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

ABSTRACT: Chronic ?-adrenoceptor antagonist (?-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 ?-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 ?-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?

SUBMITTER: Marshall GE 

PROVIDER: S-EPMC3307334 | biostudies-literature | 2012 Apr

REPOSITORIES: biostudies-literature

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

Marshall Gillian E GE   Russell Julie A JA   Tellez James O JO   Jhund Pardeep S PS   Currie Susan S   Dempster John J   Boyett Mark R MR   Kane Kathleen A KA   Rankin Andrew C AC   Workman Antony J AJ  

Pflugers Archiv : European journal of physiology 20111208 4

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 curren  ...[more]

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