| An outwardly rectifying chloride channel in human atrial cardiomyocytes. | |
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MedLine Citation:
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PMID: 16426403 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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INTRODUCTION: Among a range of chloride channels, outwardly rectifying Cl- channels have been reported in the heart of various species. Although the anionic current carried by this channel has been subjected to intense electrophysiological investigations, paradoxically no examination of single-channel currents has been reported for human cardiomyocytes. METHODS AND RESULTS: Using the cell-attached and cell-free configurations of the patch-clamp technique, we have characterized the properties of an outwardly rectifying chloride current (ORCC) at the unitary level in freshly isolated human atrial cardiomyocytes. In excised inside-out patches, the channel presented a nonlinear I/V relationship with a conductance of 76.5 +/- 14.7 pS in the positive voltage range and 8.1 +/- 2 pS in the negative voltage range, indicating an outward rectification. Preincubation with the protein kinase C activator phorbol 12-myristate 13-acetate (PMA) significantly increased the number of spontaneously active channels observed. The channel was Cl- selective (Cl- to Na+ permeability ratio, PCl/PNa= 18) with the permeability sequence I- > Br- > Cl- > F- > gluconate. It was blocked by the classical Cl- channels blockers glibenclamide, NPPB, SITS, and DIDS. Channel activity was not dependent upon internal calcium concentration. In the cell-attached configuration, ORCC channel activation was observed under perfusion of a hypotonic solution. CONCLUSION: Human atrial myocytes express an outwardly rectifying Cl- channel that is sensitive to PKC activation. This channel shares biophysical and pharmacological properties with the swelling-activated chloride current implicated in cardiac pathologies such as myocardial ischemia and dilated cardiopathies. |
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Authors:
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Marie Demion; Romain Guinamard; Antoun El Chemaly; Mohammad Rahmati; Patrick Bois |
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Publication Detail:
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Type: Comparative Study; In Vitro; Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Journal of cardiovascular electrophysiology Volume: 17 ISSN: 1045-3873 ISO Abbreviation: J. Cardiovasc. Electrophysiol. Publication Date: 2006 Jan |
Date Detail:
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Created Date: 2006-01-23 Completed Date: 2006-05-04 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 9010756 Medline TA: J Cardiovasc Electrophysiol Country: United States |
Other Details:
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Languages: eng Pagination: 60-8 Citation Subset: IM |
Affiliation:
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Institut de Physiologie et Biologie Cellulaires, CNRS UMR 6187, Université de Poitiers, Poitiers Cedex, France. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Aged Cell Membrane Permeability / drug effects, physiology Cells, Cultured Chloride Channels / drug effects, metabolism* Chlorides / metabolism* Female Glyburide / pharmacology Heart Atria / cytology*, drug effects, metabolism Humans Hypoglycemic Agents / pharmacology Male Membrane Potentials / physiology Myocytes, Cardiac / cytology, drug effects, metabolism* Patch-Clamp Techniques Protein Kinase C / pharmacology |
| Chemical | |
Reg. No./Substance:
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0/Chloride Channels; 0/Chlorides; 0/Hypoglycemic Agents; 10238-21-8/Glyburide; EC 2.7.11.13/Protein Kinase C |
| Comments/Corrections | |
Comment In:
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J Cardiovasc Electrophysiol. 2006 Jan;17(1):69-71
[PMID:
16426404
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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