Parameters in the Hund & Rudy (2004) canine epicardial (epi) cell electrophysiology model were altered to model differences in isolated endocardial (endo), midmyocardial (M) and epi cell current densities and kinetics, Ca²⁺ transients, and action potentials (APs), their duration (APD) and rate dependence. Maximal conductances and fluxes were scaled with respect to epi values according to published experimental estimates: the late Na⁺ current I_Na,L by 1.15 and 1.7 for endo and M cells respectively; the transient outward K⁺ current I_to1 by 0.5 and 1.0; the slow delayed rectifier K⁺ current I_Ks by 0.9 and 0.3; the Na⁺-Ca²⁺ exchanger current I_NaCa by 0.4 and 0.5; and the Ca²⁺ uptake flux J_up by 0.6 and 0.7. The time course of reactivation of I_to1 was modelled by altering the slow inactivation time constant to give values of 390, 456 and 264 ms at –80 mV in endo, M and epi cells, respectively. The activation time constant of the M cell rapid delayed rectifier K⁺ current I_Kr was twice that in epi and endo cells at all membrane potentials. Computed APs (Fig. 1A) quantitatively reproduce experimentally recorded APs and APD rate dependence (Fig. 1B). When the cell models were incorporated into a 15 mm virtual tissue strand composed of equal fractions of endo, M and epi tissue, electrotonic coupling reduces the transmural APD dispersion, prolongs the mean APD by ∼20 ms, and smooths the gradient in APD (Fig. 1C). The conduction velocity of the depolarisation wavefront is approximately constant throughout the strand. The spatial distribution of repolarisation will be reflected in the ECG T wave. The 3D ventricular wall is heterogeneous, rotationally anisotropic and orthotropic. However, the normal sinus rhythm ensures near-synchronous activation of the endocardial surface and so the excitation wavefront throughout the ventricles approximates a transmural plane wave. The 1D strand is therefore a computationally efficient model of the ventricular wall that can be used to study, for example, the transmural effects of anti-arrhythmic drugs (Aslanidi et al. 2004).