In 2003, Small-Conductance of Ca2+-activated K+ channels( SK) are first reported to present in Cardiac myocytes, which is expressed more abundant in the atria compared with the ventricles. Genetic knockout of the SK channels results in the delay in cardiac repolarization and showed inducible atrial fibrillation(AF). The purpose of this study was to confirm whether SK channels are involved in electrical remodeling of human chronic atrial fibrillation (CAF).The ionic currents were recorded using whole-cell Conventional patch clamp techniques(35 appendages from patients with SR and 18 appendages from patients with CAF). SK2 channel protein expressions were assayed by western blot technique(12 appendages from patients with SR and 24 preparations from patients with CAF). Our result indicate that SK channels present in patients atrial with SR Group and CAF Group ,identified it with SK channel blocker apamin (100nmol/L) . SK channels are voltage-independent and inwardly rectifying . The SK channel current densities were significantly increased in CAF(n=24,[Ca2+]i=500nmol/L,p<0.05) compare to SR (n=49, [Ca2+]i=500nmol/L). The increased proportion of SK channel current densities in CAF(n=8,[Ca2+]i=1000nmol/L,p<0.05) were larger than in SR (n=10,[Ca2+]i=1000nmol/L). it manifested that SK is more sensitive to intracellular Ca2+ in CAF than in SR.Western bloting result demonstrated that SK2 protein level is significant decrease in CAF than in SR.Our results showed SK channels present in patients atrial with SR and CAF ;SK channel density in CAF were significantly increase than in SR.In patients with CAF, the SK channels are more sensitive to [Ca2+]i. Compared with SR,the protein level of SK2 was down-regulation in Patients atrial with CAF.these results indicated the increase densities of SK channel in CAF maybe depend on the more sensitive to [Ca2+]i and higher intracellular Calcium level,which lead to increase channels activity ,not by the numbers of channels.It might be one of the treatment targets of patients with Atrial Fibrillation,involving in human atrial electric remodeling in CAF.