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Article: Involvement of anion channel(s) in the modulation of the transient outward K+ channel in rat ventricular myocytes

TitleInvolvement of anion channel(s) in the modulation of the transient outward K+ channel in rat ventricular myocytes
Authors
Issue Date2004
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpcell.physiology.org/
Citation
American Journal Of Physiology - Cell Physiology, 2004, v. 287 n. 1 56-1, p. C163-C170 How to Cite?
AbstractThe cardiac Ca2+-independent transient outward K+ current (Ito), a major repolarizing ionic current, is markedly affected by Cl- substitution and anion channel blockers. We reexplored the mechanism of the action of anions on Ito by using whole cell patch-clamp in single isolated rat cardiac ventricular myocytes. The transient outward current was sensitive to blockade by 4-aminopyridine (4-AP) and was abolished by Cs+ substitution for intracellular K +. Replacement of most of the extracellular Cl- with less permeant anions, aspartate (Asp-) and glutamate (Glu-), markedly suppressed the current. Removal of external Na+ or stabilization of F-actin with phalloidin did not significantly affect the inhibitory action of less permeant anions on Ito. In contrast, the permeant Cl- substitute Br- did not markedly affect the current, whereas F- substitution for Cl- induced a slight inhibition. The Ito elicited during Br- substitution for Cl- was also sensitive to blockade by 4-AP. The ability of Cl - substitutes to induce rightward shifts of the steady-state inactivation curve of Ito was in the following sequence: NO 3 - > Cl- ≈ Br- > gluconate- > Glu- > Asp-. Depolymerization of actin filaments with cytochalasin D (CytD) induced an effect on the steady-state inactivation of Ito similar to that of less permeant anions. Fluorescent phalloidin staining experiments revealed that CytD-pretreatment significantly decreased the intensity of FITC-phalloidin staining of F-actin, whereas Asp- substitution for Cl- was without significant effect on the intensity. These results suggest that the Ito channel is modulated by anion channel(s), in which the actin cytoskeleton may be implicated.
Persistent Identifierhttp://hdl.handle.net/10722/162916
ISSN
2015 Impact Factor: 3.395
2015 SCImago Journal Rankings: 1.893
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLai, XGen_US
dc.contributor.authorYang, Jen_US
dc.contributor.authorZhou, SSen_US
dc.contributor.authorZhu, Jen_US
dc.contributor.authorLi, GRen_US
dc.contributor.authorWong, TMen_US
dc.date.accessioned2012-09-05T05:25:14Z-
dc.date.available2012-09-05T05:25:14Z-
dc.date.issued2004en_US
dc.identifier.citationAmerican Journal Of Physiology - Cell Physiology, 2004, v. 287 n. 1 56-1, p. C163-C170en_US
dc.identifier.issn0363-6143en_US
dc.identifier.urihttp://hdl.handle.net/10722/162916-
dc.description.abstractThe cardiac Ca2+-independent transient outward K+ current (Ito), a major repolarizing ionic current, is markedly affected by Cl- substitution and anion channel blockers. We reexplored the mechanism of the action of anions on Ito by using whole cell patch-clamp in single isolated rat cardiac ventricular myocytes. The transient outward current was sensitive to blockade by 4-aminopyridine (4-AP) and was abolished by Cs+ substitution for intracellular K +. Replacement of most of the extracellular Cl- with less permeant anions, aspartate (Asp-) and glutamate (Glu-), markedly suppressed the current. Removal of external Na+ or stabilization of F-actin with phalloidin did not significantly affect the inhibitory action of less permeant anions on Ito. In contrast, the permeant Cl- substitute Br- did not markedly affect the current, whereas F- substitution for Cl- induced a slight inhibition. The Ito elicited during Br- substitution for Cl- was also sensitive to blockade by 4-AP. The ability of Cl - substitutes to induce rightward shifts of the steady-state inactivation curve of Ito was in the following sequence: NO 3 - > Cl- ≈ Br- > gluconate- > Glu- > Asp-. Depolymerization of actin filaments with cytochalasin D (CytD) induced an effect on the steady-state inactivation of Ito similar to that of less permeant anions. Fluorescent phalloidin staining experiments revealed that CytD-pretreatment significantly decreased the intensity of FITC-phalloidin staining of F-actin, whereas Asp- substitution for Cl- was without significant effect on the intensity. These results suggest that the Ito channel is modulated by anion channel(s), in which the actin cytoskeleton may be implicated.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.subject.meshActins - Metabolismen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAnions - Metabolismen_US
dc.subject.meshAspartic Acid - Pharmacologyen_US
dc.subject.meshChloride Channels - Metabolismen_US
dc.subject.meshCytochalasin D - Pharmacologyen_US
dc.subject.meshElectric Conductivityen_US
dc.subject.meshHeart Ventriclesen_US
dc.subject.meshHomeostasisen_US
dc.subject.meshIon Channels - Metabolismen_US
dc.subject.meshMyocytes, Cardiac - Metabolismen_US
dc.subject.meshNucleic Acid Synthesis Inhibitors - Pharmacologyen_US
dc.subject.meshPatch-Clamp Techniquesen_US
dc.subject.meshPermeabilityen_US
dc.subject.meshPotassium Channels - Physiologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.titleInvolvement of anion channel(s) in the modulation of the transient outward K+ channel in rat ventricular 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.doi10.1152/ajpcell.00297.2003en_US
dc.identifier.pmid14973147-
dc.identifier.scopuseid_2-s2.0-2942660220en_US
dc.identifier.hkuros101176-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-2942660220&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume287en_US
dc.identifier.issue1 56-1en_US
dc.identifier.spageC163en_US
dc.identifier.epageC170en_US
dc.identifier.isiWOS:000221926100019-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLai, XG=7101868372en_US
dc.identifier.scopusauthoridYang, J=8360091600en_US
dc.identifier.scopusauthoridZhou, SS=25927738800en_US
dc.identifier.scopusauthoridZhu, J=14034937700en_US
dc.identifier.scopusauthoridLi, GR=7408462932en_US
dc.identifier.scopusauthoridWong, TM=7403531434en_US

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