In addition to its central role in excitation-contraction coupling (ECCl, calcium is heavily implicated in the genesis of arrhythmias, including atrial fibrillation (AF). In contrast to ventricular myocytes, there is comparatively little quantitative information on Ca 2 + handling in atrial cells. A thorough appreciation of physiological Ca2 + handling is necessary to understand fully the pathological significance of changes leading to AF. The aim of this thesis was to perform a quantitative assessment of atrial Ca 2 + handling and report the effects of angiotensin-lion Ca2 +- current. Differences in ultrastructure between atrial and ventricular cells are likely to be significant. The extensiveness of t-tubules was investigated in rabbit and pig atrial cells in comparison with ventricular cells. No t-tubules were observed in rabbit atrial cells, however, a subset of pig atrial cells showed a t-tubule network, albeit less extensive than that of ventricular myocytes. Ca2 + transients in rabbit atrial cells were spatio-temporally non-uniform, initiated at the cell edge and spreading to the cell centre. The importance of CICR in atrial cells was highlighted by the reduced transient amplitude in the absence of SR and the high contribution of the SR to Ca2 + removal. The centripetal spread was not greatly affected by increasing Ca2 + influx, or SR ci+ release, possibly due to the buffering power of atrial cells, which was greater than that of ventricular cells. Surprisingly ECC gain was not significantly different between atrial and ventricular cells, however it is suggested that differences in stimulus underlie this result. Data presented here highlight that not only the differences in ultrastructure, but also fundamental ci+ handling properties are responsible for atrial-ventricu lar tissue differences. Initial experiments to investigate the effects of angiotensin-I I suggest that this does not have a significant impact on ci+ influx, however further work to fully assess its effects in atrial cells is required.