From the Department of Medicine (S.K., J. Duc, D.A., G.F.T.), Division of
Molecular and Cellular Cardiology, Johns Hopkins University, Baltimore,
Maryland; Department of Neurobiology and Behavior (J. Dixon, D.M.), State
University of New York at Stony Brook; Department of Medicine I (S.K., M.N.,
G.S.), Ludwig Maximilians University of Munich (Germany); and Department of
Medicine III (D.J.B.), University of Cologne (Germany).
Correspondence to Gordon Tomaselli, MD, 720 N Rutland Ave, Ross 844, Johns Hopkins University, Baltimore, MD 21205. E-mail gtomasel{at}welchlink.welch.jhu.edu
Background—Despite advances in
medical therapy, congestive heart failure remains a major cause of
death in the developed world. A disproportionate number of the deaths
of patients with heart failure are sudden and presumed to be
arrhythmic. Heart failure in humans and in animal models is associated
with prolongation of the action potential duration (APD), the result of
downregulation of K+ currents—prominently, the
Ca2+-independent transient outward current
(Ito). The mechanism for the reduction of
Ito in heart failure is unknown. The
K+ channel
Methods and Results—We used ribonuclease protection assays and
whole-cell electrophysiological
recording to study changes in the level of Kv4.3 mRNA and
Ito in human tissues and isolated
ventricular myocytes, respectively. We found that the level
of Kv4.3 mRNA decreased by 30% in failing hearts compared with
nonfailing controls. Furthermore, this reduction correlated with the
reduction in peak Ito density measured in
ventricular myocytes isolated from adjacent regions of the
heart. There was no significant change in the steady-state level of any
other mRNA studied (HERG, Kv1.4, Kir2.1, Kvß1.3, and
the
Conclusions—These data provide further support for the hypothesis
that Kv4.3 encodes all or part of the native cardiac
Ito in humans and that part of the
downregulation of this current in heart failure may be
transcriptionally regulated.
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports
Molecular Basis of Transient Outward Potassium Current Downregulation in Human Heart Failure
A Decrease in Kv4.3 mRNA Correlates With a Reduction in Current Density
-subunit Kv4.3, a homolog of the
Drosophila Shal family, is most likely to encode all or
part of the native cardiac Ito in
humans. 1C subunit of the Ca2+ channel). mRNAs encoding
Kv1.2, Kv1.5, and Kv2.1 were found in low abundance in human
ventricle.
Key Words: currents • sodium • potassium • heart failure • repolarization
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C. Antzelevitch Molecular basis for the transmural distribution of the transient outward current J. Physiol., May 15, 2001; 533(1): 1 - 1. [Full Text] [PDF]
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B. Rosati, Z. Pan, S. Lypen, H.-S. Wang, I. Cohen, J. E Dixon, and D. McKinnon Regulation of KChIP2 potassium channel {beta} subunit gene expression underlies the gradient of transient outward current in canine and human ventricle J. Physiol., May 15, 2001; 533(1): 119 - 125. [Abstract] [Full Text] [PDF]
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P. B. Adamson and E. Vanoli Early autonomic and repolarization abnormalities contribute to lethal arrhythmias in chronic ischemic heart failure: Characteristics of a novel heart failure model in dogs with postmyocardial infarction left ventricular dysfunction J. Am. Coll. Cardiol., May 1, 2001; 37(6): 1741 - 1748. [Abstract] [Full Text] [PDF]
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T. González, M. Longobardo, R. Caballero, E. Delpón, J. Tamargo, and C. Valenzuela Effects of Bupivacaine and a Novel Local Anesthetic, IQB-9302, on Human Cardiac K+ Channels J. Pharmacol. Exp. Ther., April 13, 2001; 296(2): 573 - 583. [Abstract] [Full Text]
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M. Nabauer Tuning Repolarization in the Heart : A Multitude of Potassium Channels and Regulatory Pathways Circ. Res., March 16, 2001; 88(5): 453 - 455. [Full Text] [PDF]
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T.-T. Zhang, K. Takimoto, A. F. R. Stewart, C. Zhu, and E. S. Levitan Independent Regulation of Cardiac Kv4.3 Potassium Channel Expression by Angiotensin II and Phenylephrine Circ. Res., March 16, 2001; 88(5): 476 - 482. [Abstract] [Full Text] [PDF]
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 C.-C. Shieh, M. Coghlan, J. P. Sullivan, and M. Gopalakrishnan Potassium Channels: Molecular Defects, Diseases, and Therapeutic Opportunities Pharmacol. Rev., December 1, 2000; 52(4): 557 - 594. [Abstract] [Full Text] [PDF]
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J. L. Greenstein, R. Wu, S. Po, G. F. Tomaselli, and R. L. Winslow Role of the Calcium-Independent Transient Outward Current Ito1 in Shaping Action Potential Morphology and Duration Circ. Res., November 24, 2000; 87(11): 1026 - 1033. [Abstract] [Full Text] [PDF]
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P. G.A. Volders, M. A. Vos, B. Szabo, K. R. Sipido, S.H.M. de Groot, A. P.M. Gorgels, H. J.J. Wellens, and R. Lazzara Progress in the understanding of cardiac early afterdepolarizations and torsades de pointes: time to revise current concepts Cardiovasc Res, June 1, 2000; 46(3): 376 - 392. [Full Text] [PDF]
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Y. A. Kuryshev, T. I. Gudz, A. M. Brown, and B. A. Wible KChAP as a chaperone for specific K+ channels Am J Physiol Cell Physiol, May 1, 2000; 278(5): C931 - C941. [Abstract] [Full Text] [PDF]
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L. C. Baker, B. London, B.-R. Choi, G. Koren, and G. Salama Enhanced Dispersion of Repolarization and Refractoriness in Transgenic Mouse Hearts Promotes Reentrant Ventricular Tachycardia Circ. Res., March 3, 2000; 86(4): 396 - 407. [Abstract] [Full Text] [PDF]
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E. Cerbai, A. Crucitti, L. Sartiani, P. De Paoli, R. Pino, M. L. Rodriguez, G. Gensini, and A. Mugelli Long-term treatment of spontaneously hypertensive rats with losartan and electrophysiological remodeling of cardiac myocytes Cardiovasc Res, January 14, 2000; 45(2): 388 - 396. [Abstract] [Full Text] [PDF]
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T. Kiyosue and M. Arita Altered expression of cardiac K+ channel genes during sub-acute and healing phases of myocardial infarction Cardiovasc Res, October 1, 1999; 44(1): 13 - 16. [Full Text] [PDF]
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Y. A. Kuryshev, G. M. Brittenham, H. Fujioka, P. Kannan, C.-C. Shieh, S. A. Cohen, and A. M. Brown Decreased Sodium and Increased Transient Outward Potassium Currents in Iron-Loaded Cardiac Myocytes : Implications for the Arrhythmogenesis of Human Siderotic Heart Disease Circulation, August 10, 1999; 100(6): 675 - 683. [Abstract] [Full Text] [PDF]
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P. Schaffer, B. Pelzmann, E. Bernhart, P. Lang, H. Machler, B. Rigler, and B. Koidl Repolarizing currents in ventricular myocytes from young patients with tetralogy of Fallot Cardiovasc Res, August 1, 1999; 43(2): 332 - 343. [Abstract] [Full Text] [PDF]
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G. F. Tomaselli and E. Marban Electrophysiological remodeling in hypertrophy and heart failure Cardiovasc Res, May 1, 1999; 42(2): 270 - 283. [Full Text] [PDF]
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D. M. Roden and S. Kupershmidt From genes to channels: normal mechanisms Cardiovasc Res, May 1, 1999; 42(2): 318 - 326. [Abstract] [Full Text] [PDF]
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F. Aimond, J. L Alvarez, J.-M. Rauzier, P. Lorente, and G. Vassort Ionic basis of ventricular arrhythmias in remodeled rat heart during long-term myocardial infarction Cardiovasc Res, May 1, 1999; 42(2): 402 - 415. [Abstract] [Full Text] [PDF]
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U. C. Hoppe, D. C. Johns, E. Marban, and B. O'Rourke Manipulation of Cellular Excitability by Cell Fusion : Effects of Rapid Introduction of Transient Outward K+ Current on the Guinea Pig Action Potential Circ. Res., April 30, 1999; 84(8): 964 - 972. [Abstract] [Full Text] [PDF]
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M. Song, G. Helguera, M. Eghbali, N. Zhu, M. M. Zarei, R. Olcese, L. Toro, and E. Stefani Remodeling of Kv4.3 Potassium Channel Gene Expression under the Control of Sex Hormones J. Biol. Chem., August 17, 2001; 276(34): 31883 - 31890. [Abstract] [Full Text] [PDF]
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C. A. Ufret-Vincenty, D. J. Baro, W. J. Lederer, H. A. Rockman, L. E. Quinones, and L. F. Santana Role of Sodium Channel Deglycosylation in the Genesis of Cardiac Arrhythmias in Heart Failure J. Biol. Chem., July 20, 2001; 276(30): 28197 - 28203. [Abstract] [Full Text] [PDF]
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G. J. Rozanski and Z. Xu Glutathione and K+ channel remodeling in postinfarction rat heart Am J Physiol Heart Circ Physiol, June 1, 2002; 282(6): H2346 - H2355. [Abstract] [Full Text] [PDF]
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Z. Kassiri, C. Zobel, T.-T. T. Nguyen, J. D. Molkentin, and P. H. Backx Reduction of Ito Causes Hypertrophy in Neonatal Rat Ventricular Myocytes Circ. Res., March 22, 2002; 90(5): 578 - 585. [Abstract] [Full Text] [PDF]
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