β-adrenergic stimulation increases the heart rate by accelerating the electrical activity of the pacemaker of the heart, the sinoatrial node (SAN). Ionic mechanisms underlying the actions of β-adrenergic stimulation are not clear yet. Isoprenaline (ISO), a β-agonist, shifts the If activation curve to more positive potentials resulting in an increase of If, which has been suggested to be the main mechanism underlying the effect of β-adrenergic stimulation. However, ISO has been found to increase firing rate of rabbit SAN cells when If is blocked. ISO also increases ICa,L, Ist, IKr and IKs. Recently, ISO has also been reported to shift the activation curve of IKr to more negative potentials, increase the rate of its deactivation and increases the intracellular Ca2+ transient, which can also contribute to chronotropy. The aim of this study was to analyse the ionic mechanisms underlying the chronotropy of β-adrenergic stimulation using two distinct and well established computational models of the electrical activitiy of rabbit SAN cells. We modified the Zhang et al. (2000) and Kurata et al. (2008) models of the electrical activity for the central and peripheral rabbit SAN cells by incorporating equations for the known dose-dependent actions of ISO on various ionic channel conductances (ICa,L, Ist, IKr and IKs), kinetics of IKr and If, and the intracellular Ca2+ transient. These equations were constructed from experimental data. To investigate the ionic basis of the effects of ISO, we measured the chronotropic effect of a range of ISO concentrations when ISO exerted all its actions or just a subset of them. In both the Zhang et al. and Kurata et al. SAN models, the chronotropic effect of ISO is shown to be an integrated action of ISO on ICa,L, If, Ist, IKr and IKs, among which an increase in the rate of deactivation of IKr plays a relatively more important role, though the effect of ISO on [Ca2+]i also plays a significant role.