To determine whether Ca~(2+) activated Cl~-current (I_(Cl(Ca))) contributes to the functional remodeling of the failing heart. Methods Whole cell patch-clamp recording technique was employed to record the I_(Cl(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 I_(Cl(Ca)) induced by intracellular Ca~(2+) release trigged by L-type Ca~(2+) current (I_(Ca,L)) was significantly decreased in heart failare (HF) cells compared to Nor cells.At membrane voltage of 20mV,the I_(Cl(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 I_(Ca,L) density did not show difference between two groups.The time constant of current decay of I_(Cl(Ca)) was similar in both types of cells.On the other hand,in intra cellular Ca~(2+) clamped mode,where the [Ca~(2+)]_i was maintained at 100nmol/L,I_(Cl(Ca)) density be increased significantly in HF cells when the membrane voltage at +30mV or higher.Conclusions Our results suggest that I_(Cl(Ca)) density was decreased in pacing induced failing heart but the channel function be enhanced.Impaired Ca~(2+) handing in HF cells rather than reduced I_(Cl(Ca)) channel function itself may have caused this abnormality.The I_(Cl(Ca)) density reduction might contribute to the prolongation of action potential in failing heart.The I_(Cl(Ca)) channel function up-regulation is likely to cause cardiac arrhythmia by inducing a delayed after depolarization,when Ca~(2+) overload occurred in diastolic failing heart cells. To determine whether Ca ~ (2+) activated Cl ~ -current (I_ (Cl (Ca))) contributes to the functional remodeling of the failing heart. Methods Whole cell patch-clamp recording technique was employed to record the I_ (Cl Ca2 +) 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 I_ (Cl (Ca)) induced by intracellular Ca ~ (2+) release trigged by L-type Ca 2+ (I_ (Ca, L)) was significantly decreased in heart failure Cl (Ca) density was 3.02 ± 0.54 pA / pF in Nor (n = 6) vs.1.31 ± 0.25 pA / pF in HF (n = 8) Ca, L) density did not show difference between two groups. The time constant of current decay of I_ (Cl (Ca)) was similar in both types of cells. mode, where the [Ca ~ (2 +)] _ i was maintained at 100nm ol / L, I_ (Cl (Ca)) density be increased significantly in HF cells when the membrane voltage at + 30mV or higher. Conclusions Our results suggest that I_ (Cl (Ca)) density was decreased in pacing induced failing heart but the the (Cl (Ca)) channel function itself may have caused this abnormality. I_ (Cl (Ca)) density reduction contribute contribute to the prolongation of action potential in failing heart. The I_ (Cl (Ca)) channel function up-regulation is likely to cause cardiac arrhythmia by inducing a delayed after depolarization, when Ca ~ (2+) overload occurred in diastolic failing heart cells.