CCK regulates pancreatic enzyme secretion via short duodenal-pancreatic reflexes in pigs
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/315312
- author
- Evilevitch, Lena LU ; Weström, Björn LU and Pierzynowski, Stefan LU
- organization
- publishing date
- 2003
- 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
- 10.1080/00365520310000708
- language
- English
- LU publication?
- yes
- id
- 415177ef-5dd1-4cc7-a066-504f0f7aeacd (old id 315312)
- date added to LUP
- 2016-04-01 16:21:29
- date last changed
- 2022-01-28 19:06:52
@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}},
keywords = {{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/10.1080/00365520310000708}},
doi = {{10.1080/00365520310000708}},
volume = {{38}},
year = {{2003}},
}