File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Transmembrane chloride currents in human atrial myocytes

TitleTransmembrane chloride currents in human atrial myocytes
Authors
Keywordscardiac arrhythmias
cell swelling
chloride channels
cystic fibrosis transmembrane conductance regulator
electrophysiology
Issue Date1996
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpcell.physiology.org/
Citation
American Journal Of Physiology - Cell Physiology, 1996, v. 270 n. 2 39-2, p. C500-C507 How to Cite?
AbstractThe present study was designed to evaluate the presence of basal, swelling-induced, and cAMP-dependent Cl- currents in human atrial myocytes studied with the whole cell patch-clamp technique. Under basal conditions, a small outwardly rectifying background conductance was noted that reversed close to 0 mV and was not altered by Cl- replacement. Isoproterenol (1 μM), forskolin (3 μM), and 8-bromoadenosine 3',5'-cyclic monophosphate (50 μM) did not increase membrane conductance, even when responsiveness to isoproterenol was confirmed by an increase in Ca2+ current and when perforated-patch techniques (nystatin) were used. Exposure to hyposmotic solutions increased cell volume and induced a whole cell conductance that showed outward rectification, was inhibited by 4,4'-diisothiocyanostilbene- 2,2'-disulfonic acid (100 μM), and responded to changes in Cl- gradient in a fashion consistent with a Cl--selective conductance, with estimated relative permeabilities of 1, 0.25, and 0.07 for Cl-, methanesulfonate, and aspartate, respectively. The results suggest that human atrial cells lack basal and adenosine 3',5'-cyclic monophosphate-dependent Cl- current but manifest a substantial Cl- conductance in the presence of cell swelling.
Persistent Identifierhttp://hdl.handle.net/10722/162148
ISSN
2021 Impact Factor: 5.282
2020 SCImago Journal Rankings: 1.432
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLi, GRen_US
dc.contributor.authorFeng, Jen_US
dc.contributor.authorWang, Zen_US
dc.contributor.authorNattel, Sen_US
dc.date.accessioned2012-09-05T05:17:39Z-
dc.date.available2012-09-05T05:17:39Z-
dc.date.issued1996en_US
dc.identifier.citationAmerican Journal Of Physiology - Cell Physiology, 1996, v. 270 n. 2 39-2, p. C500-C507en_US
dc.identifier.issn0363-6143en_US
dc.identifier.urihttp://hdl.handle.net/10722/162148-
dc.description.abstractThe present study was designed to evaluate the presence of basal, swelling-induced, and cAMP-dependent Cl- currents in human atrial myocytes studied with the whole cell patch-clamp technique. Under basal conditions, a small outwardly rectifying background conductance was noted that reversed close to 0 mV and was not altered by Cl- replacement. Isoproterenol (1 μM), forskolin (3 μM), and 8-bromoadenosine 3',5'-cyclic monophosphate (50 μM) did not increase membrane conductance, even when responsiveness to isoproterenol was confirmed by an increase in Ca2+ current and when perforated-patch techniques (nystatin) were used. Exposure to hyposmotic solutions increased cell volume and induced a whole cell conductance that showed outward rectification, was inhibited by 4,4'-diisothiocyanostilbene- 2,2'-disulfonic acid (100 μM), and responded to changes in Cl- gradient in a fashion consistent with a Cl--selective conductance, with estimated relative permeabilities of 1, 0.25, and 0.07 for Cl-, methanesulfonate, and aspartate, respectively. The results suggest that human atrial cells lack basal and adenosine 3',5'-cyclic monophosphate-dependent Cl- current but manifest a substantial Cl- conductance in the presence of cell swelling.en_US
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpcell.physiology.org/en_US
dc.relation.ispartofAmerican Journal of Physiology - Cell Physiologyen_US
dc.subjectcardiac arrhythmias-
dc.subjectcell swelling-
dc.subjectchloride channels-
dc.subjectcystic fibrosis transmembrane conductance regulator-
dc.subjectelectrophysiology-
dc.subject.meshAnimalsen_US
dc.subject.meshAtrial Functionen_US
dc.subject.meshCell Membrane - Physiologyen_US
dc.subject.meshChlorides - Antagonists & Inhibitors - Physiologyen_US
dc.subject.meshCyclic Amp - Physiologyen_US
dc.subject.meshElectric Conductivityen_US
dc.subject.meshGuinea Pigsen_US
dc.subject.meshHumansen_US
dc.subject.meshMesylates - Pharmacologyen_US
dc.subject.meshMyocardium - Cytologyen_US
dc.subject.meshOsmotic Pressureen_US
dc.titleTransmembrane chloride currents in human atrial myocytesen_US
dc.typeArticleen_US
dc.identifier.emailLi, GR:grli@hkucc.hku.hken_US
dc.identifier.authorityLi, GR=rp00476en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid8779912-
dc.identifier.scopuseid_2-s2.0-0029947379en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0029947379&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume270en_US
dc.identifier.issue2 39-2en_US
dc.identifier.spageC500en_US
dc.identifier.epageC507en_US
dc.identifier.isiWOS:A1996TV84400012-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLi, GR=7408462932en_US
dc.identifier.scopusauthoridFeng, J=7403884361en_US
dc.identifier.scopusauthoridWang, Z=7410039597en_US
dc.identifier.scopusauthoridNattel, S=36048738800en_US
dc.identifier.issnl0363-6143-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats