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Sodium accumulation promotes diastolic dysfunction in end-stage heart failure following Serca2 knockout

  1. William E. Louch1,4,
  2. Karina Hougen1,4,
  3. Halvor K. Mørk1,4,
  4. Fredrik Swift1,4,
  5. Jan M. Aronsen1,4,
  6. Ivar Sjaastad1,2,4,
  7. Henrik M. Reims3,
  8. Borghild Roald3,
  9. Kristin B. Andersson1,4,
  10. Geir Christensen1,4,
  11. Ole M. Sejersted1,4

Article first published online: 29 JAN 2010

DOI: 10.1113/jphysiol.2009.183517

Issue

The Journal of Physiology

The Journal of Physiology

Volume 588, Issue 3, pages 465–478, February 2010

Additional Information

How to Cite

Louch, W. E., Hougen, K., Mørk, H. K., Swift, F., Aronsen, J. M., Sjaastad, I., Reims, H. M., Roald, B., Andersson, K. B., Christensen, G. and Sejersted, O. M. (2010), Sodium accumulation promotes diastolic dysfunction in end-stage heart failure following Serca2 knockout. The Journal of Physiology, 588: 465–478. doi: 10.1113/jphysiol.2009.183517

Author Information

  1. 1

    Institute for Experimental Medical Research

  2. 2

    Department of Cardiology

  3. 3

    Department of Pathology, Oslo University Hospital Ullevaal, Oslo, Norway

  4. 4

    Centre for Heart Failure Research, Faculty of Medicine, University of Oslo, Oslo, Norway

*Corresponding author W. E. Louch: Institute for Experimental Medical Research, 4.etg. Kirurgisk Bygning, Oslo University Hospital Ullevaal, 0407 Oslo, Norway.  Email: w.e.louch@medisin.uio.no

Publication History

  1. Issue published online: 29 JAN 2010
  2. Article first published online: 29 JAN 2010
  3. (Received 20 October 2009; accepted after revision 5 December 2009; first published online 14 December 2009)

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References

  • Andersson KB, Birkeland JA, Finsen AV, Louch WE, Sjaastad I, Wang Y, Chen J, Molkentin JD, Chien KR, Sejersted OM & Christensen G (2009a). Moderate heart dysfunction in mice with inducible cardiomyocyte-specific excision of the Serca2 gene. J Mol Cell Cardiol 47, 180–187.
  • Andersson KB, Finsen AV, Sjåland C, Winer LH, Sjaastad I, Ødegaard A, Louch WE, Wang Y, Chen J, Chien KR, Sejersted OM & Christensen G (2009b). Mice carrying a conditional Serca2flox allele for the generation of Ca2+ handling-deficient mouse models. Cell Calcium 46, 219–225.
  • Andersson KB, Winer LH, Mork HK, Molkentin JD & Jaisser F (2009c). Tamoxifen administration routes and dosage for inducible Cre-mediated gene disruption in mouse hearts. Transgenic Res DOI: 10.1007/s11248-009-9342-4.
  • Baartscheer A, Schumacher CA & Fiolet JW (1997). Small changes of cytosolic sodium in rat ventricular myocytes measured with SBFI in emission ratio mode. J Mol Cell Cardiol 29, 3375–3383.
  • Baartscheer A, Schumacher CA, Van Borren MM, Belterman CN, Coronel R & Fiolet JW (2003). Increased Na+/H+-exchange activity is the cause of increased [Na+]i and underlies disturbed calcium handling in the rabbit pressure and volume overload heart failure model. Cardiovasc Res 57, 1015–1024.
  • Berry RG, Despa S, Fuller W, Bers DM & Shattock MJ (2007). Differential distribution and regulation of mouse cardiac Na+/K+-ATPase α1 and α2 subunits in T-tubule and surface sarcolemmal membranes. Cardiovasc Res 73, 92–100.
  • Bers DM (2001). Excitation-Contraction Coupling and Cardiac Contractile Force. Kluwer Academic Publishers, Dordrecht , The Netherlands .
  • Bers DM (2006). Altered cardiac myocyte Ca regulation in heart failure. Physiology (Bethesda) 21, 380–387.
  • Brini M (2009). Plasma membrane Ca2+-ATPase: from a housekeeping function to a versatile signalling role. Pflugers Arch 457, 657–664.
  • Campbell AM, Wuytack F & Fambrough DM (1993). Differential distribution of the alternative forms of the sarcoplasmic/endoplasmic reticulum Ca2+-ATPase, SERCA2b and SERCA2a, in the avian brain. Brain Res 605, 67–76.
  • Cheng H, Lederer WJ & Cannell MB (1993). Calcium sparks: elementary events underlying excitation-contraction coupling in heart muscle. Science 262, 740–744.
  • Despa S, Islam MA, Weber CR, Pogwizd SM & Bers DM (2002). Intracellular Na+ concentration is elevated in heart failure but Na/K pump function is unchanged. Circulation 105, 2543–2548.
  • Drummond GB (2009). Reporting ethical matters in The Journal of Physiology: standards and advice. J Physiol 587, 713–719.
    Direct Link:
  • Everts ME, Andersen JP, Clausen T & Hansen O (1989). Quantitative determination of Ca2+-dependent Mg2+-ATPase from sarcoplasmic reticulum in muscle biopsies. Biochem J 260, 443–448.
  • Finsen AV, Christensen G & Sjaastad I (2005). Echocardiographic parameters discriminating myocardial infarction with pulmonary congestion from myocardial infarction without congestion in the mouse. J Appl Physiol 98, 680–689.
  • Hasenfuss G & Pieske B (2002). Calcium cycling in congestive heart failure. J Mol Cell Cardiol 34, 951–969.
  • Hasenfuss G, Schillinger W, Lehnart SE, Preuss M, Pieske B, Maier LS, Prestle J, Minami K, Just H (1999). Relationship between Na+-Ca2+-exchanger protein levels and diastolic function of failing human myocardium. Circulation 99(5), 641–648.
  • Henderson SA, Goldhaber JI, So JM, Han T, Motter C, Ngo A, Chantawansri C, Ritter MR, Friedlander M, Nicoll DA, Frank JS, Jordan MC, Roos KP, Ross RS & Philipson KD (2004). Functional adult myocardium in the absence of Na+-Ca2+ exchange: cardiac-specific knockout of NCX1. Circ Res 95, 604–611.
  • Iwamoto T, Watano T & Shigekawa M (1996). A novel isothiourea derivative selectively inhibits the reverse mode of Na+/Ca2+ exchange in cells expressing NCX1. J Biol Chem 271, 22391–22397.
  • Khan H, Metra M, Blair JE, Vogel M, Harinstein ME, Filippatos GS, Sabbah HN, Porchet H, Valentini G & Gheorghiade M (2009). Istaroxime, a first in class new chemical entity exhibiting SERCA-2 activation and Na-K-ATPase inhibition: a new promising treatment for acute heart failure syndromes? Heart Fail Rev 14, 277–287.
  • Louch WE, Mork HK, Sexton J, Stromme TA, Laake P, Sjaastad I & Sejersted OM (2006). T-tubule disorganization and reduced synchrony of Ca2+ release in murine cardiomyocytes following myocardial infarction. J Physiol 574, 519–533.
    Direct Link:
  • Mork HK, Sjaastad I, Sejersted OM & Louch WE (2009). Slowing of cardiomyocyte Ca2+ release and contraction during heart failure progression in post-infarction mice. Am J Physiol Heart Circ Physiol 296, H1069–H1079.
  • Muller-Ehmsen J, Wang J, Schwinger RH & McDonough AA (2001). Region specific regulation of sodium pump isoform and Na,Ca-exchanger expression in the failing human heart – right atrium vs left ventricle. Cell Mol Biol (Noisy -le-grand) 47, 373–381.
  • Ozdemir S, Bito V, Holemans P, Vinet L, Mercadier JJ, Varro A & Sipido KR (2008). Pharmacological inhibition of Na/Ca exchange results in increased cellular Ca2+ load attributable to the predominance of forward mode block. Circ Res 102, 1398–1405.
  • Pieske B, Maier LS, Piacentino V III, Weisser J, Hasenfuss G & Houser S (2002). Rate dependence of [Na+]i and contractility in nonfailing and failing human myocardium. Circulation 106, 447–453.
  • Pogwizd SM, Schlotthauer K, Li L, Yuan W & Bers DM (2001). Arrhythmogenesis and contractile dysfunction in heart failure: roles of sodium-calcium exchange, inward rectifier potassium current, and residual β-adrenergic responsiveness. Circ Res 88, 1159–1167.
  • Sah R, Ramirez RJ, Oudit GY, Gidrewicz D, Trivieri MG, Zobel C & Backx PH (2003). Regulation of cardiac excitation–contraction coupling by action potential repolarization: role of the transient outward potassium current (Ito). J Physiol 546, 5–18.
    Direct Link:
  • Satoh H, Ginsburg KS, Qing K, Terada H, Hayashi H & Bers DM (2000). KB-R7943 block of Ca2+ influx via Na+/Ca2+ exchange does not alter twitches or glycoside inotropy but prevents Ca2+ overload in rat ventricular myocytes. Circulation 101, 1441–1446.
  • Schwinger RH, Wang J, Frank K, Muller-Ehmsen J, Brixius K, McDonough AA & Erdmann E (1999). Reduced sodium pump α1, α3, and β1-isoform protein levels and Na+,K+-ATPase activity but unchanged Na+-Ca2+ exchanger protein levels in human heart failure. Circulation 99, 2105–2112.
  • Shammas RL, Khan NU, Nekkanti R & Movahed A (2007). Diastolic heart failure and left ventricular diastolic dysfunction: what we know, and what we don't know! Int J Cardiol 115, 284–292.
  • Sossalla S, Wagner S, Rasenack EC, Ruff H, Weber SL, Schondube FA, Tirilomis T, Tenderich G, Hasenfuss G, Belardinelli L & Maier LS (2008). Ranolazine improves diastolic dysfunction in isolated myocardium from failing human hearts – role of late sodium current and intracellular ion accumulation. J Mol Cell Cardiol 45, 32–43.
  • Swift F, Birkeland JA, Tovsrud N, Enger UH, Aronsen JM, Louch WE, Sjaastad I & Sejersted OM (2008). Altered Na+/Ca2+-exchanger activity due to downregulation of Na+/K+-ATPase α2-isoform in heart failure. Cardiovasc Res 78, 71–78.
  • Swift F, Tovsrud N, Enger UH, Sjaastad I & Sejersted OM (2007). The Na+/K+-ATPase α2-isoform regulates cardiac contractility in rat cardiomyocytes. Cardiovasc Res 75, 109–117.
  • Thomas MJ, Sjaastad I, Andersen K, Helm PJ, Wasserstrom JA, Sejersted OM & Ottersen OP (2003). Localization and function of the Na+/Ca2+-exchanger in normal and detubulated rat cardiomyocytes. J Mol Cell Cardiol 35, 1325–1337.
  • Wang Y, Tandan S, Cheng J, Yang C, Nguyen L, Sugianto J, Johnstone JL, Sun Y & Hill JA (2008). Ca2+/calmodulin-dependent protein kinase II-dependent remodelling of Ca2+ current in pressure overload heart failure. J Biol Chem 283, 25524–25532.
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