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Science 2 May 1997:
Vol. 276. no. 5313, pp. 800 - 806
DOI: 10.1126/science.276.5313.800
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Reports

Defective Excitation-Contraction Coupling in Experimental Cardiac Hypertrophy and Heart Failure

A. M. Gómez, H. H. Valdivia, H. Cheng, Miriam R. Lederer, L. F. Santana, M. B. Cannell, S. A. McCune, R. A. Altschuld, W. J. Lederer *

Cardiac hypertrophy and heart failure caused by high blood pressure were studied in single myocytes taken from hypertensive rats (Dahl SS/Jr) and SH-HF rats in heart failure. Confocal microscopy and patch-clamp methods were used to examine excitation-contraction (EC) coupling, and the relation between the plasma membrane calcium current (ICa) and evoked calcium release from the sarcoplasmic reticulum (SR), which was visualized as "calcium sparks." The ability of ICa to trigger calcium release from the SR in both hypertrophied and failing hearts was reduced. Because ICa density and SR calcium-release channels were normal, the defect appears to reside in a change in the relation between SR calcium-release channels and sarcolemmal calcium channels. beta -Adrenergic stimulation largely overcame the defect in hypertrophic but not failing heart cells. Thus, the same defect in EC coupling that develops during hypertrophy may contribute to heart failure when compensatory mechanisms fail.

A. M. Gómez, L. F. Santana, W. J. Lederer, Department of Physiology and the Medical Biotechnology Center, University of Maryland School of Medicine, 725 West Lombard Street, Baltimore, MD 21201, USA.
H. H. Valdivia, Department of Physiology, University of Wisconsin Medical School, Madison, WI 53706, USA.
H. Cheng, Medical Biotechnology Center, University of Maryland School of Medicine, 725 West Lombard Street, Baltimore, MD 21201, and Section of Cardiovascular Research, National Institute of Aging, Baltimore, MD 21224, USA.
M. R. Lederer, Department of Physiology, University of Maryland School of Medicine, 725 West Lombard Street, Baltimore, MD 21201, USA.
M. B. Cannell, Department of Physiology and the Medical Biotechnology Center, University of Maryland School of Medicine, 725 West Lombard Street, Baltimore, MD 21201, USA, and Department of Pharmacology and Clinical Pharmacology, St. George's Hospital Medical School, London SW17 ORE, UK.
S. A. McCune, Department of Food Science and Technology, Ohio State University, Columbus, OH 43210, USA.
R. A. Altschuld, Department of Medical Biochemistry, Ohio State University, Columbus, OH 43210, USA.
*   To whom correspondence should be addressed. E-mail: jlederer{at}umabnet.ab.umd.edu

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   Abstract »    Full Text »    PDF »
Electric currents applied during refractory period enhance contractility and systolic calcium in the ferret heart.
S. Mohri, J. Shimizu, Y. Mika, I. Shemer, J. Wang, S. Ben-Haim, and D. Burkhoff (2003)
Am J Physiol Heart Circ Physiol 284, H1119-H1123
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Contractile Reserve and Calcium Regulation Are Depressed in Myocytes From Chronically Unloaded Hearts.
K. Ito, M. Nakayama, F. Hasan, X. Yan, M. D. Schneider, and B. H. Lorell (2003)
Circulation 107, 1176-1182
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Reduced contraction strength with increased intracellular [Ca2+] in left ventricular trabeculae from failing rat hearts.
M.-L. Ward, A. J Pope, D. S Loiselle, and M. B Cannell (2003)
J. Physiol. 546, 537-550
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Protein Kinase A Phosphorylation of the Cardiac Calcium Release Channel (Ryanodine Receptor) in Normal and Failing Hearts. ROLE OF PHOSPHATASES AND RESPONSE TO ISOPROTERENOL.
S. Reiken, M. Gaburjakova, S. Guatimosim, A. M. Gomez, J. D'Armiento, D. Burkhoff, J. Wang, G. Vassort, W. J. Lederer, and A. R. Marks (2003)
J. Biol. Chem. 278, 444-453
   Abstract »    Full Text »    PDF »
Regulation of cardiac excitation-contraction coupling by action potential repolarization: role of the transient outward potassium current (Ito).
R. Sah, R. J Ramirez, G. Y Oudit, D. Gidrewicz, M. G Trivieri, C. Zobel, and P. H Backx (2003)
J. Physiol. 546, 5-18
   Abstract »    Full Text »    PDF »
Heart failure - a challenge to our current concepts of excitation-contraction coupling.
I. Sjaastad, J A. Wasserstrom, and O. M Sejersted (2003)
J. Physiol. 546, 33-47
   Abstract »    Full Text »    PDF »
Targeting calcium cycling proteins in heart failure through gene transfer.
F. del Monte and R. J Hajjar (2003)
J. Physiol. 546, 49-61
   Abstract »    Full Text »    PDF »
The cardiac ryanodine receptor (calcium release channel): Emerging role in heart failure and arrhythmia pathogenesis.
M. Scoote and A. J Williams (2002)
Cardiovasc Res 56, 359-372
   Abstract »    Full Text »    PDF »
Heart Failure and the Ryanodine Receptor: Does Occam's Razor Rule?.
D.A. Eisner and A.W. Trafford (2002)
Circ. Res. 91, 979-981
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Abnormal Ca2+ Release, but Normal Ryanodine Receptors, in Canine and Human Heart Failure.
M. T. Jiang, A. J. Lokuta, E. F. Farrell, M. R. Wolff, R. A. Haworth, and H. H. Valdivia (2002)
Circ. Res. 91, 1015-1022
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Structural and functional implications of the phospholamban hinge domain: impaired SR Ca2+ uptake as a primary cause of heart failure.
A. G Schmidt, J. Zhai, A. N Carr, M. J Gerst, J. N Lorenz, P. Pollesello, A. Annila, B. D Hoit, and E. G Kranias (2002)
Cardiovasc Res 56, 248-259
   Abstract »    Full Text »    PDF »
Alternans Goes Subcellular: A "Disease" of the Ryanodine Receptor?.
B. Pieske and J. Kockskamper (2002)
Circ. Res. 91, 553-555
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Depressed Ryanodine Receptor Activity Increases Variability and Duration of the Systolic Ca2+ Transient in Rat Ventricular Myocytes.
M.E. Diaz, D.A. Eisner, and S.C. O'Neill (2002)
Circ. Res. 91, 585-593
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Defective intracellular Ca2+ signaling contributes to cardiomyopathy in Type 1 diabetic rats.
K. M. Choi, Y. Zhong, B. D. Hoit, I. L. Grupp, H. Hahn, K. W. Dilly, S. Guatimosim, W. J. Lederer, and M. A. Matlib (2002)
Am J Physiol Heart Circ Physiol 283, H1398-H1408
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L-Type Ca2+ Channel Density and Regulation Are Altered in Failing Human Ventricular Myocytes and Recover After Support With Mechanical Assist Devices.
X. Chen, V. Piacentino III, S. Furukawa, B. Goldman, K. B. Margulies, and S. R. Houser (2002)
Circ. Res. 91, 517-524
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Myocardial infarction in rat eliminates regional heterogeneity of AP profiles, Ito K+ currents, and [Ca2+]i transients.
R. Kaprielian, R. Sah, T. Nguyen, A. D. Wickenden, and P. H. Backx (2002)
Am J Physiol Heart Circ Physiol 283, H1157-H1168
   Abstract »    Full Text »    PDF »
Normal contractions triggered by ICa,L in ventricular myocytes from rats with postinfarction CHF.
I. Sjaastad, J. Bokenes, F. Swift, J. A. Wasserstrom, and O. M. Sejersted (2002)
Am J Physiol Heart Circ Physiol 283, H1225-H1236
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Increased Exchange Current but Normal Ca2+ Transport via Na+-Ca2+ Exchange During Cardiac Hypertrophy After Myocardial Infarction.
A. M. Gomez, B. Schwaller, H. Porzig, G. Vassort, E. Niggli, and M. Egger (2002)
Circ. Res. 91, 323-330
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Echocardiographic quantification of left ventricular asynchrony predicts an acute hemodynamic benefit of cardiac resynchronization therapy.
O. A. Breithardt, C. Stellbrink, A. P. Kramer, A. M. Sinha, A. Franke, R. Salo, B. Schiffgens, E. Huvelle, A. Auricchio, and PATH-CHF Study Group (2002)
J. Am. Coll. Cardiol. 40, 536-545
   Abstract »    Full Text »    PDF »
What is wrong with positive inotropic drugs? Lessons from basic science and clinical trials.
B Swynghedauw and D Charlemagne (2002)
Eur. Heart J. Suppl. 4, D43-D49
   Abstract »    PDF »


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