Advertisement

Cardiac Action Potentials, Ion Channels, and Gap Junctions

  • Jacques M. T. de Bakker
  • Harold V. M. van Rijen
Chapter

Abstract

Interplay between various ion channels in the membrane of cardiomyocytes is responsible for depolarization and repolarization of the heart cells, whereas cell-to-cell coupling, mediated by gap junction proteins, is involved in propagation of the action potential through the heart. In this chapter, the different phases of the action potential of heart cells are discussed and the role and characteristics of the most important ion channels that are active during these phases are conferred. Differences in the expression of the various ion and gap junction channels under normal conditions are described. Also discussed are changes in ion and gap junction channel expression and distribution that occur in cardiac disease. Finally, the role of ligand-gated and stretch-activated ion channels is addressed briefly.

Keywords

Sodium Channel Action Potential Duration Sodium Current Plateau Phase Arrhythmogenic Right Ventricular Cardiomyopathy 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

References

  1. 1.
    Noble D. The Initiation of the Heart Beat, second edition. Oxford: Clarendon Press, 1979.Google Scholar
  2. 2.
    Kanno S, Saffitz JE. The role of myocardial gap junctions in electrical conduction and arrhythmogenesis. Cardiovasc Pathol 2001; 10:169–77.PubMedCrossRefGoogle Scholar
  3. 3.
    Boron WF, Boulpaep EL. Medical Physiology: A Cellular and Molecular Approach, second edition. Philadelphia: Elsevier/Saunders, 2009.Google Scholar
  4. 4.
    Hille B. Ion Channels of Excitable Membranes, third edition, Sunderland: Sinauer Associates Inc., 2001Google Scholar
  5. 5.
    Marban E, Yamagishi T, Tomaselli GF. Structure and function of voltage-gated sodium channels. J Physiol 1998; 508:647–57.PubMedCrossRefGoogle Scholar
  6. 6.
    Bennett PB, Shin HG. Biophysics of cardiac sodium channels. In: Zipes DP, Jalife J, editors. Cardiac Electrophysiology from Cell to Bedside, third edition. Philadelphia: WB Saunders Company, 1999:67–78.Google Scholar
  7. 7.
    van Veen TA, Stein M, Royer A, et al. Impaired impulse propagation in Scn5a-knockout mice: combined contribution of excitability, connexin expression, and tissue architecture in relation to aging. Circulation 2005; 112:1927–35.PubMedCrossRefGoogle Scholar
  8. 8.
    Balke CW, Marban E, O’Rourke B. Calcium channels: structure, function and regulation. In: Zipes DP, Jalife J, editors. Cardiac Electrophysiology from Cell to Bedside, third edition. Philadelphia: WB Saunders Company, 1999:8–21.Google Scholar
  9. 9.
    Snyders DJ. Structure and function of cardiac potassium channels. Cardiovasc Res 1999; 42: 377–90.PubMedCrossRefGoogle Scholar
  10. 10.
    Calloe K, Cordeiro JM, Di Diego JM, et al. A transient outward potassium current activator recapitulates the electrocardiographic manifestations of Brugada Syndrome. Cardiovasc Res 2009; 81(4):686–94.PubMedGoogle Scholar
  11. 11.
    Zareba W, Cygankiewicz I. Long QT syndrome and short QT syndrome. Prog Cardiovasc Dis 2008; 51:264–78.PubMedCrossRefGoogle Scholar
  12. 12.
    Fedida D, Eldstrom J, Hesketh JC, et al. Kv1.5 is an important component of repolarizing K+ current in canine atrial myocytes. Circ Res 2003; 93:744–51.PubMedCrossRefGoogle Scholar
  13. 13.
    Tristani-Firouzi M, Chen J, Mitcheson JS, et al. Molecular biology of K(+) channels and their role in cardiac arrhythmias. Am J Med 2001; 110:50–9.PubMedCrossRefGoogle Scholar
  14. 14.
    Taggart P, Lab M. Cardiac mechano-electric feedback and electrical restitution in humans. Prog Biophys Mol Biol 2008; 97:452–60.PubMedCrossRefGoogle Scholar
  15. 15.
    Viswanathan PC, Rudy Y. Cellular arrhythmogenic effects of congenital and acquired long-QT syndrome in the heterogeneous myocardium. Circulation 2000; 101:1192–8.PubMedCrossRefGoogle Scholar
  16. 16.
    Tomaselli GF, Marban E. Electrophysiological remodeling in hypertrophy and heart failure. Cardiovasc Res 1999; 42:270–83.PubMedCrossRefGoogle Scholar
  17. 17.
    Näbauer M, Beuckelmann DJ, Erdmann E. Characteristics of transient outward current in human ventricular myocytes from patients with terminal heart failure. Circ Res 1993; 73: 386–94.PubMedCrossRefGoogle Scholar
  18. 18.
    Dhein S. Cardiovascular Gap Junctions. Basel: Karger, 2006.Google Scholar
  19. 19.
    van Rijen HV, Eckardt D, Degen J, et al. Slow conduction and enhanced anisotropy increase the propensity for ventricular tachyarrhythmias in adult mice with induced deletion of connexin43. Circulation 2004; 109:1048–55.PubMedCrossRefGoogle Scholar
  20. 20.
    Van Rijen HVM, van Veen AB, van Kempen MJA, et al. Impaired conduction in the bundle branches of mouse hearts lacking the gap junction protein connexin40. Circulation 2001; 103: 1591–8.PubMedCrossRefGoogle Scholar
  21. 21.
    Kreuzberg MM, Schrickel JW, Ghanem A, et al. Connexin30.2 containing gap junction channels decelerate impulse propagation through the atrioventricular node. Proc Natl Acad Sci U S A 2006; 103:5959–64.PubMedCrossRefGoogle Scholar
  22. 22.
    Shaw RM, Rudy Y. Ionic mechanisms of propagation in cardiac tissue. Roles of the sodium and L-type calcium currents during reduced excitability and decreased gap junction coupling. Circ Res 1997; 81:727–41.PubMedCrossRefGoogle Scholar
  23. 23.
    Rohr S, Kucera JP, Fast VG, et al. Paradoxical improvement of impulse conduction in cardiac tissue by partial cellular uncoupling. Science 1997; 275:841–4.PubMedCrossRefGoogle Scholar
  24. 24.
    Elenes S, Martinez AD, Delmar M, et al. Heterotypic docking of Cx43 and Cx45 connexons blocks fast voltage gating of Cx43. Biophys J 2001; 81:1406–18.PubMedCrossRefGoogle Scholar
  25. 25.
    Beauchamp P, Yamada KA, Baertschi AJ, et al. Relative contributions of connexins 40 and 43 to atrial impulse propagation in synthetic strands of neonatal and fetal murine cardiomyocytes. Circ Res 2006; 99:1216–24.PubMedCrossRefGoogle Scholar
  26. 26.
    Severs NJ, Coppen SR, Dupont E, et al. Gap junction alterations in human cardiac disease. Cardiovasc Res 2004; 62:368–77.PubMedCrossRefGoogle Scholar
  27. 27.
    Poelzing S, Rosenbaum DS. Altered connexin43 expression produces arrhythmia substrate in heart failure. Am J Physiol Heart Circ Physiol 2004; 287:H1762–70.PubMedCrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media, LLC 2010

Authors and Affiliations

  • Jacques M. T. de Bakker
    • 1
  • Harold V. M. van Rijen
  1. 1.Department of Experimental CardiologyAcademic Medical CenterAmsterdamThe Netherlands

Personalised recommendations