A model with which to elucidate the mechanism of Ca 2+ release from, and Ca 2+ loading in the sarcoplasmic reticulum (SR) by Ca 2+ current (I Ca ) in cardiac cells is proposed. The SR is assumed to be comprised of three functional subcompartments: (1) the main calcium store (MCS), which contains most of the calcium (both free and bound); (2) the releasable terminal (RT), which contains the calcium readily available for release; and (3) the longitudinal network of the SR (LSR), which sequesters and the transfers the sarcoplasmic calcium to the RT. A rapid increase of the Ca 2+ concentration at the outer surface of the SR (Ca e ) due to the fast component of I Ca activates and inactivates this surface, inducing the release of Ca 2+ from the RT to the sarcoplasmic space. The RT in turn is further activated and inactivated by a increase in the concentration of sarcoplasmic Ca 2+ . The Ca 2+ in the sarcoplasmic space is then sequestered by the LSR, leading to the reactivation of the RT. Further increase of Ca e due to the slow component of I Ca enhances the entry of Ca 2+ into the MCS to be bound by the binding substance. The free Ca 2+ released from the Ca-binding substance complex is transferred to the RT for subsequent release. The activation, inactivation and reactivation are Ca 2+ -mediated and time-dependent. The proposed model yields simulation of the many events qualitatively similar to those observed experimentally in skinned cardiac cells.