In the human and other mammals, the functioning of the sinoatrial node (SAN) declines with age. A key feature is a slow down in the intrinsic heart rate (i.e., increase of the pacemaking cycle length) (Alings and Bouman, 1993). Experimental data has shown that ageing is associated with both a decrease in the SAN myocyte population (Shiraishi et al., 1992) and a possible reduction in Na+ channel expression (Alings and Bouman, 1993). It is unclear how these changes affect the pacemaker activity of the SAN. In this study, we have constructed an anatomical model of the SAN: a section through the rabbit SAN was discretised (resolution, 35 μm) to generate a two-dimensional discrete lattice model. Each node of the lattice is represented by a model of a SAN or atrial cell as appropriate (Zhang et al., 2000). In the SAN, Cm (cell capacitance) changes from 20 pF in the centre to 65 pF in the periphery and ionic current densities are functions of Cm (Zhang et al., 2000). Each node is electrically connected to its neighbours with a junctional conductance of 25 nS (SAN-SAN or SAN-atrial) or 175 nS (atrial-atrial). In simulations, the electrical connection length (L) at the border between the SAN and atrium varied between 0.4 mm to 2.2 mm. The decrease in myocyte population (nodes made either empty or non-excitable) varied between 5-20 % and was randomly distributed across the SAN tissue. The Na+ current density in the SAN was reduced by 20-100 %. Cycle length was measured as the time interval between two successive action potentials recorded from the atrium. A decrease of 10 % in the SAN myocyte density increased the pacemaking cycle length by 10 % when L=1.0 mm, and 20 % when L= 1.2 mm. Reduction of Na+ current density by 50 % increased the cycle length by 14 % when L=1.0 mm or 1.2 mm. 100 % reduction of Na+ current density did not abolish the pacemaker activity, but caused the SAN to fail to drive the atrium – the phenomenon of SAN exit block. When considered together, myocyte loss and reduction of Na+ current density slowed down the pacemaker activity additively. We conclude that aging induced changes in the SAN myocyte population and SAN Na+ channel density could contribute to the slow down of the pacemaker activity.