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Article: Regulation of pancreatic exocrine function: A role for cell-to-cell communication?

TitleRegulation of pancreatic exocrine function: A role for cell-to-cell communication?
Authors
KeywordsChemicals And Cas Registry Numbers
Issue Date1987
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.pancreasjournal.com
Citation
Pancreas, 1987, v. 2 n. 3, p. 262-271 How to Cite?
AbstractThe effect of heptanol, an alkanol which decreases gap junctional permeability, was investigated in the perfused rat pancreas. Under basal conditions, heptanol (3.5 mM) caused a three- to fourfold increase of pancreatic juice, protein, and amylase outputs. The effect on enzyme secretion was fully reversible upon removal of the alkanol and was not secondary to the release of acetylcholine from nerve endings, since it was not prevented by addition of atropine (10 -6 M) to the perfusate. By contrast, another alkanol, hexanol (3 mM), which does not decrease coupling between acinar cells in spite of anesthetic properties analogous to those of heptanol, did not alter pancreatic secretion. The effect of heptanol was not mediated by a significant stimulation of cyclic AMP, nor did the alkanol increase the secretion of lactic dehydrogenase, a cytosolic marker. Analysis of the numerical density of freeze-fractured and immunolabeled gap junctions between acinar cells did not show differences between heptanol-perfused and control pancreases. In addition, heptanol did not alter carbachol (10 -6 M and 10 -5 M)-evoked amylase release. Since heptanol blocks cell coupling, apparently without interfering with the main intracellular pathways triggering enzyme release, we suggest that downregulation of direct cell-to-cell communications increases pancreatic exocrine secretion. Thus, cell coupling is probably involved in the regulation of the secretory activity of acinar cells.
Persistent Identifierhttp://hdl.handle.net/10722/132783
ISSN
2015 Impact Factor: 2.738
2015 SCImago Journal Rankings: 1.114
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorBruzzone, Ren_HK
dc.contributor.authorTrimble, ERen_HK
dc.contributor.authorGjinovci, Aen_HK
dc.contributor.authorTraub, Oen_HK
dc.contributor.authorWillecke, Ken_HK
dc.contributor.authorMeda, Pen_HK
dc.date.accessioned2011-03-28T09:28:56Z-
dc.date.available2011-03-28T09:28:56Z-
dc.date.issued1987en_HK
dc.identifier.citationPancreas, 1987, v. 2 n. 3, p. 262-271en_HK
dc.identifier.issn0885-3177en_HK
dc.identifier.urihttp://hdl.handle.net/10722/132783-
dc.description.abstractThe effect of heptanol, an alkanol which decreases gap junctional permeability, was investigated in the perfused rat pancreas. Under basal conditions, heptanol (3.5 mM) caused a three- to fourfold increase of pancreatic juice, protein, and amylase outputs. The effect on enzyme secretion was fully reversible upon removal of the alkanol and was not secondary to the release of acetylcholine from nerve endings, since it was not prevented by addition of atropine (10 -6 M) to the perfusate. By contrast, another alkanol, hexanol (3 mM), which does not decrease coupling between acinar cells in spite of anesthetic properties analogous to those of heptanol, did not alter pancreatic secretion. The effect of heptanol was not mediated by a significant stimulation of cyclic AMP, nor did the alkanol increase the secretion of lactic dehydrogenase, a cytosolic marker. Analysis of the numerical density of freeze-fractured and immunolabeled gap junctions between acinar cells did not show differences between heptanol-perfused and control pancreases. In addition, heptanol did not alter carbachol (10 -6 M and 10 -5 M)-evoked amylase release. Since heptanol blocks cell coupling, apparently without interfering with the main intracellular pathways triggering enzyme release, we suggest that downregulation of direct cell-to-cell communications increases pancreatic exocrine secretion. Thus, cell coupling is probably involved in the regulation of the secretory activity of acinar cells.en_HK
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.pancreasjournal.comen_HK
dc.relation.ispartofPancreasen_HK
dc.subjectChemicals And Cas Registry Numbersen_US
dc.titleRegulation of pancreatic exocrine function: A role for cell-to-cell communication?en_HK
dc.typeArticleen_HK
dc.identifier.emailBruzzone, R: bruzzone@hkucc.hku.hken_HK
dc.identifier.authorityBruzzone, R=rp01442en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid3628228-
dc.identifier.scopuseid_2-s2.0-0023481685en_HK
dc.identifier.volume2en_HK
dc.identifier.issue3en_HK
dc.identifier.spage262en_HK
dc.identifier.epage271en_HK
dc.identifier.isiWOS:A1987H557200004-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridBruzzone, R=7006793327en_HK
dc.identifier.scopusauthoridTrimble, ER=7005267920en_HK
dc.identifier.scopusauthoridGjinovci, A=6701391657en_HK
dc.identifier.scopusauthoridTraub, O=7005923056en_HK
dc.identifier.scopusauthoridWillecke, K=7101817466en_HK
dc.identifier.scopusauthoridMeda, P=7005822187en_HK

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