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Department of Experimental Cardiology, Masonic Medical Research Laboratory, Utica, New York 13501-1787
This study examines the amplitude of sodium-calcium
exchange current (INaCa) in epicardial,
midmyocardial, and endocardial canine ventricular myocytes. Whole cell
currents were recorded at 37°C using standard or
perforated-patch voltage-clamp techniques in the absence of potassium,
calcium-activated chloride, and sodium-pump currents.
INaCa was triggered by release of calcium from the
sarcoplasmic reticulum or by rapid removal of external sodium.
INaCa was large in midmyocardial myocytes and
significantly smaller in endocardial myocytes, regardless of the method
used to activate INaCa. INaCa at 
80 mV was 0.316 ± 0.013, 0.293 ± 0.016, and
0.210 ± 0.007 pC/pF, respectively, in midmyocardial,
epicardial, and endocardial myocytes when activated by the calcium
transient. When triggered by sodium removal, peak
INaCa was 0.74 ± 0.04, 0.57 ± 0.04, and 0.50 ± 0.03 pA/pF, respectively, in midmyocardial, epicardial, and endocardial myocytes. Epicardial INaCa was
smaller than midmyocardial INaCa when activated by
removal of external sodium but was comparable to epicardial and
midmyocardial INaCa when activated by the normal calcium transient, implying possible transmural differences in excitation-contraction coupling. Our results suggest that
INaCa differences contribute to transmural
electrical heterogeneity under normal and pathological states. A large
midmyocardial INaCa may contribute to the prolonged
action potential of these cells as well as to the development of
triggered activity under calcium-loading conditions.
cardiac myocytes; sodium-calcium exchanger; excitation-contraction coupling
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