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Remodelling of human atrial K+ currents but not ion channel expression by chronic β-blockade

Chronic β-adrenoceptor antagonist (β-blocker) treatment in patients is associated with a potentially anti-arrhythmic prolongation of the atrial action potential duration (APD), which may involve remodelling of repolarising K + currents. The aim of this study was to investigate the effects of chronic...

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Bibliographic Details
Published in:Pflügers Archiv 2012-04, Vol.463 (4), p.537-548
Main Authors: Marshall, Gillian E., Russell, Julie A., Tellez, James O., Jhund, Pardeep S., Currie, Susan, Dempster, John, Boyett, Mark R., Kane, Kathleen A., Rankin, Andrew C., Workman, Antony J.
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Language:English
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Summary:Chronic β-adrenoceptor antagonist (β-blocker) treatment in patients is associated with a potentially anti-arrhythmic prolongation of the atrial action potential duration (APD), which may involve remodelling of repolarising K + currents. The aim of this study was to investigate the effects of chronic β-blockade on transient outward, sustained and inward rectifier K + currents (I TO , I KSUS and I K1 ) in human atrial myocytes and on the expression of underlying ion channel subunits. Ion currents were recorded from human right atrial isolated myocytes using the whole-cell-patch clamp technique. Tissue mRNA and protein levels were measured using real time RT-PCR and Western blotting. Chronic β-blockade was associated with a 41% reduction in I TO density: 9.3 ± 0.8 (30 myocytes, 15 patients) vs 15.7 ± 1.1 pA/pF (32, 14), p  
ISSN:0031-6768
1432-2013
DOI:10.1007/s00424-011-1061-z