The underlying mechanisms for the electrophysiological abnormalities that develop as a consequence of cirrhosis of the liver have been studied by recording three different K+ currents in mammalian heart tissue. Single myocytes from the atria and ventricles of sham-operated and bile ductligated (BDL) cirrhotic adult rats were current and voltage clamped using standard whole cell methods. In ventricular myocytes from cirrhotic animals, measurements of the current-voltage relationships, voltage dependence of inactivation, and reactivation kinetics of K+ currents showed that the only significant functional changes (within the physiological range of membrane potentials) were decreases in the density of expression of 1) I(t), a Ca(2+)-independent transient outward K+ current, and 2) Isus, a delayed rectifier K+ current. The decreases in I(t) and Isus contribute to the prolonged Q-T interval of the electrocardiogram that has been described in cirrhotic patients. Measurement of K+ currents in atrial myocytes demonstrated that there were no significant differences in any of the K+ current densities between sham and BDL animals, although reactivation kinetics of I(t) were slowed somewhat.