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

Evilevitch, Lena LU ; Weström, Björn LU and Pierzynowski, Stefan LU (2003) In Scandinavian Journal of Gastroenterology 38(2). p.201-206
Abstract
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... (More)
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. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
CCK-A receptors, exocrine pancreas, regulation
in
Scandinavian Journal of Gastroenterology
volume
38
issue
2
pages
201 - 206
publisher
Taylor & Francis
external identifiers
  • pmid:12678338
  • wos:000181797300012
  • scopus:0037300797
ISSN
1502-7708
DOI
language
English
LU publication?
yes
id
415177ef-5dd1-4cc7-a066-504f0f7aeacd (old id 315312)
date added to LUP
2007-09-03 07:13:47
date last changed
2018-05-29 10:30:44
@article{415177ef-5dd1-4cc7-a066-504f0f7aeacd,
  abstract     = {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.},
  author       = {Evilevitch, Lena and Weström, Björn and Pierzynowski, Stefan},
  issn         = {1502-7708},
  keyword      = {CCK-A receptors,exocrine pancreas,regulation},
  language     = {eng},
  number       = {2},
  pages        = {201--206},
  publisher    = {Taylor & Francis},
  series       = {Scandinavian Journal of Gastroenterology},
  title        = {CCK regulates pancreatic enzyme secretion via short duodenal-pancreatic reflexes in pigs},
  url          = {http://dx.doi.org/},
  volume       = {38},
  year         = {2003},
}