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Am J Physiol Heart Circ Physiol 282: H880-H889, 2002; doi:10.1152/ajpheart.01138.2000
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Vol. 282, Issue 3, H880-H889, March 2002

Effects of sustained beta -adrenergic stimulation on ionic currents of cultured adult guinea pig cardiomyocytes

Li-Ming Zhang1, Zhiguo Wang1, and Stanley Nattel1,2

1 Research Center and Department of Medicine, Montreal Heart Institute, Montreal H1T 1C8, and University of Montreal, Montreal H3C 3J7; and 2 Department of Pharmacology and Therapeutics, McGill University, Montreal, Quebec H3G 1Y6, Canada

Short-term stimulation of beta -receptors is known to affect cardiac ion channels; however, the impact of longer-term stimulation on intrinsic channel function is poorly understood. To evaluate this, cultured guinea pig ventricular myocytes were exposed to isoproterenol (10 nM), vehicle, or isoproterenol plus propranolol (1 µM) for 48 h. Sustained exposure to isoproterenol decreased the density of the inward rectifier (IK1), slow delayed rectifier (IKs), and L-type Ca2+ (ICa L) currents, effects that were fully prevented by propranolol. Changes in K+ currents were prevented by the beta 1-selective antagonist CGP-20712A, unaffected by the beta 2-antagonist ICI-118,551, and mimicked by the membrane-permeable cAMP analog 8-bromo-cAMP. Isoproterenol did not alter the current-voltage relationship of the K+ currents but increased the density of T-type Ca2+ current (ICa T) and thereby increased the proportion of the total Ca2+ current at more negative potentials. We conclude that sustained exposure to isoproterenol reduces IK1, IKs, and ICa L density and increases the density of ICa T. The direct ionic current remodeling effects of sustained beta -adrenoceptor stimulation resemble changes reported with heart failure and may be important in arrhythmogenic ionic remodeling.

ion-channel regulation; cardiac arrhythmias; calcium channels; potassium channels; sympathetic nervous system


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