Skip to main content

Gap Junctions: Functional Effects of Molecular Structure and Tissue Distribution

  • Chapter
Analytical and Quantitative Cardiology

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 430))

Abstract

Abnormal conduction is fundamental to the pathogenesis of both atrial fibrillation and ventricular tachycardia/fibrillation. Normal atrial and ventricular myocytes express different combinations of multiple gap junction channel proteins and are interconnected by gap junctions in markedly different spatial distributions. These observations suggest that the disparate anisotropic conduction properties of atrial and ventricular muscle are determined, in part, by both structural and molecular features of gap junctions. Alterations in gap junctional coupling likely contribute to conduction abnormalities underlying reentrant atrial or ventricular arrhythmias.

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

Access this chapter

Chapter
USD 29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD 39.99
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD 54.99
Price excludes VAT (USA)
  • Compact, lightweight 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

Institutional subscriptions

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Page E. Cardiac gap junctions. In: The Heart and Cardiovascular System (Fozzard HA, Haber E, Jennings RB, Katz AM, Morgan HE, eds). New York: Raven Press, 1992;1003–1047.

    Google Scholar 

  2. Makowski L, Caspar DL, Phillips WC, Goodenough DA. Gap junction structure: analysis of X-ray diffraction data. J Cell Biol 1977;74:629–645.

    Article  PubMed  CAS  Google Scholar 

  3. Beyer EC, Goodenough DA, Paul DL. Connexin family of gap junction proteins. J Membr Biol 1990;116:187–194.

    Article  PubMed  CAS  Google Scholar 

  4. Kanter HL, Saffitz JE, Beyer EC. Cardiac myocytes express multiple gap junction proteins. Circ Res 1992;70:438–444.

    Article  PubMed  CAS  Google Scholar 

  5. Davis LM, Kanter HL, Beyer EC, Saffitz JE. Distinct gap junction protein phenotypes in cardiac tissues with disparate conduction properties. J Am Coll Cardiol 1994;24:1124–1132.

    Article  PubMed  CAS  Google Scholar 

  6. Veenstra RD. Size and selectivity of gap junction channels formed from different connexins. J Bioenergetics Biomembranes 1996;28:317–337.

    Article  Google Scholar 

  7. Dillon SM, Allessie MA, Ursell PC, Wit AL. Influences of anisotropic tissue structure and reentrant circuits in the epicardial border zone of subacute canine infarcts. Circ Res 1988;63:182–206.

    Article  PubMed  CAS  Google Scholar 

  8. Veenstra RD, Wang H-Z, Beyer EC, Brink PR. Selective dye and ionic permeability of gap junction channels formed by connexin45. Circ Res 1994;75:483–490.

    Article  PubMed  CAS  Google Scholar 

  9. Moreno AP, Saez JC, Fishman GI, Spray DC. Human connexin43 gap junction channels. Regulation of unitary conductances by phosphorylation. Circ Res 1994;74:1050–1057.

    Article  PubMed  CAS  Google Scholar 

  10. Hoyt RH, Cohen ML, Saffitz JE. Distribution and three-dimensional structure of intercellular junctions in canine myocardium. Circ Res 1989;64:563–574.

    Article  PubMed  CAS  Google Scholar 

  11. Luke RA, Saffitz JE. Remodeling of ventricular conduction pathways in healed canine infarct border zones. J Clin Invest 1991;87:1594–1602.

    Article  PubMed  CAS  Google Scholar 

  12. Severs NJ. The cardiac gap junction and intercalated disk. Int J Cardiol 1990;26; 137–173.

    Article  PubMed  CAS  Google Scholar 

  13. Saffitz JE, Kanter HL, Green KG, Tolley TK, Beyer EC. Tissue-specific determinants of anisotropic conduction velocity in canine atrial and ventricular myocardium. Circ Res 1994;74:1065–1070.

    Article  PubMed  CAS  Google Scholar 

  14. Kanter HL, Beyer EC, Green KG, Saffitz JE. Multiple connexins colocalize in canine cardiac myocyte gap junctions. Circ Res 1993;74:344–350.

    Article  Google Scholar 

  15. Bastide B, Neyses L, Ganten D, Paul M, Willecke F, Traub O. Gap junction protein connexin40 is preferentially expressed in vascular endothelium and conductive bundles of rat myocardium and is increased under hypertensive conditions. Circ Res 1993;73:1138–1149.

    Article  PubMed  CAS  Google Scholar 

  16. Chen S, Davis LM, Westphale EM, Beyer EC, Saffitz JE. Expression of multiple gap junction proteins in human fetal and infant hearts. Ped Res 1994;36:561–566.

    Article  CAS  Google Scholar 

  17. Spach MS, Miller WT III, Geselowitz DB, Barr RRC, Kootsey JM, Johnson EA. The discontinuous nature of propagation in normal canine cardiac muscle: evidence for recurrent discontinuities of intracellular resistance that affect the membrane currents. Circ Res 1981;48:39–54.

    Article  PubMed  CAS  Google Scholar 

  18. Reaume AG, de Sousa PA, Kulkarni S, Langille BL, Zhu D, Davies TC, Jeneja SC, Kidder GM, Rossant J. Cardiac malformation in neonatal mice lacking connexin43. Science 1995;267:1831–1834.

    Article  PubMed  CAS  Google Scholar 

  19. Guerrero PA, Schuessler RB, Beyer EC, Saffitz JE. Mice heterozygous for a Cx43 null mutation exhibit a conduction defect. Circulation 1996;94:1–8.

    Article  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Editor information

Editors and Affiliations

Rights and permissions

Reprints and permissions

Copyright information

© 1997 Springer Science+Business Media New York

About this chapter

Cite this chapter

Saffitz, J.E. (1997). Gap Junctions: Functional Effects of Molecular Structure and Tissue Distribution. In: Sideman, S., Beyar, R. (eds) Analytical and Quantitative Cardiology. Advances in Experimental Medicine and Biology, vol 430. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5959-7_25

Download citation

  • DOI: https://doi.org/10.1007/978-1-4615-5959-7_25

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4613-7731-3

  • Online ISBN: 978-1-4615-5959-7

  • eBook Packages: Springer Book Archive

Publish with us

Policies and ethics