Demonstration of calcium-activated transient outward chloride current and delayed rectifier potassium currents in Swine atrial myocytes

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 (Ito), ultra-rapid delayed rectifier potassium current (IKur), and rapid and slow delayed rectifier K+ currents (IKr and IKs) 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 Ito was activated upon depolarization voltage steps to between –10 and +60 mV from –50 mV in pig atrial cells, and the Ito was sensitive to the inhibition by the blockade of L-type calcium (Ca2+) current, showed a “bell-shaped” I–V relationship, typical of Ito2 (i.e. ICl.Ca). The Ito2 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. IKur was found in pig atrial myocytes, and the current showed properties of weak inward rectification and use- and frequency-dependent reduction. IKur was resistant to tetraethylammonium, but sensitive to inhibition by 4-aminopyridine (4-AP) (IC50 = 71.7 ± 3.5 μmol/l). In addition, E-4031-sensitive IKr and chromanol 293B-sensitive IKs were observed in pig atrial myocytes. Blockade of Ito2, IKur, IKr or IKs with corresponding blockers significantly prolonged atrial action potentials. These results indicate that Ca2+-activated Ito2, 4-AP-sensitive IKur, E-4031-sensitive IKr, and 293B-sensitive IKs are present in pig atrial myocytes, and these currents play important roles in action potential repolarization of pig atria.