Aim To study the effects of simvastatin on L-type calcium current and Cav1.2 protein levels in atrial myocytes of rats with diastolic heart failure. Methods 30 SD rats were randomly divided into 3 groups: control group, DHF group, Simvastatin group. DHF model was produced by abdominal aortic coarctation in the rats in the operating group. The rats in Simvastatin group were given with Simvastatin 2 mg/(kg·d) by intragastric administration for 4 weeks, the others were treated with equal isotonic Na chloride. After 4 weeks, hemorheology was assessed by catheterization. Single atrial myocytes were isolated by enzymatic dissociation and L-type calcium current were investigated using a whole-cell patch-clamp technique. The expression levels of ICa-L alpha-subunit (Cav1.2) in atrial myocytes were measured by Western-blot analysis. Results (1) Compared with control group, DHF rats exhibited increases in LVSP, LVEDP and Tau. They also showed a decrease in -dp/dtmax. Compared with DHF group, LVSP, LVEDP and Tau were decreased and -dp/dtmax was increased in Simvastatin group. There were no differences in heart rate, the maximum ascendsus ratio for +dp/dtmax and Cm among three groups. (2) Compared with control group, the peak densities of atrial ICa-L in DHF group were decreased, while activation curves, inactivation curves and recovery curves were not altered. Compared with the DHF group, Simvastatin increased the peak density of atrial ICa-L and made the inactivation curves shift to more positive potentials in DHF rats, but did not change activation curves and recovery curves. (3) Campared with control group, DHF rats exhibited decreases in the protein levels of Cav1.2 in atrial myocytes. Simvastatin increased Cav1.2 protein levels in atrial myocytes in DHF rats. Conclusion Simvastatin increases the peak density of atrial ICa-L in DHF rats and the effects are related with the increases in Cav1.2 protein levels.