The effect of acidosis on the electrical activity of isolated rat atrial myocytes was investigated using the patch clamp technique. Reducing the pH of the bathing solution from 7.4 to 6.5 shortened the action potential. Acidosis had no significant effect on transient outward or inward rectifier currents, but increased steady-state outward current. This increase was still present, although reduced, when intracellular Ca²⁺ was buffered by BAPTA; BAPTA also inhibited acidosis-induced shortening of the action potential. 5 mM Ni²⁺ had no significant effect on the acidosis-induced shortening of the action potential. Acidosis also increased inward current at -80 mV and depolarised the resting membrane potential. Acidosis activated an inwardly rectifying Cl^- current that was blocked by DIDS, which also inhibited the acidosis-induced depolarisation of the resting membrane potential. It is concluded that an acidosis-induced increase in steady-state outward K⁺ current underlies the shortening of the action potential and that an acidosis-induced increase in inwardly rectifying Cl^- current underlies the depolarisation of the resting membrane potential during acidosis.