To study the role of calcium dependent currents in regulation of the action potential (AP) duration in short and long action potential cardiac myocytes, we simulated the effect of known mechanisms producing positive inotropy with two models: the Luo-Rudy II model for guinea pig ventricle (GP-model) representing long AP myocytes and the rat atrial model (RA-model) as exemplifying myocytes with short APs. The specific interventions useed were 1) activation of stretch-gated cationic channels, 2) increase of [Na⁺]_i , 3) simulated ß-adrenoceptor stimulation, and 4) calcium accumulation into the SR. These all caused an augmentation of the calcium transients in both model cells. In the RA-model all of these interventions caused an increase of the AP duration, whereas in the GP model the AP duration decreased in all but with the simulated ß-stimulation it produced AP lengthening as in the AP model. Based on the simulations we conclude that regardless of which of the above mechanisms was promoting changes in the calcium transient, the change in the shape of APs is significantly contributed by the increase of the calcium transient itself. The results also implicated that the AP duration is controlled differently in cardiac myocytes with short and long AP duration during inotropic interventions. In myocytes with short APs, an increase of the calcium transient promotes an inward current via Na⁺/Ca²⁺ -exchanger which lengthens the AP. This effect is similar regardless of the mechanism causing the increase of the calcium transient. In myocytes with long AP the calcium transient increase as such decreases the AP duration via calcium-dependent inactivation of the L-type calcium current. However, L-type current increase (as with ß-stimulation) is likely to increase the AP duration despite of the simultaneous calcium transient augmentation. The modelling and simulations explain the evident dispersion of AP changes in myocytes with short and long AP during inotropic interventions that increase the calcium transients.