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- Publisher Website: 10.1073/pnas.84.14.4901
- Scopus: eid_2-s2.0-0023378034
- PMID: 2440035
- WOS: WOS:A1987J172500054
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Article: Gap junctional coupling modulates secretion of exocrine pancreas.
Title | Gap junctional coupling modulates secretion of exocrine pancreas. |
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Authors | |
Keywords | Chemicals And Cas Registry Numbers |
Issue Date | 1987 |
Publisher | National 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? |
Abstract | Dispersed 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 Identifier | http://hdl.handle.net/10722/132671 |
ISSN | 2023 Impact Factor: 9.4 2023 SCImago Journal Rankings: 3.737 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Meda, P | en_HK |
dc.contributor.author | Bruzzone, R | en_HK |
dc.contributor.author | Chanson, M | en_HK |
dc.contributor.author | Bosco, D | en_HK |
dc.contributor.author | Orci, L | en_HK |
dc.date.accessioned | 2011-03-28T09:28:06Z | - |
dc.date.available | 2011-03-28T09:28:06Z | - |
dc.date.issued | 1987 | en_HK |
dc.identifier.citation | Proceedings Of The National Academy Of Sciences Of The United States Of America, 1987, v. 84 n. 14, p. 4901-4904 | en_HK |
dc.identifier.issn | 0027-8424 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/132671 | - |
dc.description.abstract | Dispersed 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.language | eng | en_US |
dc.publisher | National Academy of Sciences. The Journal's web site is located at http://www.pnas.org | en_HK |
dc.relation.ispartof | Proceedings of the National Academy of Sciences of the United States of America | en_HK |
dc.subject | Chemicals And Cas Registry Numbers | en_US |
dc.title | Gap junctional coupling modulates secretion of exocrine pancreas. | en_HK |
dc.type | Article | en_HK |
dc.identifier.email | Bruzzone, R: bruzzone@hkucc.hku.hk | en_HK |
dc.identifier.authority | Bruzzone, R=rp01442 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1073/pnas.84.14.4901 | - |
dc.identifier.pmid | 2440035 | - |
dc.identifier.scopus | eid_2-s2.0-0023378034 | en_HK |
dc.identifier.volume | 84 | en_HK |
dc.identifier.issue | 14 | en_HK |
dc.identifier.spage | 4901 | en_HK |
dc.identifier.epage | 4904 | en_HK |
dc.identifier.isi | WOS:A1987J172500054 | - |
dc.publisher.place | United States | en_HK |
dc.identifier.scopusauthorid | Meda, P=7005822187 | en_HK |
dc.identifier.scopusauthorid | Bruzzone, R=7006793327 | en_HK |
dc.identifier.scopusauthorid | Chanson, M=7004131733 | en_HK |
dc.identifier.scopusauthorid | Bosco, D=7005328418 | en_HK |
dc.identifier.scopusauthorid | Orci, L=35468097500 | en_HK |
dc.identifier.issnl | 0027-8424 | - |