Cellular electrophysiology is not fully understood in the atrium of pig heart. The objective of the present study was to determine whether transient outward current (I t o ), ultra-rapid delayed rectifier potassium current (I K u r ), and rapid and slow delayed rectifier K + currents (I K r and I K s ) were present in pig atrium. The whole-cell patch technique was applied to record membrane currents and action potentials in myocytes isolated from pig atrium. It was found that an I t o was activated upon depolarization voltage steps to between -10 and +60 mV from -50 mV in pig atrial cells, and the I t o was sensitive to the inhibition by the blockade of L-type calcium (Ca 2 + ) current, showed a ''bell-shaped'' I-V relationship, typical of I t o 2 (i.e. I C l . C a ). The I t o 2 was inhibited by the chloride (Cl - ) channel blocker anthracene-9-carboxylic acid (9-AC, 200 μmol/l) or 4,4'-diisothiocyanostilben-2,2'disulfonic acid (200 μmol/l), and by Cl - substitution in the superfusate. I K u r was found in pig atrial myocytes, and the current showed properties of weak inward rectification and use- and frequency-dependent reduction. I K u r was resistant to tetraethylammonium, but sensitive to inhibition by 4-aminopyridine (4-AP) (IC 5 0 = 71.7 +/- 3.5 μmol/l). In addition, E-4031-sensitive I K r and chromanol 293B-sensitive I K s were observed in pig atrial myocytes. Blockade of I t o 2 , I K u r , I K r or I K s with corresponding blockers significantly prolonged atrial action potentials. These results indicate that Ca 2 + -activated I t o 2 , 4-AP-sensitive I K u r , E-4031-sensitive I K r , and 293B-sensitive I K s are present in pig atrial myocytes, and these currents play important roles in action potential repolarization of pig atria.