Objective To determine whether Ca2+ activated Cl- current (ICl(Ca)) contributes to the functional remodeling of the failing heart. Methods Whole cell patch-clamp recording technique was employed to record the ICl(Ca) in cardiac myocytes enzymatically isolated from rapidly pacing induced canine failing hearts at room temperature and compared that of the normal hearts (Nor). Results The current density of DIDS (200M) sensitive ICl(Ca) induced by intracellular Ca2+ release trigged by L-type Ca2+ current (ICa,L) was significantly decreased in heart failare (HF) cells compared to Nor cells. At membrane voltage of 20mV, the ICl(Ca) density was 3.02±0.54 pA/pF in Nor (n=6) vs. 1.31±0.25 pA/pF in HF (n=8) cells, (P<0.01), while the averaged ICa,L density did not show difference between two groups. The time constant of current decay of ICl(Ca) was similar in both types of cells. On the other hand, in intra cellular Ca2+ clamped mode, where the [Ca2+]i was maintained at 100nmol/L, ICl(Ca) density be increased significantly in HF cells when the membrane voltage at +30mV or higher. Conclusions Our results suggest that ICl(Ca) density was decreased in pacing induced failing heart but the channel function be enhanced. Impaired Ca2+ handing in HF cells rather than reduced ICl(Ca) channel function itself may have caused this abnormality. The ICl(Ca) density reduction might contribute to the prolongation of action potential in failing heart. The ICl(Ca) channel function up-rugulation is likely to cause cardiac arrhythmia by inducing a delayed after depolarization, when Ca2+ overload occurred in diastolic failing heart cells.