CCK regulates pancreatic enzyme secretion via short duodenal-pancreatic reflexes in pigs
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Background: Different routes of administration of CCK-33 and blockage of CCK-A and muscarinic (m(3)) receptors are used in this study to evaluate the mechanisms by which cholecystokinin can stimulate the exocrine pancreas. Methods: The experiment was performed on eight anaesthetized pigs during control conditions and after administration of the CCK-A and m(3) receptor antagonists, Tarazepide and 4-DAMP, respectively. Catheters were surgically implanted in the pancreatic duct for juice collection and in the gastric and right gastro-epipoic arteries and in the jugular vein, so that infusions of CCK-33 could be made exclusively to the duodenum/stomach, duodenum/pancreas or general circulation, respectively. Results: Infusion of a low dose of CCK-33 (13 pmol kg(-1)) to the general circulation did not affect pancreatic protein or trypsin output. When the same dose was given directly to the duodenum/stomach or the duodenum/pancreas, pancreatic output increased during both control conditions and after Tarazepide and/or 4-DAMP treatment, though the increase in trypsin Output was lower after Tarazepide and/or 4-DAMP blockade. A high dose of CCK-33 (130 pmol kg(-1)) given peripherally stimulated the pancreatic secretion, but this response was totally abolished in Tarazepide and 4-Damp treated animals. Conclusions: Pancreatic enzyme secretion due to CCK-33 stimulation depends on the presence of short duodenal-pancreatic peptidergic reflexes evoked mainly via low sensitive, probably CCK-B, receptors located in the duodenum/stomach. Pancreatic secretion evoked by peripheral CCK-33 in pharmacological doses was independent Of m(3) receptors blockade but depended on CCK-A receptors located elsewhere than in the duodenum/pancreas.
|Enheter & grupper|
Ämnesklassifikation (UKÄ) – OBLIGATORISK
|Tidskrift||Scandinavian Journal of Gastroenterology|
|Status||Published - 2003|
|Peer review utförd||Ja|