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CCK regulates pancreatic enzyme secretion via short duodenal-pancreatic reflexes in pigs

Evilevitch, Lena (author)
Lund University,Lunds universitet,Biologiska institutionen,Naturvetenskapliga fakulteten,Department of Biology,Faculty of Science
Weström, Björn (author)
Lund University,Lunds universitet,Funktionell zoologi,Biologiska institutionen,Naturvetenskapliga fakulteten,Functional zoology,Department of Biology,Faculty of Science
Pierzynowski, Stefan (author)
Lund University,Lunds universitet,Funktionell zoologi,Biologiska institutionen,Naturvetenskapliga fakulteten,Functional zoology,Department of Biology,Faculty of Science
 (creator_code:org_t)
2011-03-08
2003
English.
In: Scandinavian Journal of Gastroenterology. - : Informa UK Limited. - 1502-7708 .- 0036-5521. ; 38:2, s. 201-206
  • Journal article (peer-reviewed)
Abstract Subject headings
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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.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Gastroenterologi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Gastroenterology and Hepatology (hsv//eng)

Keyword

CCK-A receptors
exocrine pancreas
regulation

Publication and Content Type

art (subject category)
ref (subject category)

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Evilevitch, Lena
Weström, Björn
Pierzynowski, St ...
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