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(Circulation. 1999;99:641-648.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
Relationship Between Na+-Ca2+–Exchanger Protein Levels and Diastolic Function of Failing Human Myocardium
From Zentrum Innere Medizin (G.H., W.S., S.E.L., B.P., L.S.M., J.P.), Abteilung Kardiologie und Pneumologie, Universität Göttingen, Göttingen, FRG; Medizinische Klinik III (M.P., H.J.), Universität Freiburg, Freiburg, FRG; and Klinik für Thorax- und Kardiovascularchirurgie (K.M.), Herzzentrum Nordrhein-Westfalen, Bad Oeynhausen, FRG.
Correspondence to Gerd Hasenfuss, MD, Universität Göttingen, Zentrum Innere Medizin, Abteilung Kardiologie und Pneumologie, Robert-Koch-Straße 40, 37075 Göttingen, FRG. E-mail hasenfus{at}med.uni-goettingen.de
Background—In the failing human heart, sarcoplasmic reticulum (SR) calcium handling is impaired, and therefore, calcium elimination and diastolic function may depend on the expression of sarcolemmal Na+-Ca2+ exchanger.
Methods and Results—Force-frequency relations were studied in ventricular muscle strip preparations from failing human hearts (n=29). Protein levels of Na+-Ca2+ exchanger and SR Ca2+-ATPase were measured in the same hearts. Hearts were divided into 3 groups by discriminant analysis according to the behavior of diastolic function when stimulation rate of muscle strips was increased from 30 to 180 min-1. At 180 compared with 30 min-1, diastolic force was increased by 160%, maximum rate of force decline was decreased by 46%, and relaxation time was unchanged in group III. In contrast, in group I, diastolic force and maximum rate of force decline did not change, and relaxation time decreased by 20%. Na+-Ca2+ exchanger was 66% higher in group I than in group III. Na+-Ca2+ exchanger was inversely correlated with the frequency-dependent rise of diastolic force when stimulation rate was increased (r=-0.74; P<0.001). Compared with nonfailing human hearts (n=6), SR Ca2+-ATPase was decreased and Na+-Ca2+ exchanger unchanged in group III, whereas Na+-Ca2+ exchanger was increased and SR Ca2+-ATPase unchanged in group I. Results with group II hearts were between those of group I and group III hearts.
Conclusions—By discriminating failing human hearts according to their diastolic function, we identified different phenotypes. Disturbed diastolic function occurs in hearts with decreased SR Ca2+-ATPase and unchanged Na+-Ca2+ exchanger, whereas increased expression of the Na+-Ca2+ exchanger is associated with preserved diastolic function.
Key Words: heart failure • calcium • myocardium • sarcoplasmic reticulum • diastole • proteins
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E. TAKIMOTO, A. YAO, H. TOKO, H. TAKANO, M. SHIMOYAMA, M. SONODA, K. WAKIMOTO, T. TAKAHASHI, H. AKAZAWA, M. MIZUKAMI, et al. Sodium calcium exchanger plays a key role in alteration of cardiac function in response to pressure overload FASEB J, March 1, 2002; 16(3): 373 - 378. [Abstract] [Full Text] [PDF]
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K. R Sipido, P. G.A Volders, M. A Vos, and F. Verdonck Altered Na/Ca exchange activity in cardiac hypertrophy and heart failure: a new target for therapy? Cardiovasc Res, March 1, 2002; 53(4): 782 - 805. [Abstract] [Full Text] [PDF]
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F. del Monte, S. E. Harding, G. W. Dec, J. K. Gwathmey, and R. J. Hajjar Targeting Phospholamban by Gene Transfer in Human Heart Failure Circulation, February 26, 2002; 105(8): 904 - 907. [Abstract] [Full Text] [PDF]
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J. G. Muller, Y. Isomatsu, S. V. Koushik, M. O'Quinn, L. Xu, C. S. Kappler, E. Hapke, M. R. Zile, S. J. Conway, and D. R. Menick Cardiac-Specific Expression and Hypertrophic Upregulation of the Feline Na+-Ca2+ Exchanger Gene H1-Promoter in a Transgenic Mouse Model Circ. Res., February 8, 2002; 90(2): 158 - 164. [Abstract] [Full Text] [PDF]
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C. R. Weber, V. Piacentino III, K. S. Ginsburg, S. R. Houser, and D. M. Bers Na+-Ca2+ Exchange Current and Submembrane [Ca2+] During the Cardiac Action Potential Circ. Res., February 8, 2002; 90(2): 182 - 189. [Abstract] [Full Text] [PDF]
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U. Schotten, M. Greiser, D. Benke, K. Buerkel, B. Ehrenteidt, C. Stellbrink, J. F Vazquez-Jimenez, F. Schoendube, P. Hanrath, and M. Allessie Atrial fibrillation-induced atrial contractile dysfunction: a tachycardiomyopathy of a different sort Cardiovasc Res, January 1, 2002; 53(1): 192 - 201. [Abstract] [Full Text] [PDF]
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K. Sugishita, Z. Su, F. Li, K. D. Philipson, and W. H. Barry Gender Influences [Ca2+]i During Metabolic Inhibition in Myocytes Overexpressing the Na+-Ca2+ Exchanger Circulation, October 23, 2001; 104(17): 2101 - 2106. [Abstract] [Full Text] [PDF]
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F. del Monte, E. Williams, D. Lebeche, U. Schmidt, A. Rosenzweig, J. K. Gwathmey, E. D. Lewandowski, and R. J. Hajjar Improvement in Survival and Cardiac Metabolism After Gene Transfer of Sarcoplasmic Reticulum Ca2+-ATPase in a Rat Model of Heart Failure Circulation, September 18, 2001; 104(12): 1424 - 1429. [Abstract] [Full Text] [PDF]
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H. Kubo, K. B. Margulies, V. Piacentino III, J. P. Gaughan, and S. R. Houser Patients With End-Stage Congestive Heart Failure Treated With {beta}-Adrenergic Receptor Antagonists Have Improved Ventricular Myocyte Calcium Regulatory Protein Abundance Circulation, August 28, 2001; 104(9): 1012 - 1018. [Abstract] [Full Text] [PDF]
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S. J Conway and S. V Koushik Cardiac sodium-calcium exchanger: a double-edged sword Cardiovasc Res, August 1, 2001; 51(2): 194 - 197. [Full Text] [PDF]
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S. Adachi-Akahane and Y. Kurachi New Era for Translational Research in Cardiac Arrhythmias Circ. Res., June 8, 2001; 88(11): 1095 - 1096. [Full Text] [PDF]
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E. Braunwald Congestive heart failure: a half century perspective Eur. Heart J., May 2, 2001; 22(10): 825 - 836. [PDF]
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S. Y. Boateng, R. U. Naqvi, M. U. Koban, M. H. Yacoub, K. T. MacLeod, and K. R. Boheler Low-dose ramipril treatment improves relaxation and calcium cycling after established cardiac hypertrophy Am J Physiol Heart Circ Physiol, March 1, 2001; 280(3): H1029 - H1038. [Abstract] [Full Text] [PDF]
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K. L. Golden, J. Ren, J. O'Connor, A. Dean, S. E. DiCarlo, and J. D. Marsh In vivo regulation of Na/Ca exchanger expression by adrenergic effectors Am J Physiol Heart Circ Physiol, March 1, 2001; 280(3): H1376 - H1382. [Abstract] [Full Text] [PDF]
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A Baartscheer Adenovirus gene transfer of SERCA in heart failure. A promising therapeutic approach ? Cardiovasc Res, February 1, 2001; 49(2): 249 - 252. [Full Text] [PDF]
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G. Isenberg How can overexpression of Na+,Ca2+-exchanger compensate the negative inotropic effects of downregulated SERCA? Cardiovasc Res, January 1, 2001; 49(1): 1 - 6. [Full Text] [PDF]
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C. M.N. Terracciano, K. D. Philipson, and K. T. MacLeod Overexpression of the Na+/Ca2+ exchanger and inhibition of the sarcoplasmic reticulum Ca2+-ATPase in ventricular myocytes from transgenic mice Cardiovasc Res, January 1, 2001; 49(1): 38 - 47. [Abstract] [Full Text] [PDF]
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P. M. Heerdt, J. W. Holmes, B. Cai, A. Barbone, J. D. Madigan, S. Reiken, D. L. Lee, M. C. Oz, A. R. Marks, and D. Burkhoff Chronic Unloading by Left Ventricular Assist Device Reverses Contractile Dysfunction and Alters Gene Expression in End-Stage Heart Failure Circulation, November 28, 2000; 102(22): 2713 - 2719. [Abstract] [Full Text] [PDF]
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K. R. Sipido Local Ca2+ Release in Heart Failure : Timing Is Important Circ. Res., November 24, 2000; 87(11): 966 - 968. [Full Text] [PDF]
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N. Satoh, T. M. Suter, R. Liao, and W. S. Colucci Chronic {alpha}-Adrenergic Receptor Stimulation Modulates the Contractile Phenotype of Cardiac Myocytes In Vitro Circulation, October 31, 2000; 102(18): 2249 - 2254. [Abstract] [Full Text] [PDF]
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K. R. Sipido, P. G. A. Volders, S. H. M. de Groot, F. Verdonck, F. Van de Werf, H. J. J. Wellens, and M. A. Vos Enhanced Ca2+ Release and Na/Ca Exchange Activity in Hypertrophied Canine Ventricular Myocytes : Potential Link Between Contractile Adaptation and Arrhythmogenesis Circulation, October 24, 2000; 102(17): 2137 - 2144. [Abstract] [Full Text] [PDF]
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S. M. Pogwizd Increased Na+-Ca2+ Exchanger in the Failing Heart Circ. Res., October 13, 2000; 87(8): 641 - 643. [Full Text] [PDF]
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I. A. Hobai and B. O'Rourke Enhanced Ca2+-Activated Na+-Ca2+ Exchange Activity in Canine Pacing-Induced Heart Failure Circ. Res., October 13, 2000; 87(8): 690 - 698. [Abstract] [Full Text] [PDF]
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P. Trouve, F. Carre, I. Belikova, C. Leclercq, T. Dakhli, L. Soufir, I. Coquard, J. Ramirez-Gil, and D. Charlemagne Na+-K+-ATPase alpha 2-isoform expression in guinea pig hearts during transition from compensation to decompensation Am J Physiol Heart Circ Physiol, October 1, 2000; 279(4): H1972 - H1981. [Abstract] [Full Text] [PDF]
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S. Gupta, A. J.C Prahash, and I. S Anand Myocyte contractile function is intact in the post-infarct remodeled rat heart despite molecular alterations Cardiovasc Res, October 1, 2000; 48(1): 77 - 88. [Abstract] [Full Text] [PDF]
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W. H. Barry Na+-Ca2+ Exchange in Failing Myocardium : Friend or Foe? Circ. Res., September 29, 2000; 87(7): 529 - 531. [Full Text] [PDF]
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W. Schillinger, P. M. L. Janssen, S. Emami, S. A. Henderson, R. S. Ross, N. Teucher, O. Zeitz, K. D. Philipson, J. Prestle, and G. Hasenfuss Impaired Contractile Performance of Cultured Rabbit Ventricular Myocytes After Adenoviral Gene Transfer of Na+-Ca2+ Exchanger Circ. Res., September 29, 2000; 87(7): 581 - 587. [Abstract] [Full Text] [PDF]
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K. Ito, X. Yan, M. Tajima, Z. Su, W. H. Barry, and B. H. Lorell Contractile Reserve and Intracellular Calcium Regulation in Mouse Myocytes From Normal and Hypertrophied Failing Hearts Circ. Res., September 29, 2000; 87(7): 588 - 595. [Abstract] [Full Text] [PDF]
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S. Nattel and D. Li Ionic Remodeling in the Heart : Pathophysiological Significance and New Therapeutic Opportunities for Atrial Fibrillation Circ. Res., September 15, 2000; 87(6): 440 - 447. [Abstract] [Full Text] [PDF]
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L.-Q. Zhang, X.-Q. Zhang, T. I. Musch, R. L. Moore, and J. Y. Cheung Sprint training restores normal contractility in postinfarction rat myocytes J Appl Physiol, September 1, 2000; 89(3): 1099 - 1105. [Abstract] [Full Text] [PDF]
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