Although alternans of action potential duration (APD) is a robust feature of rapidly paced canine ventricle, currently available ionic models of cardiac myocytes do not recreate this phenomenon. To address this problem, we developed a new ionic model, using formulations of currents based on previous models and recent experimental data. Compared to existing models, I_K1 was decreased at depolarized potentials, the maximum conductance and rectification of I_Kr were increased and I_Kr activation kinetics were slowed. I_Ks was increased in magnitude and activation shifted to less positive voltages and I_Ca was modified to produce a smaller, more rapidly inactivating current. Finally, a simplified form of intracellular calcium dynamics was adopted. In this model, APD alternans occurred at cycle lengths = 150-210 ms, with a maximum alternans amplitude of 39 ms. APD alternans was suppressed by decreasing I_Ca magnitude or calcium-induced inactivation and by increasing the magnitude of I_K1, I_Kr, or I_Ks. These results establish an ionic basis for APD alternans, which should facilitate the development of pharmacological approaches to eliminating alternans.