Objective To determine the effect of allitridum on the ultra rapid delayed rectifier potassium current (IKUr) in single rabbit atrial cardiomyocyte, and investigate the mechanism of its anti-atrial arrhythmia. Methods The dual enzymatic method was used to separate single rabbit atrial cardiomyocyte. The drug was applied via extracellular supserfusion, and current was evoked and recorded using Axon MultiClamp 700B amplifier. Results Allitridum at 200μmol/L exerted obvious inhibitory effect on IKUr in normal rabbit atrial cardiomyocyte, and decreased the peak value from (14.5±3.2) to (7.9±1.2)pA/pF (P＜0.01, n＝15). Allitridum also resulted in a decrease in current-voltage curve, and the effect became more significant with the increase of depolarization potential, in a voltage-dependent manner. Allitridum also showed the inhibitory effect on IKUr in a dose-dependent manner, with its IC50 value of 149.6μmol/L. Allitridum caused a significant positive shift of the steady-state activation curve of IKUr, and then delayed the activation, while a markedly negative shift of the steady-state inactivation of IKUr, and so accelerated the inactivation. Furthermore, the drug markedly lengthened the time constants for IKUr recovery from inactivation, and decelerated the re-inactivation after inactivation. It decreased the channel open at many links, and reduced current density. Conclusion Allitridum derived from Chinese herb, garlic bulb, potently blocks IKUr, which might be the underlying cellular electrophysiological mechanism of its therapeutic effect on atrial arrhythmia.