The urinary bladder pressure during micturition consists of two components: initial phasic and subsequent sustained component. To investigate the excitation mechanisms underlying the sustained pressure, we recorded from membranes of isolated detrusor cells from the pig, which can be used as a model for human micturition. Parasympathomimetic agents promptly evoke a large transient inward current, and subsequently during its continuous presence oscillating inward currents of relatively small amplitudes are observed. The two types of inward current are considered to cause the phasic and sustained pressure rises, respectively. Ionic substitution and applications of channel blockers revealed that Ca²⁺-activated Cl^- channels were responsible for the large transient and oscillating inward currents. Further, the inclusion of GDPS in the patch pipette indicates that both inward currents involve G-proteins. However, applications of heparin in the patch pipette, and of xestospongin C in the bathing solution suggest a signalling pathway other than IP3 operating in the inward current oscillation, unlike the initial transient inward current. This IP3-independent inward current oscillation system required both sustained Ca²⁺ influx from the extracellular space and Ca²⁺ release from the intracellular stores. These two requirements are presumably SKF 96365-sensitive cation channels and ryanodine receptors, respectively. Experiments with various Ca²⁺ concentrations suggested that Ca²⁺ influx from the extracellular space plays a major role in pacing the oscillatory rhythm. The fact that distinct mechanisms underlie the two types of inward current may help development of clinical treatments of, for example, urinary incontinence and residual urine volume control.