I(NaCa) contributes to electrical heterogeneity within the canine ventricle.

This study examines the amplitude of sodium-calcium exchange current (I(NaCa)) in epicardial, midmyocardial, and endocardial canine ventricular myocytes. Whole cell currents were recorded at 37( degrees )C using standard or perforated-patch voltage-clamp techniques in the absence of potassium, calcium-activated chloride, and sodium-pump currents. I(NaCa) was triggered by release of calcium from the sarcoplasmic reticulum or by rapid removal of external sodium. I(NaCa) was large in midmyocardial myocytes and significantly smaller in endocardial myocytes, regardless of the method used to activate I(NaCa). I(NaCa) 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 I(NaCa) was 0.74 +/- 0.04, 0.57 +/- 0.04, and 0.50 +/- 0.03 pA/pF, respectively, in midmyocardial, epicardial, and endocardial myocytes. Epicardial I(NaCa) was smaller than midmyocardial I(NaCa) when activated by removal of external sodium but was comparable to epicardial and midmyocardial I(NaCa) when activated by the normal calcium transient, implying possible transmural differences in excitation-contraction coupling. Our results suggest that I(NaCa) differences contribute to transmural electrical heterogeneity under normal and pathological states. A large midmyocardial I(NaCa) may contribute to the prolonged action potential of these cells as well as to the development of triggered activity under calcium-loading conditions.