Although bradikinin (BK) was reported to be present in urine and cause stimulant action on ureter more than 30 years ago (Marin-Grez et al., 1980), the mechanisms of it’s action on ureteric smooth muscle have not been studied. Thus, the aim of the present study was to investigate the effects of BK on calcium (Ca2+) signalling and force of rat ureteric smooth muscle using combined confocal imaging and force measurements. Resting rat ureter always responded to BK with a complex Ca2+ transient which consisted of an initial phasic component (seen as propagating intracellular Ca2+ waves), followed by a sustained plateau component superimposed by Ca2+ oscillations which appeared as propagating intercellular Ca2+ waves. This complex Ca2+ response was accompanied by a brief phasic followed by sustained tonic contraction superimposed by brief phasic contractions. Inhibition of voltage gated L-type Ca2+ channels by Nifedipine (10µM) selectively blocked intercellular Ca2+ oscillations and phasic contraction, but had no effect on initial phasic and sustained components of Ca2+ transient and force, respectively. In Ca2+ free solution, BK showed a transient increase in Ca2+ and force which were blocked by Cyclopiazonic acid (CPA) but not Ryanodine. There was a large increase in base-line Ca2+ and force superimposed by intercellular Ca2+ oscillations associated with phasic contraction upon addition of external Ca2+ to Ca2+ free solution, following Ca2+ depletion of the SR either by BK or CPA. The data obtained suggest that in rat ureteric smooth muscle, SR Ca2+ release is coupled to marked Ca2+ entry via store operated Ca2+ channels, leading to depolarization and activation of spontaneous action potentials associated with intercellular Ca2+ oscillations and phasic contractions.