© 2000 American Heart Association, Inc.
Editorial |
Na+-Ca2+ Exchange in Failing Myocardium
Friend or Foe?
From the Division of Cardiology, University of Utah Health Sciences Center, Salt Lake City, Utah.
Correspondence to William H. Barry, MD, University of Utah Health Sciences Center, Division of Cardiology, 50 North Medical Dr, Salt Lake City, UT 84132. E-mail whbarry@med.utah.edu
Key Words: myocardium • Na+-Ca2+ exchange • sarcoplasmic reticulum
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Introduction |
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The Na+-Ca2+ exchanger (NCX) is a cation transporting protein present in the plasma membrane of animal cells. NCX transports three Na+ in exchange for one Ca2+ and thus is electrogenic; the function of the exchanger is controlled by the gradients for Na+ and Ca2+ across the cell membrane and membrane potential.1 In normal cardiac myocytes, NCX plays an important role in Ca2+ homeostasis. NCX functions in a forward mode, in which Na+ enters the cell and Ca2+ is extruded. The rate of Ca2+ extrusion by NCX is much greater than by the sarcolemmal Ca2+ pump,2 and Bridge et al3 have shown that NCX extrudes the amount of Ca2+ that enters the cell via the L-type Ca2+ channel as Ca2+ current, thus maintaining Ca2+ homeostasis on a beat-to-beat basis. As NCX extrudes Ca2+ and thus lowers Ca2+ from its peak, it contributes to relaxation in parallel with Ca2+ uptake by the sarcoplasmic reticulum (SR) Ca2+-ATPase.4 The extent to which NCX contributes to the decline of the Ca2+ transient varies between species,5 because the relative balance between the activities of these two Ca2+ removal systems is influenced by their level of expression, the [Na+]i, and the duration of the action potential. In rats and mice, which have a high level of activity of the SR Ca2+-ATPase and a relatively high [Na+]i, NCX is responsible for only
10% of relaxation. In rabbits, which have a
lower [Na+]i and SR
Ca2+-ATPase activity, NCX contributes more
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