Skip to main content
SpringerLink
Log in
Book cover

Subcellular Basis of Contractile Failure pp 115–134Cite as

Alterations of Membrane Proteins in Cardiac Hypertrophy

  • Chapter

  • 18 Accesses

Part of the book series: Developments in Cardiovascular Medicine ((DICM,volume 116))

Abstract

Hypertrophy of the heart is an adaptive mechanism to an increase in hemodynamic work. During this process, development without multiplication of the cardiac myocytes occurs and new sarcomeres are added to improve the contractility. As shown by Anversa et al. in compensatory hypertrophy of the rat (1,2), the overall result of the membrane development is an increase of the surface area parallel to the degree of hypertrophy which maintains a constant surface/volume ratio. However, some specialized membrane structures undergo a preferential development like the T-tubules (a 107% increase for the T-tubules as compared to a 33% for the sarcolemma (SL)) and the sarcoplasmic reticulum (SR) (a two fold increase). In this review on the membrane proteins of the hypertrophied myocyte, we shall take this into account to estimate their density of the receptors and their total number per myocyte or per left ventricle. We report that three types of regulation occur with enhanced, unchanged or decreased density leading to increased or unchanged total number of membrane proteins.

This is a preview of subscription content, log in via an institution.

Chapter
USD   29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD   129.00
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD   169.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info
Hardcover Book
USD   169.99
Price excludes VAT (USA)
  • Durable hardcover edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Learn about institutional subscriptions

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Anversa P, Loud AV, Giacomelli F, Wiener J. Absolute morphometric study of myocardial hypertrophy in experimental hypertension. Ultrastructure of myocytes and interstitium. Lab Invest 1978, 38: 597–609.

    Article  PubMed  CAS  Google Scholar 

  2. Anversa P, Olivetti G, Melissari M, Loud AV. Morphometric study of myocardial hypertrophy induced by abdominal aortic stenosis. Lab Invest 1979, 40: 341–349.

    PubMed  CAS  Google Scholar 

  3. Lompré AM, Schwartz K, d’Albis A, Lacombe G, Van Thiem N, Swynghedauw B. Myosin isoenzyme redistribution in chronic heart overload. Nature 1979, 282: 105–107.

    Article  PubMed  Google Scholar 

  4. Charlemagne D, Maixent JM, Preteseille M, Lelièvre L. Ouabain binding sites and (Na+, K+)-ATPase activity in rat cardiac hypertrophy. Expression of the neonatal forms. J Biol Chem 1986, 261: 185–204.

    PubMed  CAS  Google Scholar 

  5. Lelièvre W, Maixent JM, Lorente P, Mouas C, Charlemagne D, Swynghedauw B. Prolonged responsiveness to ouabain in hypertrophied rat heart: physiogical and biochemical evidence. Am J Physiol 1986, 250: H 923–931.

    Google Scholar 

  6. Feldman AM, Cates AE, Bristow MR, Van Dop C. Altered expression of a-subunits of G proteins in failing human hearts. J Mol Cell Cardiol 1989, 21: 359–365.

    Article  PubMed  CAS  Google Scholar 

  7. Tanabe T, Beam KG, Powell JA, Numa S. Restoration of excitation-contraction coupling and slow calcium curent in dysgenic muscle by dihydropyridine receptor complementary DNA. Nature 1988, 336: 134–139.

    Article  PubMed  CAS  Google Scholar 

  8. Mikami A, Imoto K, Tanabe T, Niidome T, Mori Y, Takeshima H, Narumiya S and Numa. Primary structure and functional expression of the cardiac dihydropyridine-sensitive calcium channel. Nature 1989, 340: 230–233.

    Article  PubMed  CAS  Google Scholar 

  9. Reuter H. Calcium channel modulation by neurotransmitters, enzymes and drugs. Nature 1983, 301: 569–572.

    Article  PubMed  CAS  Google Scholar 

  10. Yatani A, Codina J, Imoto Y, Reeves JP, Birnbaumer L, Brown AM. A G protein directly regulates mammalian cardiac calcium channels. Science 1987, 238: 1288–1291

    Article  PubMed  CAS  Google Scholar 

  11. Scott RH, Dolphin AC. Activation of a G protein promotes agonist responses to calcium channel ligands. Nature 1987, 330: 760–762.

    Article  PubMed  CAS  Google Scholar 

  12. Hess P, Lansman JB, Tsien RW. Different modes of Ca channel gating behaviour favoured by dihydropyridine Ca agonists and antagonists. Nature 1984, 311: 538–554.

    Article  PubMed  CAS  Google Scholar 

  13. Ten Eick RE, Bassett AL, Robertson LL. Possible electrophysiological basis for decreased contractility associated with myocardial and failure. In “Myocardial hypertrophy and failure”. Alpert NR, ed., New York, Raven press, 1983, pp 245–259.

    Google Scholar 

  14. Chatelain P, Demol D, Roba J. Comparison of [3H] nitrendipine binding to heart membranes of normotensive and spontaneously hypertensive rats. J Cardiov Pharmacol 1984, 6: 220–223.

    Article  CAS  Google Scholar 

  15. Ishii K, Kanro T, Kurobe Y, Ando J. Binding of 3H nitrendipine binding to heart membranes of normotensive and spontaneously hypertensive rats. Eur J Phannacol 1983, 88: 227–228

    Google Scholar 

  16. Mayoux E, Callens F, Swynghedauw B, Charlemagne D. Adaptional process of the cardiac Cat+ channels to pressure overload: biochemical and physiological properties of the dihydropyridine receptors in normal and hypertrophied rat hearts. J Cardiovasc Phannacol 1988, 12: 390–396.

    Article  CAS  Google Scholar 

  17. Primot I, Mayoux E, Oliviero P, Charlemagne D. DHP binding sites in hypertrophied hearts from guinea pig and rat. J Mol Cell Cardiol 1989, 21 ( Suppl. II ) S22.

    Google Scholar 

  18. Sharma V, Butters CA, Bhalla RC. Alterations in the plasma membrane properties of the myocardium of spontaneously hypertensive rats. Hypertension 1986, 8: 583–591.

    PubMed  CAS  Google Scholar 

  19. Dillon JS, Gu XH, Nayler WG. Effect of age and of hypertrophy on cardiac Cat+ antagonist binding sites. J Cardiovasc Pharmacol 1989, 14: 233–240.

    Article  PubMed  CAS  Google Scholar 

  20. Wagner JA, Reynolds IJ, Weisman HF, Dudeck P, Weisfeldt ML, Synder SH. Calcium antagonist receptors in cardiomyopathic hamster: selective increase in heart, muscle brain. Science 1986, 232: 515–518.

    Article  PubMed  CAS  Google Scholar 

  21. Andrawis N, Kuo TH, Giacomelli F. Altered calcium regulation in the cardiac plasma membrane in experimental renal hypertension. J Mol Cell Cardiol 1988, 20: 625–634.

    Article  PubMed  CAS  Google Scholar 

  22. Kleiman RB and Houser SR. Calcium currents in normal and hypertrophied isolated feline ventricular myocytes. Am J Physiol 1988, 255: H1434–H1442.

    PubMed  CAS  Google Scholar 

  23. Keung EC. Calcium current is increased in isolated adult myocytes from hypertrophied rat myocardium. Circ Res 1989, 64: 735–763,.

    Google Scholar 

  24. Mayoux E, Scamps F, Oliviero P, Vassort G, Charlemagne D. Calcium channels in normal and hypertrophied rat heart. J Mol Cell Cardiol 1989, 21 (supp. III) S18.

    Article  Google Scholar 

  25. Callens- El Amrani F, Mayoux E, Mouas C, Ventura-Clapier R, Henzel D, Charlemagne D, Swynghedauw R. Normal responsiveness to external calcium and to calcium channel modifyng agents in hypertrophied rat heart. Physiological and biochemical evidence. Personnal communication.

    Google Scholar 

  26. Tada M, Katz AM. Phosphorylation of the sarcoplasmic reticulum and sarcolemma. Annu Rev Physiol 1982, 44: 401–423.

    Article  PubMed  CAS  Google Scholar 

  27. Dixon RAF, Kobilka BK, Strader DJ, Benovic JL, Dohlman HG, Frielle T, Bolanowski MA, Bennett CD, Rands E, Diehl RE, Mumford RA, Slater EE, Sigal IS, Caron MG, Lefkowitz RJ, Strader CD. Cloning of the gene and cDNA for mammalian ß-adrenergic receptor and homology with rhodopsin. Nature 1986, 321: 75–79.

    Article  PubMed  CAS  Google Scholar 

  28. Bristow MR, Ginsburg R, Minobe W, Cubiccioti RS, Sageman WS, Lurie K, Billingham ME, Harrison DC, Stinson EB. Decreased catecholamine sensitivity and beta-adrenergic receptor density in failing human heart. N Engl J Med 1982, 307: 205–211.

    Article  PubMed  CAS  Google Scholar 

  29. Buxton ILO, Brunton LL. Direct analysis of ß-adrenergic receptor subtypes on intact adult ventricular myocytes of the rat. Circ Res 1985, 56: 126–132.

    PubMed  CAS  Google Scholar 

  30. Hadcock JR, Malbon CC. Down-regulation of 13-adrenergic receptors: agonist-induced reduction in receptor mRNA levels. Proc Nat Acad Sci USA 1988, 85: 5021–5025.

    Article  PubMed  CAS  Google Scholar 

  31. Collins S, Bolanowski A, Caron MG, Lefkowitz R. Genetic regulation of ß adrenergic receptors Annu Rev Physiol 1989, 51: 203–215.

    Article  PubMed  CAS  Google Scholar 

  32. Newman WH, Frankis MB, Webb JG. The inotropic responsiveness of the failing heart In: Abel F, Newman WH, eds Functional aspects of the normal, hypertrophied and failing heart. The Hague: Nijhoff 189–209, 1984.

    Google Scholar 

  33. Brodde, O.E. Cardiac beta-adrenergic receptors. ISI Atlas of Sciences, Pharmacology 1987, 1: 107–112.

    CAS  Google Scholar 

  34. Packer M, Leier CV. Survival in congestive heart failure during treatment with drugs with positive inotropic actions. Circulation 1987, 75: (suppl. IV) 55–63.

    Google Scholar 

  35. Hicks PE, Cavern I, Manoury P, Lefevre-Borg F, Langer SZ: Comparative analysis of beta-1 adrenoreceptor agonist and antagonist potency and selectivity of ciclopmlol, xamoterol and pindolol. J Pharmacol Exp Ther 1987, 242: 1025–1034.

    PubMed  CAS  Google Scholar 

  36. Evans DB. Modulation of cAMP: Mechanism for positive inotropic action. J Cardiovasc Pharmacol 1986, 8 (Suppl 9) S22–S29.

    PubMed  CAS  Google Scholar 

  37. Packer M, Medina N, Yushak M. Hemodynamic and clinical limitations of long-term inotropic therapy with amrinone in patients with severe chronic heart failure. Circulation 1984, 70: 1038–1047.

    Article  PubMed  CAS  Google Scholar 

  38. Kumano K, Upsher ME, Khairallah PA. Beta adrenergic receptor response coupling in hypertrophied hearts. Hypertension 1983, 17: I175–I183.

    Google Scholar 

  39. Upsher ME, Khairallah PA. Beta-adrenergic receptors in rat myocardium during the development and reversal hypertrophy and following chronic infusions of angiotensin II and epinephrine. Arch int Pharmacodyn 1985, 274: 67–79.

    Google Scholar 

  40. Ayobe MH, Tarazi RC. Reversal of changes in myocardial 13 receptors and inotropic responsiveness with regression of cardiac hypertrophy in renal hypertensive rats (RHR). Circ Res 1984, 54: 125–134.

    PubMed  CAS  Google Scholar 

  41. Woodcock EA, Finder JW, Johnston CI. Decreased cardiac adrenergic receptors in deoxycorticosterone-salt and renal hypertensive rats. Circ Res 1979, 45: 560–565.

    PubMed  CAS  Google Scholar 

  42. Chevalier B, Mansier P, Callens F, Swynghedauw B. The beta-adrenergic system is modified in compensatory system of pressure cardiac overlaod in rats: physiological and biochemical evidence. J Cardiovasc Pharmacol 1989, 13: 412–420.

    Article  PubMed  CAS  Google Scholar 

  43. Mansier P, Chevalier B, Mayoux E, Charlemagne D, Olivier L, Callens-El Amrani F, Swynghedauw B. Membrane proteins of the myocytes in cardiac overload. British J Clin Pharmacol sous presse 1989.

    Google Scholar 

  44. Varner DE, Homcy CJ, Sit SP, Manders WT, Vatner SF. Effects of pressure overload, left ventricular hypertrophy on beta-adrenergic receptors, and responsiveness to catecholamines. J Clinical Invest 1984, 73: 1473–1482.

    Article  Google Scholar 

  45. Karliner JSP, Barnes P, Brown M, Dollery C. Chronic heart failure in the guinea pigs increases cardiac al and 13 adrenoreceptors. Eur J Pharmacol 1980, 67: 115–118.

    Article  PubMed  CAS  Google Scholar 

  46. Hammond K, Lennart A, Ransnäs A, Waite JJ, Insel PA. Changes in ß-adrenergic receptors and the as subunit of Gs protein in hearts from pigs with hyperthyroidism, volume overload and after chronic dynamic exercise. J Mol Cell Cardiol 1989, vol 21 suppl II.

    Google Scholar 

  47. Inui M, Saito A, Fleischer S. Purification of the ryanodine receptor and identity with feet structures of junctional terminal cistemae of sarcoplasmic reticulum from fast skeletal muscle. J Biol Chem 1987, 262: 1740–1747.

    PubMed  CAS  Google Scholar 

  48. Campbell KP, Knudson CM, Imagawa T, Leung AT, Sutko JL, Kahl SD, Reynolds Raab C, Mattson L. Identification and characterization of the high affinity [3H] ryanodine receptor of the junctional sarcoplasmic reticulum Ca2+ release channel. J Biol Chem 1987, 262: 6460–6463.

    PubMed  CAS  Google Scholar 

  49. Fabiato A. Calcium-induced release of calcium from the cardiac sarcoplasmic reticulum. Am J Physiol 1983, 245: (Cell Physiol 14) C1–C4.

    PubMed  CAS  Google Scholar 

  50. Ikemoto N. Structure and function of the calcium pump protein of sarcoplasmic reticulum. Ann Rev Physiol 1982, 44: 297–317.

    Article  CAS  Google Scholar 

  51. Mc Lerman DH, Brandl CJ, Korczak B, Green NM. Amino-acid sequence of Calf + Mg2+-dependent ATPase from rabbit muscle sarcoplasmic reticulum, deduced from its complementary DNA sequence. Nature 1985, 316: 696–700.

    Article  Google Scholar 

  52. Brnidl CJ, Green NM, Korczak B, MacLennan DH. Two Cat+ ATPase genes: homologies and mechanistic implications of deduced amino acid sequences. Cell 1986, 44: 597–607.

    Article  Google Scholar 

  53. Brandl CJ, De Leon S, Martin DR, MacLennan DH. Adult forms of the Cat+ ATPase of sarcoplasmic reticulum. J Biol Chem 1987, 262: 3768–3774.

    PubMed  CAS  Google Scholar 

  54. Lytton J, MacLennan DH. Molecular cloning of cDNAs from human kidney coding for two alternatively spliced products of the cardiac Cat+-ATPase gene. J Biol Chem 1988, 263: 15024–15031.

    PubMed  CAS  Google Scholar 

  55. Lecarpentier Y, Martin JL, Gastineau P, Hatt PY. Load dependence of mammalian heart relaxation during cardiac hypertrophy and heart failure. Am J Physiol 1982, 242: H 855–861

    Google Scholar 

  56. Lecarpentier Y, Waldenström A, Clergue M, Chemla D, Oliviero P, Martin JL, Swynghedauw B. Major alterations in relaxation during cardiac hypertrophy induced by aortic stenosis in guinea pig. Circ Res 1987, 61: 107–116.

    PubMed  CAS  Google Scholar 

  57. Gwathmey JK, Copelas L, MacKinnon R, Schoen FJ, Feldman MD, Grossman W, Morgan JP. Abnormal intracellular calcium handling in myocardium from patients with end-stage heart failure. Circ Res 1987, 61: 70–76.

    PubMed  CAS  Google Scholar 

  58. Gwathmey JK, Morgan JP. Altered calcium handling in experimental pressure-overload hypertrophy in the ferret. Circ Res 1985, 57: 836–843.

    PubMed  CAS  Google Scholar 

  59. Alpert NR, Mulieri LA. Increased myothermal economy of isometric force generation in compensated cardiac hypertrophy induced by pulmonary artery constriction in the rabbit. A characterization of heat liberation on normal and hypertrophied right ventricular papillary muscles. Circ Res 1982, 50: 491–500.

    PubMed  CAS  Google Scholar 

  60. Kimura S, Bassett AL, Saida K, Shimizu M and Myerburg RJ. Sarcoplasmic reticulum function in skinned fibers of hypertrophied rat ventricle Am J Physiol 1989, 256: H1006–1011.

    Google Scholar 

  61. Lindenmayer GE, Sordahl LA, Harigaya S, Allen JC, Besch HR Jr, Schwartz A. Some biochemical studies on subcellular systems isolated from fresh recipient human cardiac tissue obtained during transplantation. Am J Cardiol 1971, 27: 277–283.

    Article  PubMed  CAS  Google Scholar 

  62. Ito Y, Suko J, Chidsey CA. Intracellular calcium and myocardial contractility V. calcium uptake of sarcoplasmic reticulum fractions in hypertrophied and failing rabbit hearts. J Mol Cell Cardiol 1974, 6: 237–247.

    Article  PubMed  CAS  Google Scholar 

  63. Suko J, Vogel JHK, Chidsey CA. Intracellular calcium and myocardial contractility. Reduced calcium uptake and ATPase of the sarcoplasmic reticular fraction prepared from chronically failing calf hearts. Circ Res 1970, 27: 235–247.

    PubMed  CAS  Google Scholar 

  64. Heilmann C, Lindl T, Müller W, Pette D. Characterization of cardiac microsomes from spontaneously hypertonic rats. Basic Res Cardiol 1980, 75: 92–96.

    Article  PubMed  CAS  Google Scholar 

  65. Heilmann C, Lindl T, Müller W, Pette D. Characterization of cardiac microsomes from spontaneously hypertonic rats. Basic Res Cardiol 1980, 75: 92–96.

    Article  PubMed  CAS  Google Scholar 

  66. Komuro I, Kurabayashi M, Shibazaki Y, Takaku F, Yazaki Y. Molecular cloning and characterization of Calf- Mg2+ dependent ATPase from rat cardiac sarcoplasmic reticulum. Regulation of its expression by pressure overload and developmental stage. J Clin Invest 1989, 83: 1102–1108.

    Article  PubMed  CAS  Google Scholar 

  67. Nagai R, Zarain-Herzberg A, Brandi CJ, Fujii J, Tada M, Mac Lennan DH, Alpert NR, Peiasamy M. Regulation of myocardial Cat+ ATPase and phospholamban mrna expression in response to pressure overload and thyroid hormone. Proc Natl Acad Sci USA 1989, 86:

    Google Scholar 

  68. Limas CJ, Cohn JN. Defective calcium transport by cardiac sarcoplasmic reticulum in spontaneously hypertensive rats. Circ Res 1977, (suppl I ) I62–I69.

    Google Scholar 

  69. Shull GE, Schwartz A, Lingrel JB. Amino-acid sequence of sequence of the catalytic subunit of the (Na+ + K+) ATPase deduced from a complementary DNA. Nature 1985, 316: 691–695.

    Article  PubMed  CAS  Google Scholar 

  70. Herrera VLM, Emmanuel JR, Ruiz-Opazo N. Isoform-specific modulation of Na+, K+ATPase a subunit isoforms: structural and functional implications. J Cell Biol 1987, 105: 1855–1865.

    Article  PubMed  CAS  Google Scholar 

  71. Orlowski J, Lingrel JB. Tissue-specific and developmental regulation of rat Na, K-ATPase catalytic isoform and subunit mRNAs. J Biol Chem 1988, 263: 10436–10442.

    PubMed  CAS  Google Scholar 

  72. Norgaad A, Bagger JP, Bjerregaard P. Relation of left ventricular function and Na, K-pump concentration in suspected idiopathic dilated cardiomyopathy. Am J Cardiol 1988, 61: 1312–1315.

    Article  Google Scholar 

  73. Panagia V, Michiel DF, Khatter JC. Sarcolemmal alterations in cardiac hypertrophy due to pressure overload in pigs. In function of the heart in normal and pathological states. N sperelakis ed. The Hague. Nijhöff 1983, 268–274.

    Google Scholar 

  74. Makin N, Jasmin G, Beamish RE. Sarcolemmal Na+/Ca2+ exchange during the development of genetically determined cardiomyopathy. Biochim Biophys Acta 1985, 133: 491–497.

    Google Scholar 

  75. Nirasawa Y, Akera T. Pressure-induced cardiac hypertrophy: changes in Nat, K+-ATPase and glycoside actions in cats. European J Pharmacol 1987, 137: 77–83.

    Article  CAS  Google Scholar 

  76. Lee SW, Schwartz A, Adams RJ. Decrease in Nat, K+-ATPase activity and [3H] ouabain binding sites in sarcolemma prepared from hearts of spontaneously hypertensive rats. Hypertension 1983, 5: 682–688.

    PubMed  CAS  Google Scholar 

  77. Dufilho MD, Devynk MA, Beugras JP. Quantitative changes in cardiac Na+,K+-adenosine triphosphatase of spontaneously hypertensive rats. J Cardiovasc Pharm 1984, 6: 273–280.

    Article  Google Scholar 

  78. Grupp G, Grupp IL, Melvin DB. Functional evidence in diseased human heart fibers for multiple sensitivities of the inotropic ouabain receptor Na+,K+-ATPase (NKA). In: AR Liss. Membrane Biophysics HI: Biological transport, New York, AR Liss, 1988: 215–222.

    Google Scholar 

  79. Clough DL, Pamnani MB, Haddy FJ. Decreased myocardial Nat-Kt-ATPase activity in one-kidney, one-clip hypertensive rats. Am J Physiol 1983 245: H244–H251.

    PubMed  CAS  Google Scholar 

  80. Orlowski J, Lingrel JB Regulation of multiple Na,K-ATPase genes in cultured neonatal rat cardiac myocytes. J Mol Cell Cardiol 1989, 21 suppl II.

    Google Scholar 

  81. Herrera VLM, Chobanian AV, Ruiz-Opazo N. Isoform-specific modulation of Nat, K+ATPase a-subunit gene expression in hypertension. Sciences 1988, 241: 221–223.

    Article  CAS  Google Scholar 

  82. Herrera VLM, Ruiz-Opazo N. Na-K-ATPase al ion-transport dysfunction in 2 genetic hypertension. J Mol Cell Cardiol 1989, 21 suppl II.

    Google Scholar 

  83. Charlemagne D, Orlowski J, Oliviero P, Lane L. Expression of Nat/Kt ATPase a and 13 subunit mRNAs in hypertrophied rat heart. J Mol Cell Cardiol 1989, 21 suppl II.

    Google Scholar 

  84. Hanf R, Drubaix I, Marotte F, Lelièvre L. Rat cardiac hypertrophy: altered sodium-calcium exchange activity in sarcolemmal vesicles. FEBS Letters, 1988 236: 145–149.

    Article  PubMed  CAS  Google Scholar 

  85. Will-Shahab L, Küttner I, Warbanow W. Signal transfer in cardiac muscle. Alteration of the ß-adrenoreceptor adenylate cyclase system in the hypertropied myocardium. Biomed Biochim Acta, 1986, 45: 5199-S204.

    Google Scholar 

  86. Robberecht P, Walbroeck M, Nguyen Huu A, Chatelain P, Christophe J. Rat cardiac muscarinic receptors. II. Influence of thyroid status and cardiac hypertrophy. Mol Pharmacol 1982, 21: 589–93.

    PubMed  CAS  Google Scholar 

  87. Rardon D.P., Cefali D.C., Mitchell R.D., Seiler S.M. and Jones L. R. High molecular weight proteins purified from cardiac junctional sarcosplasmic reticulum vesicles are ryanodine-sensitive calcium channels. Circ Res, 1989, 64: 779–789

    PubMed  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

  1. INSERM U 127, Hopital Lariboisière, 41 Bd de la Chapelle, 75010, Paris, France

    D. Charlemagne

Authors
  1. D. Charlemagne
    View author publications

    You can also search for this author in PubMed Google Scholar

Editor information

Borivoj Korecky Naranjan S. Dhalla

Rights and permissions

Reprints and permissions

Copyright information

© 1990 Kluwer Academic Publishers

About this chapter

Cite this chapter

Charlemagne, D. (1990). Alterations of Membrane Proteins in Cardiac Hypertrophy. In: Korecky, B., Dhalla, N.S. (eds) Subcellular Basis of Contractile Failure. Developments in Cardiovascular Medicine, vol 116. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-1513-1_8

Download citation

  • DOI: https://doi.org/10.1007/978-1-4613-1513-1_8

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4612-8813-8

  • Online ISBN: 978-1-4613-1513-1

  • eBook Packages: Springer Book Archive

Publish with us

Policies and ethics

Search

Navigation