The likelihood of developing cardiac arrhythmias increases with age (Priori et al, 2002). The purpose of the present study was to investigate changes in the cellular electrophysiological properties of the senescent myocardium that may predispose the heart to the development of arrhythmias. Single cardiac myocytes were isolated from the mid-myocardial layer of the left ventricular free wall of aged (>7 years) and young (18 month old) sheep euthanased with 200mg.kg^-1 intravenous pentobarbitone. Voltage clamp control was achieved using either the whole cell (for I_K1 measurements) or perforated patch (for action potential measurements) technique with K⁺ based solutions. All experiments were performed at 23^oC. Statistical analysis was performed using either a Students t test or Two Way ANOVA where appropriate.Membrane capacitance increased with age from 157±8 to 211±14pF (n=23-27 cells, P<0.001). Resting membrane potential was unaffected by age (− 74.5±0.8mV in young and −74.7±0.9mV in aged sheep, n=17-19 cells, P>0.4). We have also investigated whether ageing is associated with any change in the properties of I_K1.In aged sheep, I_K1 current density increased, e.g. at −130mV from −3.8±0.4pA.pF^-1 in young sheep to −7.2±0.4pA.pF^-1 in old sheep (n=10-20 cells, P<0.001). The time to peak current development at −130mV accelerated with age from 19.7±2ms (young) to 5.7±1ms (old) (P<0.0001). Furthermore, the apparent extent of inactivation of the current during a 300ms test pulse was greater in cells from aged sheep (12.8±1 vs. 27.5±3%, P<0.0001). Differences in the gating properties of I_K1 were investigated by examining the voltage dependence of channel conductance (gK/gK_max). Neither the membrane potential at which conductance is half-maximal (− 91.7mV in young and −88.2mV in old) or the voltage required to change conductance e-fold (12.3mV in young and 13.2mV in old) altered with age. In summary, ageing is associated with marked alterations in the density and kinetics of the inwardly rectifying potassium channel I_K1 that helps maintain resting membrane potential. The influence of these changes on the arrhythmogenic potential of the myocardium and the molecular determinants of the changes need to be elucidated.