Published online before print April 17, 2003, doi: 10.1161/01.RES.0000071747.61468.7F
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Submitted on February 13, 2003
Revised on April 3, 2003
Accepted on April 3, 2003
Cardiac Submembrane [Na+] Transients Sensed by Na+-Ca2+ Exchange Current
Christopher R. Weber ;
From the Department of Physiology, Loyola University Chicago, Stritch School of Medicine, Maywood, Ill.
* To whom correspondence should be addressed. E-mail: dbers{at}lumc.edu.
Na+ influx via INa during cardiac action potentials can raise bulk [Na+]i by 10 to 15 µmol/L. However, larger rises in submembrane [Na+] ([Na+]sm) local to Na+-Ca2+ exchangers (NCX) could enhance Ca2+ influx via NCX (and Ca2+-induced Ca2+ release). We tested whether INa could increase [Na+]sm, using NCX current (INCX) as a biosensor in rabbit ventricular myocytes (with [Ca2+]i buffered, [Na+]i=10 mmol/L, and other currents blocked). We measured INCX as early as 5 ms after INa. Prior INa activation did not affect INCX at physiological membrane potentials (Em=-100 to +50 mV), but for Em >+50 mV (where INCX is especially sensitive to [Na+]i), INCX shifted outward. At 5 ms and +100 mV, INa shifted INCX outward by 0.23 A/F (corresponding to 
[Na+]sm=0.24 mmol/L). The effect of INa dissipated with a time constant of 
15 ms. Thus, the impact of INa on NCX is almost undetectable at physiological Em and short lived. This suggests that INa effects on excitation-contraction coupling (via outward INCX) are minimal and limited to early during the action potential. However, local [Na+]sm during INa may be 60 times higher than bulk [Na+]i.
Key words: Na+ current • excitation-contraction coupling
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