Individual ion channels or exchangers are described with a common set of equetions for both the sinoatrial node pacemaker and ventricular cells. New experimental data are included, such as the new kinetics of the inward rectifier K⁺ channel, delayed rectifier K⁺ channel, and sustained inward current. The gating model of Shirokov et al. (J Gen Physiol 102: 1005–1030, 1993) is used for both the fast Na⁺ and L-type Ca²⁺ channels. When combined with a contraction model (Negroni and Lascano: J Mol Cell Cardiol 28: 915–929, 1996), the experimental staircase phenomenon of contraction is reconstructed. The modulation of the action potential by varying the external Ca²⁺ and K⁺ concentrations is well simulated. The conductance of I_CaL dominates membrane conductance during the action potential so that an artificial increase of I_to, I_Kr, I_Ks, or I_KATP magnifies I_CaL amplitude. Repolarizing current is provided sequentially by I_Ks, I_Kr, and I_K1. Depression of ATP production results in the shortening of action potential through the activation of I_KATP. The ratio of Ca²⁺ released from SR over Ca²⁺ entering via I_CaL (Ca²⁺ gain = ∼15) in excitation-contraction coupling well agrees with the experimental data. The model serves as a predictive tool in generating testable hypotheses.