Introduction. The KCa1.1 channel is a member of the BK family of large conductance calcium-activated potassium channels. BK channels are activated by increased intracellular Ca2+ and also by depolarizing membrane potentials and have been shown to contribute to membrane repolarization. A study by Imlach et al.(1) showed that BK channel inhibitors can cause a reduction in heart rate. The aim of this study was to determine the localisation of KCa1.1 within the heart and whether there is a differential expression of KCa1.1 in the human sinus node (SN) and right atrium (RA).Methods. Tissue was obtained from healthy donor human hearts. Sections containing SN and adjacent RA were obtained from 4 hearts, along with additional sections containing left ventricle (LV). The SN location was determined using immunohistochemistry with HCN4 (ion channel involved in pacemaking) antibodies(2). Immunohistochemistry using antibodies against KCa1.1 was used to assess protein expression in SN, RA and LV. Double labelling with vimentin (fibroblast marker), Cx43 (gap junctional protein) and Ryr2 (sarcoplasmic reticulum Ca2+ channel) antibodies was used to determine the cellular localisation of the protein within the LV. Total RNA was extracted from SN and RA. qPCR was used to examine mRNA expression of KCa1.1, Cx43 (atrial muscle marker), and TBX3 (SN marker) in SN and RA. A t-test was used to determine significant differences in expression between the regions sampled. P<0.05 was taken to be significant.Results. KCa1.1 signal within the heart was present in the cell membrane and also intracellularly. Within the LV there was co-localization of KCa1.1 and Ryr2 in the sarcoplasmic reticulum membrane. Cx43 labelling was observed at the intercalated disks and was also co-localized with KCa1.1. There was also some co-localization of vimentin with KCa1.1 within the fibroblasts. The SN showed a tendency for higher expression of KCa1.1 (P<0.09) mRNA compared to RA.Conclusion. Overall, the expression of KCa1.1 protein was found to be present at the cell surface membrane, within the sarcoplasmic reticulum membrane of cardiomyocytes, and also within fibroblasts. The results from this study suggest that the human SN has higher expression of KCa1.1 than the adjacent RA at protein and mRNA levels and therefore it may have a role in human cardiac pacemaking and potentially in arrhythmogenesis. Prolonged action potential duration is a known risk factor for the development of cardiac arrhythmias, such as early after depolarizations. KCa1.1 could be involved in the repolarization phase of the cardiac action potential, leading to a shortening of the action potential duration, and so the KCa1.1 channel may be a potential target for the treatment of this form of arrhythmia.