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Cellular Biology |
From the Department of Medicine (S.M.P.), University of Illinois, Chicago, Ill, and Department of Physiology and Cardiovascular Institute (K.S., L.L., W.Y., D.M.B.), Loyola University Chicago.
Correspondence to Donald M. Bers, PhD, Department of Physiology, Loyola University Chicago, 2160 S First Ave, Maywood, IL 60153. E-mail dbers{at}luc.edu
Abstract
AbstractVentricular
arrhythmias and contractile dysfunction are the main causes of
death in human heart failure (HF). In a rabbit HF model reproducing
these same aspects of human HF, we demonstrate that a 2-fold functional
upregulation of
Na+-Ca2+ exchange
(NaCaX) unloads sarcoplasmic reticulum (SR)
Ca2+ stores, reducing
Ca2+ transients and contractile function.
Whereas ß-adrenergic receptors (ß-ARs) are progressively
downregulated in HF, residual ß-AR responsiveness at this critical HF
stage allows SR Ca2+ load to increase,
causing spontaneous SR Ca2+ release and
transient inward current carried by NaCaX. A given
Ca2+ release produces greater arrhythmogenic
inward current in HF (as a result of NaCaX upregulation), and
50%
less Ca2+ release is required to trigger an
action potential in HF. The inward rectifier potassium current
(IK1) is
reduced by 49% in HF, and this allows greater depolarization for a
given NaCaX current. Partially blocking
IK1 in
control cells with barium mimics the greater depolarization for a given
current injection seen in HF. Thus, we present data to support a
novel paradigm in which changes in NaCaX and
IK1, and
residual ß-AR responsiveness, conspire to greatly increase the
propensity for triggered arrhythmias in HF. In addition, NaCaX
upregulation appears to be a critical link between contractile
dysfunction and arrhythmogenesis.
Key Words: heart failure excitation-contraction coupling Na+-Ca2+ exchange Ca2+ transport K+ currents
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R. A. Bassani, J. Altamirano, J. L. Puglisi, and D. M. Bers Action potential duration determines sarcoplasmic reticulum Ca2+ reloading in mammalian ventricular myocytes J. Physiol., September 1, 2004; 559(2): 593 - 609. [Abstract] [Full Text] [PDF] |
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I. A. Hobai, C. Maack, and B. O'Rourke Partial Inhibition of Sodium/Calcium Exchange Restores Cellular Calcium Handling in Canine Heart Failure Circ. Res., August 6, 2004; 95(3): 292 - 299. [Abstract] [Full Text] [PDF] |
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M. Zaugg and M. C. Schaub Cellular mechanisms in sympatho-modulation of the heart Br. J. Anaesth., July 1, 2004; 93(1): 34 - 52. [Abstract] [Full Text] [PDF] |
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R. Bouchard, R. B. Clark, A. E. Juhasz, and W. R. Giles Changes in extracellular K+ concentration modulate contractility of rat and rabbit cardiac myocytes via the inward rectifier K+ current IK1 J. Physiol., May 1, 2004; 556(3): 773 - 790. [Abstract] [Full Text] [PDF] |
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Y. Chen, B. Escoubet, F. Prunier, J. Amour, W. S. Simonides, B. Vivien, C. Lenoir, M. Heimburger, C. Choqueux, B. Gellen, et al. Constitutive Cardiac Overexpression of Sarcoplasmic/Endoplasmic Reticulum Ca2+-ATPase Delays Myocardial Failure After Myocardial Infarction in Rats at a Cost of Increased Acute Arrhythmias Circulation, April 20, 2004; 109(15): 1898 - 1903. [Abstract] [Full Text] [PDF] |
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M. J Janse Electrophysiological changes in heart failure and their relationship to arrhythmogenesis Cardiovasc Res, February 1, 2004; 61(2): 208 - 217. [Abstract] [Full Text] [PDF] |
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T.-J. Cha, J. R. Ehrlich, L. Zhang, Y.-F. Shi, J.-C. Tardif, T. K. Leung, and S. Nattel Dissociation Between Ionic Remodeling and Ability to Sustain Atrial Fibrillation During Recovery From Experimental Congestive Heart Failure Circulation, January 27, 2004; 109(3): 412 - 418. [Abstract] [Full Text] [PDF] |
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K. TASKEN and E. M. AANDAHL Localized Effects of cAMP Mediated by Distinct Routes of Protein Kinase A Physiol Rev, January 1, 2004; 84(1): 137 - 167. [Abstract] [Full Text] [PDF] |
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R. R. Makkar, M. Lill, and P.-S. Chen Stem cell therapy for myocardial repair: Is it arrhythmogenic? J. Am. Coll. Cardiol., December 17, 2003; 42(12): 2070 - 2072. [Full Text] [PDF] |
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C. I. Spencer and J. S. K. Sham Effects of Na+/Ca2+ exchange induced by SR Ca2+ release on action potentials and afterdepolarizations in guinea pig ventricular myocytes Am J Physiol Heart Circ Physiol, December 1, 2003; 285(6): H2552 - H2562. [Abstract] [Full Text] [PDF] |
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D. W. Rodenbaugh, H. L. Collins, D. G. Nowacek, and S. E. DiCarlo Increased susceptibility to ventricular arrhythmias is associated with changes in Ca2+ regulatory proteins in paraplegic rats Am J Physiol Heart Circ Physiol, December 1, 2003; 285(6): H2605 - H2613. [Abstract] [Full Text] [PDF] |
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F R Quinn, S Currie, A M Duncan, S Miller, R Sayeed, S M Cobbe, and G L Smith Myocardial infarction causes increased expression but decreased activity of the myocardial Na+--Ca2+ exchanger in the rabbit J. Physiol., November 15, 2003; 553(1): 229 - 242. [Abstract] [Full Text] [PDF] |
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C. R. Weber, V. Piacentino III, S. R. Houser, and D. M. Bers Dynamic Regulation of Sodium/Calcium Exchange Function in Human Heart Failure Circulation, November 4, 2003; 108(18): 2224 - 2229. [Abstract] [Full Text] [PDF] |
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D. M. Roden A Surprising New Arrhythmia Mechanism in Heart Failure Circ. Res., October 3, 2003; 93(7): 589 - 591. [Full Text] [PDF] |
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T. R. Shannon, S. M. Pogwizd, and D. M. Bers Elevated Sarcoplasmic Reticulum Ca2+ Leak in Intact Ventricular Myocytes From Rabbits in Heart Failure Circ. Res., October 3, 2003; 93(7): 592 - 594. [Abstract] [Full Text] [PDF] |
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D. M. Bers, D. A. Eisner, and H. H. Valdivia Sarcoplasmic Reticulum Ca2+ and Heart Failure: Roles of Diastolic Leak and Ca2+ Transport Circ. Res., September 19, 2003; 93(6): 487 - 490. [Full Text] [PDF] |
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J. R Ehrlich, T.-J. Cha, L. Zhang, D. Chartier, P. Melnyk, S. H Hohnloser, and S. Nattel Cellular electrophysiology of canine pulmonary vein cardiomyocytes: action potential and ionic current properties J. Physiol., September 15, 2003; 551(3): 801 - 813. [Abstract] [Full Text] [PDF] |
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