Calcium-activated chloride conductance in a pancreatic adenocarcinoma cell line of ductal origin (HPAF) and in freshly isolated human pancreatic duct cells
Using the whole-cell patch-clamp technique, a calcium-activated chloride conductance (CACC) could be elicited in HPAF cells by addition of 1 microM ionomycin to the bath solution (66 +/- 22 pA/pF;Vm + 60 mV) or by addition of 1 microM calcium to the pipette solution (136 +/- 17 pA/pF; Vm + 60 mV). B...
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| Veröffentlicht in: | Pflügers Archiv 1998-05, Vol.435 (6), p.796-803 |
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| creator | Winpenny, J P Harris, A Hollingsworth, M A Argent, B E Gray, M A |
| description | Using the whole-cell patch-clamp technique, a calcium-activated chloride conductance (CACC) could be elicited in HPAF cells by addition of 1 microM ionomycin to the bath solution (66 +/- 22 pA/pF;Vm + 60 mV) or by addition of 1 microM calcium to the pipette solution (136 +/- 17 pA/pF; Vm + 60 mV). Both conductances had similar biophysical characteristics, including time-dependent inactivation at hyperpolarising potentials and a linear/slightly outwardly rectifying current/voltage (I/V) curve with a reversal potential (Erev) close to the calculated chloride equilibrium potential. The anion permeability sequence obtained from shifts in Erev was I > Br >/= Cl. 4,4'-Diisothiocyanatostilbene disulphonic acid (DIDS, 500 microM) caused a 13% inhibition of the current (Vm + 60 mV) while 100 microM glibenclamide, 30 nM TS-TM-calix[4]arene and 10 microM tamoxifen, all chloride channel blockers, had no marked effects (8%, -6% and -2% inhibition respectively). Niflumic acid (100 microM) caused a voltage-dependent inhibition of the current of 48% and 17% (Vm +/- 60 mV, respectively). In freshly isolated human pancreatic duct cells (PDCs) a CACC was elicited with 1 microM calcium in the pipette solution (260 +/- 62 pA/pF; Vm + 60 mV). The presence of this CACC in human PDCs could provide a possible therapeutic pathway for treatment of pancreatic insufficiency of the human pancreas in cystic fibrosis. |
| doi_str_mv | 10.1007/s004240050586 |
| format | Article |
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Both conductances had similar biophysical characteristics, including time-dependent inactivation at hyperpolarising potentials and a linear/slightly outwardly rectifying current/voltage (I/V) curve with a reversal potential (Erev) close to the calculated chloride equilibrium potential. The anion permeability sequence obtained from shifts in Erev was I > Br >/= Cl. 4,4'-Diisothiocyanatostilbene disulphonic acid (DIDS, 500 microM) caused a 13% inhibition of the current (Vm + 60 mV) while 100 microM glibenclamide, 30 nM TS-TM-calix[4]arene and 10 microM tamoxifen, all chloride channel blockers, had no marked effects (8%, -6% and -2% inhibition respectively). Niflumic acid (100 microM) caused a voltage-dependent inhibition of the current of 48% and 17% (Vm +/- 60 mV, respectively). In freshly isolated human pancreatic duct cells (PDCs) a CACC was elicited with 1 microM calcium in the pipette solution (260 +/- 62 pA/pF; Vm + 60 mV). The presence of this CACC in human PDCs could provide a possible therapeutic pathway for treatment of pancreatic insufficiency of the human pancreas in cystic fibrosis.</description><identifier>ISSN: 0031-6768</identifier><identifier>EISSN: 1432-2013</identifier><identifier>DOI: 10.1007/s004240050586</identifier><identifier>PMID: 9518508</identifier><language>eng</language><publisher>Germany: Springer Nature B.V</publisher><subject>4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid - pharmacology ; Action Potentials ; Adenocarcinoma ; Adenocarcinoma - physiopathology ; Anions ; Calcium ; Calcium - pharmacology ; Cells ; Chelating Agents - pharmacology ; Chloride Channels - analysis ; Chloride Channels - physiology ; Egtazic Acid - pharmacology ; Electric Conductivity ; Humans ; Iodides - metabolism ; Ionomycin - pharmacology ; Male ; Pancreas ; Pancreatic Ducts - chemistry ; Pancreatic Ducts - physiopathology ; Pancreatic Neoplasms - physiopathology ; Tumor Cells, Cultured</subject><ispartof>Pflügers Archiv, 1998-05, Vol.435 (6), p.796-803</ispartof><rights>Springer-Verlag Berlin Heidelberg 1998</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c414t-758a4cca768f0d7279875d152ccc0ba6a8594a304a6212003e8fe59d829a37fd3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9518508$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Winpenny, J P</creatorcontrib><creatorcontrib>Harris, A</creatorcontrib><creatorcontrib>Hollingsworth, M A</creatorcontrib><creatorcontrib>Argent, B E</creatorcontrib><creatorcontrib>Gray, M A</creatorcontrib><title>Calcium-activated chloride conductance in a pancreatic adenocarcinoma cell line of ductal origin (HPAF) and in freshly isolated human pancreatic duct cells</title><title>Pflügers Archiv</title><addtitle>Pflugers Arch</addtitle><description>Using the whole-cell patch-clamp technique, a calcium-activated chloride conductance (CACC) could be elicited in HPAF cells by addition of 1 microM ionomycin to the bath solution (66 +/- 22 pA/pF;Vm + 60 mV) or by addition of 1 microM calcium to the pipette solution (136 +/- 17 pA/pF; Vm + 60 mV). Both conductances had similar biophysical characteristics, including time-dependent inactivation at hyperpolarising potentials and a linear/slightly outwardly rectifying current/voltage (I/V) curve with a reversal potential (Erev) close to the calculated chloride equilibrium potential. The anion permeability sequence obtained from shifts in Erev was I > Br >/= Cl. 4,4'-Diisothiocyanatostilbene disulphonic acid (DIDS, 500 microM) caused a 13% inhibition of the current (Vm + 60 mV) while 100 microM glibenclamide, 30 nM TS-TM-calix[4]arene and 10 microM tamoxifen, all chloride channel blockers, had no marked effects (8%, -6% and -2% inhibition respectively). Niflumic acid (100 microM) caused a voltage-dependent inhibition of the current of 48% and 17% (Vm +/- 60 mV, respectively). In freshly isolated human pancreatic duct cells (PDCs) a CACC was elicited with 1 microM calcium in the pipette solution (260 +/- 62 pA/pF; Vm + 60 mV). The presence of this CACC in human PDCs could provide a possible therapeutic pathway for treatment of pancreatic insufficiency of the human pancreas in cystic fibrosis.</description><subject>4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid - pharmacology</subject><subject>Action Potentials</subject><subject>Adenocarcinoma</subject><subject>Adenocarcinoma - physiopathology</subject><subject>Anions</subject><subject>Calcium</subject><subject>Calcium - pharmacology</subject><subject>Cells</subject><subject>Chelating Agents - pharmacology</subject><subject>Chloride Channels - analysis</subject><subject>Chloride Channels - physiology</subject><subject>Egtazic Acid - pharmacology</subject><subject>Electric Conductivity</subject><subject>Humans</subject><subject>Iodides - metabolism</subject><subject>Ionomycin - pharmacology</subject><subject>Male</subject><subject>Pancreas</subject><subject>Pancreatic Ducts - chemistry</subject><subject>Pancreatic Ducts - physiopathology</subject><subject>Pancreatic Neoplasms - physiopathology</subject><subject>Tumor Cells, Cultured</subject><issn>0031-6768</issn><issn>1432-2013</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kcFuFSEUhonR1Nvq0qUJcWHqYvTAwADL5sa2Jk10oevJKTBemhm4wkyTPosvK3N7Y9SFK1h8_wfn_IS8YvCeAagPBUBwASBB6u4J2TDR8oYDa5-SDUDLmk51-jk5LeUOALjQ_IScGMm0BL0hP7c42rBMDdo53OPsHbW7MeXgPLUpusXOGK2nIVKk-3rNHudgKTofk8VsQ0wTUuvHkY4hepoGegiNtEq-19j59ZeLy3cUo1slQ_ZlNz7QUNJ4eG23TBj_NK_pg6-8IM8GHIt_eTzPyLfLj1-3183N56tP24ubxgom5kZJjcJarGMO4BRXRivpmOTWWrjFDrU0AlsQ2HHG60q8Hrw0TnODrRpce0bePnr3Of1YfJn7KZT1Bxh9WkqvjOpAM1PB8_-CDEwrZNcaVdE3_6B3acmxjtFrpU3dPV-h5hGyOZWS_dDvc5gwP1RTv5bb_1Vu5V8fpcvt5N1v-thm-wt73p9j</recordid><startdate>19980501</startdate><enddate>19980501</enddate><creator>Winpenny, J P</creator><creator>Harris, A</creator><creator>Hollingsworth, M A</creator><creator>Argent, B E</creator><creator>Gray, M A</creator><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7TK</scope><scope>7TS</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope></search><sort><creationdate>19980501</creationdate><title>Calcium-activated chloride conductance in a pancreatic adenocarcinoma cell line of ductal origin (HPAF) and in freshly isolated human pancreatic duct cells</title><author>Winpenny, J P ; Harris, A ; Hollingsworth, M A ; Argent, B E ; Gray, M A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c414t-758a4cca768f0d7279875d152ccc0ba6a8594a304a6212003e8fe59d829a37fd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid - pharmacology</topic><topic>Action Potentials</topic><topic>Adenocarcinoma</topic><topic>Adenocarcinoma - physiopathology</topic><topic>Anions</topic><topic>Calcium</topic><topic>Calcium - pharmacology</topic><topic>Cells</topic><topic>Chelating Agents - pharmacology</topic><topic>Chloride Channels - analysis</topic><topic>Chloride Channels - physiology</topic><topic>Egtazic Acid - pharmacology</topic><topic>Electric Conductivity</topic><topic>Humans</topic><topic>Iodides - metabolism</topic><topic>Ionomycin - pharmacology</topic><topic>Male</topic><topic>Pancreas</topic><topic>Pancreatic Ducts - chemistry</topic><topic>Pancreatic Ducts - physiopathology</topic><topic>Pancreatic Neoplasms - physiopathology</topic><topic>Tumor Cells, Cultured</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Winpenny, J P</creatorcontrib><creatorcontrib>Harris, A</creatorcontrib><creatorcontrib>Hollingsworth, M A</creatorcontrib><creatorcontrib>Argent, B E</creatorcontrib><creatorcontrib>Gray, M A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Physical Education Index</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><jtitle>Pflügers Archiv</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Winpenny, J P</au><au>Harris, A</au><au>Hollingsworth, M A</au><au>Argent, B E</au><au>Gray, M A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Calcium-activated chloride conductance in a pancreatic adenocarcinoma cell line of ductal origin (HPAF) and in freshly isolated human pancreatic duct cells</atitle><jtitle>Pflügers Archiv</jtitle><addtitle>Pflugers Arch</addtitle><date>1998-05-01</date><risdate>1998</risdate><volume>435</volume><issue>6</issue><spage>796</spage><epage>803</epage><pages>796-803</pages><issn>0031-6768</issn><eissn>1432-2013</eissn><abstract>Using the whole-cell patch-clamp technique, a calcium-activated chloride conductance (CACC) could be elicited in HPAF cells by addition of 1 microM ionomycin to the bath solution (66 +/- 22 pA/pF;Vm + 60 mV) or by addition of 1 microM calcium to the pipette solution (136 +/- 17 pA/pF; Vm + 60 mV). Both conductances had similar biophysical characteristics, including time-dependent inactivation at hyperpolarising potentials and a linear/slightly outwardly rectifying current/voltage (I/V) curve with a reversal potential (Erev) close to the calculated chloride equilibrium potential. The anion permeability sequence obtained from shifts in Erev was I > Br >/= Cl. 4,4'-Diisothiocyanatostilbene disulphonic acid (DIDS, 500 microM) caused a 13% inhibition of the current (Vm + 60 mV) while 100 microM glibenclamide, 30 nM TS-TM-calix[4]arene and 10 microM tamoxifen, all chloride channel blockers, had no marked effects (8%, -6% and -2% inhibition respectively). Niflumic acid (100 microM) caused a voltage-dependent inhibition of the current of 48% and 17% (Vm +/- 60 mV, respectively). In freshly isolated human pancreatic duct cells (PDCs) a CACC was elicited with 1 microM calcium in the pipette solution (260 +/- 62 pA/pF; Vm + 60 mV). The presence of this CACC in human PDCs could provide a possible therapeutic pathway for treatment of pancreatic insufficiency of the human pancreas in cystic fibrosis.</abstract><cop>Germany</cop><pub>Springer Nature B.V</pub><pmid>9518508</pmid><doi>10.1007/s004240050586</doi><tpages>8</tpages></addata></record> |
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| identifier | ISSN: 0031-6768 |
| ispartof | Pflügers Archiv, 1998-05, Vol.435 (6), p.796-803 |
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| subjects | 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid - pharmacology Action Potentials Adenocarcinoma Adenocarcinoma - physiopathology Anions Calcium Calcium - pharmacology Cells Chelating Agents - pharmacology Chloride Channels - analysis Chloride Channels - physiology Egtazic Acid - pharmacology Electric Conductivity Humans Iodides - metabolism Ionomycin - pharmacology Male Pancreas Pancreatic Ducts - chemistry Pancreatic Ducts - physiopathology Pancreatic Neoplasms - physiopathology Tumor Cells, Cultured |
| title | Calcium-activated chloride conductance in a pancreatic adenocarcinoma cell line of ductal origin (HPAF) and in freshly isolated human pancreatic duct cells |
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