Robust electrophysiological and functional evidence shows the importance of L-type Cav1.3 channels in sinoatrial node pacemaker activity. Genetic ablation or pharmacologic inhibition of Cav1.3 in mice severely reduce pacemaker activity and loss of function in Cav1.3 channels leads to congenital sinoatrial dysfunction in humans. Cav1.3 channels show more hyperpolarised half-activation voltage and faster activation kinetics compared to cardiac excitation-contraction coupling Cav1.2 isoform and Cav1.3-dependent current (ICav1.3) supplies inward current during diastolic depolarisation. However, little is still known about its quantitative contribution in rabbit sinoatrial node cells. Therefore, we developed a 3D computational model of single rabbit sinoatrial node myocytes, starting from previously validated "membrane" and "calcium-clock" models of cardiac pacemaking. In particular, the model includes detailed descriptions of I) Calcium Release Units organization; II) membrane current formulations and III) β-adrenergic signalling cascade. Formulation of ICav1.3 gained from mouse sinoatrial myocytes was included, while the Cav1.2 current was modified so that the sum of the Cav1.2 (ICav1.2) and Cav1.3 (ICav1.3) components would reproduce the original ICaL I/V relationship. Additionally, key ion channels (Cav1.3, Cav1.2, sodium-calcium exchanger and small-conductance calcium-activated potassium channels) were spatially colocalized with Ryanodine receptor channels. A common-pool (0D) version of the model was developed as well by including the Cav1.3 and β-AR cascade formulations in the original Severi-DiFrancesco rabbit sinoatrial single cell model. Numerical simulations show that the mathematical models reproduce basal pacemaker activity, main Action Potential features and cell-wide Calcium Transient features. Further validation was performed against available experimental data on ion channel blocks and autonomic nervous stimulation. In conclusion, we show the relevance of Cav1.3 channels contribution to rabbit sinoatrial activity using a computational model that will allow further highly detailed investigation of pacemaking mechanisms (e.g. β-adrenergic cascade and channel compartmentalization).