To explore the ionic basis of the strengthening effect of intermittent hypoxic adaptation (IHA) on the electric stability of heart, the effects of intermittent hypoxia on the transient outward current (Ito) in rat ventricular myocytes were investigated by using whole-cell patch-clamp recording techniques. After 28-day (H28) exposure (6 h/d) to intermittent hypoxia, the density of Ito in the right, but not in the left, ventricular myocytes was dramatically increased as compared with the normoxia control (16.18 +/- 4.61 vs 6.32 +/- 1.35 pA/pF, P < 0.05), while the Ito density of the myocytes isolated from both sides of ventricles in 42-day-exposure group (H42) did not show significant difference. Except for a more negative shift of the steady-state inactivation curves (half-inactivation voltages: -38.9 +/- 2.3 vs -32.8 +/- 5.9 mV in the left ventricle and -41.9 +/- 4.5 vs -33.5 +/- 3.5 mV in the right ventricle) in the H42 group, all the other parameters for activation, inactivation and recovery kinetics of Ito of each group remained unchanged. It is speculated that the change in the current density of Ito may be responsible for the different hemodynamic responses of the ventricles to the early stage of hypoxia. The alteration in inactivation may participate in the cardioprotective effect of IHA.