We simulated mechanisms that increase Ca²⁺ transients with two models: the Luo-Rudy II model for guinea pig (GP) ventricle (GP model) representing long action potential (AP) myocytes and the rat atrial (RA) model exemplifying myocytes with short APs. The interventions were activation of stretch-gated cationic channels, increase of intracellular Na⁺ concentration ([Na⁺]_i), simulated -adrenoceptor stimulation, and Ca²⁺ accumulation into the sarcoplasmic reticulum (SR). In the RA model, interventions caused an increase of AP duration. In the GP model, AP duration decreased except in the simulated -stimulation where it lengthened APs as in the RA model. We conclude that the changes in the APs are significantly contributed by the increase of the Ca²⁺ transient itself. The AP duration is controlled differently in cardiac myocytes with short and long AP durations. With short APs, an increase of the Ca²⁺ transient promotes an inward current via Na⁺/Ca²⁺-exchanger lengthening the AP. This effect is similar regardless of the mechanism causing the increase of the Ca²⁺ transient. With long APs the Ca²⁺ transient increase decreases the AP duration via inactivation of the L-type Ca²⁺ current. However, L-type current increase (as with -stimulation) increases the AP duration despite the simultaneous Ca²⁺ transient augmentation. The results explain the dispersion of AP changes in myocytes with short and long APs during interventions increasing the Ca²⁺ transients.