Following pulmonary artery banding (PAB), the contractile function of right ventricle (RV) diminishes over time. Subsequently, the right atrium (RA) has to contract against a higher after load, but it is unknown to what extent ventricular dysfunction has an effect on the atrial contractility. We hypothesized that right ventricular pressure overload may have an affect on atrial contractility and Ca²⁺-transport protein expression. Therefore, we induced pressure overload (PO) of the right ventricle by pulmonary artery banding for 10 weeks in rabbits and examined the changes in the expression of Ca²⁺-transport proteins in the atrium. We demonstrate that PAB significantly decreased the expression of Serca2a while expression of NCX-1 was significantly upregulated in the RA but not in the left atria (LA) of rabbit hearts indicating that pressure is the major trigger. Decrease in Serca2a expression was concomitant with a significant decrease in sarcolipin (SLN) possibly indicating a compensatory role of SLN. The decreased expression of SLN was unable to completely restore SR Ca²⁺-uptake function of Serca2a. Functional contractile assessments in isolated trabeculae showed no difference between PAB- and sham-operated rabbits at 1 Hz, but displayed an enhanced force development at higher frequencies and in presence of isoproterenol, while twitch timing was unaffected. Our results indicate that right ventricular mechanical overload due to PAB affects the expression of the calcium handling proteins in the RA in rabbits.