Objective To investigate the effects of sodium tanshinoneⅡA sulfonate (STS) on rapidly activating component of delayed rectifier K current (IKr) in sinoatrial node cells (SNCs) from neonatal rats. Methods The SNCs were isolated and cultured from the sinus node tissues derived from neonatal rats (＜24 hours old) by enzymatic dispersion with differential attachment as well as 5’-bromodeoxyufidine (5-BrdU). IKr currents in the STS treated cells were measured by whole-cell configuration with patch-clamp technique. Results The frequency of SNCs beat was significantly increased by 30μmol/L STS, from (157.2±10.3) to (268.1±12.6) times/min. This dose of STS induced the current densities of IKr,tail increased from (54.6±4.7) to (86.3±8.3) pA/pF (n＝10, P＜0.01). IKr,tail was excited by 1 to 100μmol/L STS in a dose-dependent fashion, with a half maximal effective concentration (EC50) of (29.3±1.02)μmol/L and Hill coefficient of 1.05. Investigation of gating mechanism showed that the effect was associated with the increase of STS concentration enhancing the steady-state activation and the recovery of inactivation of IKr,tail currents in SNCs, but hade little effect on the steady-state inactivation of IKr. Conclusion STS improves the densities of IKr, and then shortens repolarization duration and enhances pulse frequency of SNCs.