We have developed a model of Ca²⁺ handling in the ferret ventricular myocytes. This model includes a novel L-type Ca²⁺ channel, detailed intracellular Ca²⁺ movements, and graded Ca²⁺-induced Ca²⁺ release (CICR). The model successfully reproduces data from voltage-clamp experiments including the voltage and time dependent changes in [Ca²⁺]_i, I_CaL inactivation and recovery kinetics, and Ca²⁺ sparks. The development of graded CICR is critically dependent on spatial heterogeneity and the physical arrangement of calcium channels in opposition to ryanodine sensitive release channels. The model contains spatially distinct subsystems representing the subsarcolemmal regions where the junctional SR abuts the T-tubular membrane, and where the L-type Ca²⁺ channels and the SR ryanodine receptors (RyRs) are localized. There are 8 different types of subsystem in our model, with between 1 and 8 L-type Ca²⁺ channels distributed binomially. This model exhibits graded Ca²⁺-induced Ca²⁺ release and provides a quantitative description of Ca²⁺ dynamics not requiring Monte-Carlo simulations. Activation of RyRs and release of Ca²⁺ from the SR depends critically on Ca²⁺ entry through L-type Ca²⁺ channels. In turn, Ca²⁺ channel inactivation is critically dependent on release of stored intracellular Ca²⁺. Inactivation of the L-type Ca²⁺ current (I_CaL) depends on both transmembrane voltage and the local [Ca²⁺]_i near the channel, which results in distinctive inactivation properties. The molecular mechanisms underlying many I_CaL gating properties are unclear, but [Ca²⁺]_i dynamics clearly play a fundamental role.