Sarcolipin (SLN) is a key regulator of sarco(endo)plasmic reticulum (SR) Ca²⁺-ATPase (SERCA), and its expression is altered in diseased atrial myocardium. To determine the precise role of SLN in atrial Ca²⁺ homeostasis, we developed a SLN knockout (sln−/−) mouse model and demonstrated that ablation of SLN enhances atrial SERCA pump activity. The present study is designed to determine the long-term effects of enhanced SERCA activity on atrial remodeling in the sln−/− mice. Calcium transient measurements show an increase in atrial SR Ca²⁺ load and twitch Ca²⁺ transients. Patch-clamping experiments demonstrate activation of the forward mode of sodium/calcium exchanger, increased L-type Ca²⁺ channel activity, and prolongation of action potential duration at 90% repolarization in the atrial myocytes of sln−/− mice. Spontaneous Ca²⁺ waves, delayed afterdepolarization, and triggered activities are frequent in the atrial myocytes of sln−/− mice. Furthermore, loss of SLN in atria is associated with increased interstitial fibrosis and altered expression of genes encoding collagen and other extracellular matrix proteins. Our results also show that the sln−/− mice are susceptible to atrial arrhythmias upon aging. Together, these findings indicate that ablation of SLN results in increased SERCA activity and SR Ca²⁺ load, which, in turn, could cause abnormal intracellular Ca²⁺ handling and atrial remodeling.