Exchange protein directly activated by cAMP mediates slow delayed-rectifier current remodeling by sustained β-adrenergic activation in guinea pig hearts.


RATIONALE β-Adrenoceptor activation contributes to sudden death risk in heart failure. Chronic β-adrenergic stimulation, as occurs in patients with heart failure, causes potentially arrhythmogenic reductions in slow delayed-rectifier K(+) current (IKs). OBJECTIVE To assess the molecular mechanisms of IKs downregulation caused by chronic β-adrenergic… (More)
DOI: 10.1161/CIRCRESAHA.113.302982


  • Presentations referencing similar topics