Cardiac submembrane Na$^+$ transients sensed by Na$^+$-Ca$^2+$ exchange current.
C. Weber, K. Ginsburg, and D. Bers.
Circ. Res. 92 (9): 950--952 (May 2003)

Na$^+$ influx via INa during cardiac action potentials can raise bulk Na$^+$i by 10 to 15 micromol/L. However, larger rises in submembrane Na$^+$ (Na$^+$sm) local to Na$^+$-Ca$^2+$ exchangers (NCX) could enhance Ca$^2+$ influx via NCX (and Ca$^2+$-induced Ca$^2+$ release). We tested whether INa could increase Na$^+$sm, using NCX current (INCX) as a biosensor in rabbit ventricular myocytes (with Ca$^2+$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 DeltaNa$^+$sm=0.24 mmol/L). The effect of INa dissipated with a time constant of approximately 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 DeltaNa$^+$sm during INa may be 60 times higher than bulk DeltaNa$^+$i.
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