stimulants. Feeding and duodenal oleate or amino acids also stimulate the release of pancreatic polypeptide (PP), which may be involved in the control of pancreatic secretion in response to endogenous stimulants, including CCK. Perfusion of the intact intestine with graded amounts of oleate (0.5-16 mmol/h) produced dose-dependent increments in plasma CCK and pancreatic protein similar to those obtained with intravenous infusion of graded doses of CCK (0.85-255 pmol X kg-1 X h-1). Oleate perfusion of isolated Thiry loops (30 cm long) made of duodenojejunal (D-J) and ileal (I) segments also stimulated protein secretion but elevated plasma CCK only after perfusion of the D-J but not of the I loop. We conclude that 1) the endogenous CCK released by various luminal stimulants drives the pancreatic protein secretion; 2) the release of CCK is confined to the foregut; and 3) PP concomitantly released by various intestinal stimulants may contribute to the control of pancreatic secretion induced by endogenous CCK.