The sinoatrial node (SAN) has spontaneous activity and sets the heart rate. The intrinsic heart rate (heart rate in absence of autonomic agonists) is faster in the neonate as compared to the adult. Intracellular Ca²⁺ plays an important role in the spontaneous activity. Ca²⁺ is released from the sarcoplasmic reticulum (SR) through the RYR2 Ca²⁺ release channel into the cytosol; it is then removed either into the SR via the SR Ca²⁺ pump (SERCA2a) or out of the cell via the Na⁺-Ca²⁺ exchanger (NCX1). Removal of Ca²⁺ via NCX1 produces an inward current, which contributes to the initiation of a spontaneous action potential in the SAN. Ca²⁺ reenters the cell via the Ca²⁺ channels, Ca_v1.2 and Ca_v1.3. The aim of this study was to investigate Ca²⁺ handling proteins in the SAN and right atrium (RA) during post-natal development. 11 neonatal (2-7 days of age) and 11 adult male (~6 months of age) New Zealand white rabbits were killed humanly and the expression of Ca²⁺ handling proteins at the mRNA level was measured using quantitative PCR (qPCR) and the distribution of Ca²⁺ handling proteins was measured using immunohistochemistry. Cx43 (major gap junction channel in heart) was used as a negative marker of the SAN, and caveolin3 (membrane bound protein) was used as a marker of myocytes and was a useful tool to measure cell diameter. Tables 1 and 2 summarise the qPCR and immunohistochemistry data. Our data show that during development there is a complex change in the expression and distribution of Ca²⁺ handling proteins. Interestingly, using caveolin3, our data also show that there is a significant increase in cell diameter in the SAN and atrial muscle with age. We conclude that there are complex developmental changes in Ca²⁺ handling proteins in the SAN, as well as in the RA, and these changes may, in part, explain the observed decrease in the intrinsic heart rate from the neonate to the adult. The results also may have implications for excitation-contraction coupling in the atrial muscle.