After enzymatic dispersion of the muscle of the guinea- pig gastric fundus, single elongated cells were observed which differed from archetypal smooth muscle cells due to their knurled, tuberose or otherwise irregular surface morphology. These, but not archetypal smooth muscle cells, consistently displayed spontaneous localised (i.e. non-propagating) intracellular calcium ([Ca²⁺]_i) release events. Such calcium events were novel in their magnitude and kinetic profiles. They included short transient events, plateau events and events which coalesced spatially or temporally (compound events). Quantitative analysis of the events with an automatic detection programme showed that their spatio-temporal characteristics (full width and full duration at half maximum amplitude) were approximately exponentially distributed. Their amplitude distribution suggested the presence of two release modes. Carbachol application caused an initial cell-wide calcium transient followed by an increase in localised calcium release events. Pharmacological analysis suggested that localised calcium release was largely dependent on external calcium entry acting on both inositol trisphosphate receptors (IP3Rs) and ryanodine receptors (RyRs) to release stored calcium. Nominally calcium-free external solution immediately and reversibly abolished all localised calcium release without blocking the initial transient calcium release response to carbachol. This was inhibited by 2-APB (100 µM), ryanodine (10 or 50µM) or 1µM U-73122. 2-APB (100µM), 10µM xestospongin C (XeC) or 1µM U-73122 blocked both spontaneous localised calcium release and localised release stimulated by 10µM carbachol. Ryanodine (50µM) also inhibited spontaneous release, but enhanced localised release in response to carbachol. This study represents the first characterisation of localised calcium release events in cells from the gastric fundus.