Article Text

PDF
Late sodium current in the pathophysiology of cardiovascular disease: consequences of sodium–calcium overload
  1. D Noble,
  2. P J Noble
  1. University Laboratory of Physiology, Oxford, UK
  1. Correspondence to:
    Dr Denis Noble
    University Laboratory of Physiology, Parks Road, Oxford OX1 3PT, UK; denis.noble{at}physiol.ox.ac.uk

Abstract

Late sodium current in cardiac cells is very small compared with the fast component, but as it flows throughout the action potential it may make a substantial contribution to sodium loading during each cardiac cycle. Late sodium current may contribute to triggering arrhythmia in two ways: by causing repolarisation failure (early afterdepolarisations); and by triggering late afterdepolarisations attributable to calcium oscillations in sodium–calcium overload conditions. Reduction of late sodium current would therefore be expected to have therapeutic benefits, particularly in disease states such as ischaemia in which sodium–calcium overload is a major feature.

  • EAD, early afterdepolarisation
  • IbNa, sodium background current
  • ICa, L, L-type inward calcium current
  • IKr, rapid delayed potassium current
  • IpNa, persistent sodium current
  • [Na+]i, intracellular sodium concentration

Statistics from Altmetric.com

Footnotes

  • Competing interests: None declared.

Request permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.