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Electrophysiological Studies of Wild-Type and Mutant Na+-Ca2+ Exchange Proteins

  • Larry V. Hryshko
  • Debora A. Nicoll
  • Satoshi Matsuoka
  • Dmitri Levitsky
  • Zhaoping Li
  • James N. Weiss
  • Kenneth D. Philipson
Part of the Developments in Cardiovascular Medicine book series (DICM, volume 168)

Abstract

In cardiac muscle, Na+-Ca2+ exchange is the primary mechanism for transsarcolemmal Ca2+ efflux (for reviews, see [1–3]). The majority of Ca2+ entering through L-type Ca2+ channels during the action potential is removed by this mechanism [4,5]. Recently, it has been postulated that Na+-Ca2+ exchange may also play a role in the Ca2+-induced Ca2+-release mechanism during cardiac contractions [6–8]. That is, Ca2+ entry through reverse Na+-Ca2+ exchange may trigger an additional release of Ca2+ from the sarcoplasmic reticulum. Although the contribution of this mechanism to physiological excitation-contraction coupling has not been unequivocally established [9–11], this postulation raises the possibility that Na+-Ca2+ exchange plays a prominent role in both contraction and relaxation of cardiac muscle.

Keywords

Xenopus Oocyte Exchange Current Exchange Protein Niflumic Acid Transport Site 
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.

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Copyright information

© Kluwer Academic Publishers 1996

Authors and Affiliations

  • Larry V. Hryshko
  • Debora A. Nicoll
  • Satoshi Matsuoka
  • Dmitri Levitsky
  • Zhaoping Li
  • James N. Weiss
  • Kenneth D. Philipson

There are no affiliations available

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