Endogenous oxytocin is known to produce a range of physiological actions through its G-protein-coupled receptor (Gimpl & Farenholz, 2001). Due to its uterotonic effects, oxytocin is also given clinically as an intravenous bolus to minimise bleeding during surgical curettage; it has recently been associated with prolongation of the QT interval of the electrocardiogram when given in this fashion (Charbit et al. 2004). Therefore, the present study was conducted to determine whether or not oxytocin exerts a direct modulatory effect on ventricular cardiomyocyte electrophysiology. Guinea-pigs were humanely killed and ventricular myocytes isolated from the hearts by enzymatic and mechanical dispersion. Recordings were made from ventricular myocytes using the whole-cell patch-clamp recording technique at 37°C (pipette dialysate was potassium-based except for sodium-calcium exchange current measurements). Isolated cells were superfused with a standard Tyrode solution, and with Tyrode solution to which oxytocin (10nM) was added. Application of oxytocin resulted in a prolongation of action potential duration at 90% repolarisation (APD₉₀) by 10.4 ± 2.1% (mean ± S.E.M.; n = 7 cells). Under whole cell voltage-clamp, oxytocin was seen to increase amplitude of L-type calcium current (I_Ca,L) at +10 mV by 40.1 ± 8.4% (n = 6 cells). Sodium-calcium exchange current (I_NaCa) was measured as Ni-sensitive difference current during a voltage-ramp protocol, under conditions in which overlapping currents were inhibited (e.g. Zhang et al. 2001). Oxytocin augmented both inward and outward I_NaCa (current at +60 mV was increased by 57.4 ± 14.6%; n= 5 cells). These findings demonstrate that oxytocin can modulate ventricular APD₉₀, I_Ca,L and I_NaCa.