We used intracellular microelectrodes to study the electrophysiological effects of low barium concentrations (1--4 x 10(-5) M) on sheep cardiac Purkinje fibers. The main effect of barium was an increase in action potential duration (APD) both at -60 mV (APD-60) and at 100% repolarization (APD100). The prolongation of APD was greater at a lower (30/min) than at a higher driving rate (120/min). Barium significantly modified the normal linear relationship between driving rate and APD. The effects of barium on APD were enhanced by lowering [K+]0 and antagonized by increasing [Ca2+]0. Barium caused a slowing of phase 3 repolarization, a steepening of diastolic depolarization and induced spontaneous activity in the resting potential range during the interruption of the drive. The first spontaneous action potential was usually preceded by an oscillatory potential. By means of several procedures (lowering [K+]0, increasing [Ca2+]0, increasing the driving rate) it was possible to identify two separate mechanism underlying the initiation of spontaneous activity: (1) enhancement of normal diastolic depolarization and (2) induction of oscillatory afterpotentials. Finally, barium induced repetitive activity through early afterdepolarizations. We conclude that in Purkinje fibers low barium concentrations cause a lengthening of APD and can induce spontaneous activity by means of at least three different mechanisms. The main factor underlying the barium effects seems to be a reduction in potassium conductance.