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Article: Gap junctional coupling modulates secretion of exocrine pancreas.

TitleGap junctional coupling modulates secretion of exocrine pancreas.
Authors
KeywordsChemicals And Cas Registry Numbers
Issue Date1987
PublisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.org
Citation
Proceedings Of The National Academy Of Sciences Of The United States Of America, 1987, v. 84 n. 14, p. 4901-4904 How to Cite?
AbstractDispersed pancreatic acini were studied to assess the function of junctional coupling between adult secretory cells. Nonstimulated control cells were extensively coupled to their neighbors throughout each acinus. Addition of heptanol caused their uncoupling and increased their basal amylase release. Neurotensin, secretin, and vasoactive intestinal peptide (VIP) stimulated amylase secretion without uncoupling acinar cells. Heptanol rapidly and markedly uncoupled the neurotensin-, secretin-, and VIP-stimulated acinar cells and increased their amylase secretion in an additive manner. By contrast, the secretory response to carbamoylcholine (carbachol), a secretagogue that, alone, uncoupled acinar cells, was not affected by heptanol. Basal as well as neurotensin-, secretin-, and VIP-stimulated output returned to the lower control values following removal of heptanol and recovery of normal coupling. The data provide evidence that blockage of gap junctional coupling increases the basal secretion of exocrine pancreas as well as the response of the gland to a variety of secretagogues.
Persistent Identifierhttp://hdl.handle.net/10722/132671
ISSN
2015 Impact Factor: 9.423
2015 SCImago Journal Rankings: 6.883
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorMeda, Pen_HK
dc.contributor.authorBruzzone, Ren_HK
dc.contributor.authorChanson, Men_HK
dc.contributor.authorBosco, Den_HK
dc.contributor.authorOrci, Len_HK
dc.date.accessioned2011-03-28T09:28:06Z-
dc.date.available2011-03-28T09:28:06Z-
dc.date.issued1987en_HK
dc.identifier.citationProceedings Of The National Academy Of Sciences Of The United States Of America, 1987, v. 84 n. 14, p. 4901-4904en_HK
dc.identifier.issn0027-8424en_HK
dc.identifier.urihttp://hdl.handle.net/10722/132671-
dc.description.abstractDispersed pancreatic acini were studied to assess the function of junctional coupling between adult secretory cells. Nonstimulated control cells were extensively coupled to their neighbors throughout each acinus. Addition of heptanol caused their uncoupling and increased their basal amylase release. Neurotensin, secretin, and vasoactive intestinal peptide (VIP) stimulated amylase secretion without uncoupling acinar cells. Heptanol rapidly and markedly uncoupled the neurotensin-, secretin-, and VIP-stimulated acinar cells and increased their amylase secretion in an additive manner. By contrast, the secretory response to carbamoylcholine (carbachol), a secretagogue that, alone, uncoupled acinar cells, was not affected by heptanol. Basal as well as neurotensin-, secretin-, and VIP-stimulated output returned to the lower control values following removal of heptanol and recovery of normal coupling. The data provide evidence that blockage of gap junctional coupling increases the basal secretion of exocrine pancreas as well as the response of the gland to a variety of secretagogues.en_HK
dc.languageengen_US
dc.publisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.orgen_HK
dc.relation.ispartofProceedings of the National Academy of Sciences of the United States of Americaen_HK
dc.subjectChemicals And Cas Registry Numbersen_US
dc.titleGap junctional coupling modulates secretion of exocrine pancreas.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.doi10.1073/pnas.84.14.4901-
dc.identifier.pmid2440035-
dc.identifier.scopuseid_2-s2.0-0023378034en_HK
dc.identifier.volume84en_HK
dc.identifier.issue14en_HK
dc.identifier.spage4901en_HK
dc.identifier.epage4904en_HK
dc.identifier.isiWOS:A1987J172500054-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridMeda, P=7005822187en_HK
dc.identifier.scopusauthoridBruzzone, R=7006793327en_HK
dc.identifier.scopusauthoridChanson, M=7004131733en_HK
dc.identifier.scopusauthoridBosco, D=7005328418en_HK
dc.identifier.scopusauthoridOrci, L=35468097500en_HK

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