Effects of Ba2+ on the K+ currents of guinea pig ventricular muscle were studied using the single sucrose-gap voltage-clamp technique. Ba2+ decreased the late (1- or 2-s) current at any potential level, with stronger suppression in the slope conductance at resting potential level than at depolarized voltages above 0 mV. During depolarizing pulses beyond -40 mV, Ba2+ reduced both the time-dependent and time-independent current components, indicating suppression of both outward and background K+ currents (IK and IK1, respectively), whereas tail currents after repolarization to -40 mV increased, with their time courses having double exponentials. These apparent conflicting results between IK and the tail current could not be explained by extracellular K+ fluctuation, because 20 mM Cs+ alone depressed both factors, but an additional application of Ba2+ caused an increase in both components compared with those in the former condition. On hyperpolarization below -60 mV, a time-dependent decrease in the inward current was observed after Ba2+ application without an activation of If. The decrease was stronger and faster at negative potential levels. These results are compatible with a time- and voltage-dependent blocking action of Ba2+ on the inward rectifier K+ current reported in other cardiac and noncardiac tissues. In two components of the tail currents after repolarization from depolarizing voltage steps during Ba2+ application, the faster one can probably be attributed to this blocking action of IK1, whereas the slower one can be attributed to the deactivation of IK. This time-dependent component of IK1 may contribute to the generation of Ba2+-induced automaticity at the depolarized state.