Freshly dispersed smooth muscle cells were studied at 37°C using the amphotericin B perforated patch configuration of the patch clamp technique. Currents were recorded using Cs⁺ rich pipette solutions to block K⁺ currents. Two components of current, with electrophysiological and pharmacological properties typical of T and L type calcium currents, were recorded. When steady state inactivation curves for the L current were fitted with a Boltzmann equation, this yielded a V_1/2 of -41 ± 3 mV. In contrast, the T current inactivated with a V_1/2 of -76 ± 2 mV. The L currents were reduced in a concentration dependent manner by nifedipine (IC50 = 225 ± 84 nM), Ni²⁺ (IC₅₀= 324 ± 74 µM) and mibefradil (IC₅₀= 2.6 ± 1.1 µM) but were enhanced when external Ca²⁺ was substituted with Ba²⁺. The T current was little affected by nifedipine at concentrations below 300 nM but was increased in amplitude when external Ca²⁺ was substitution with Ba²⁺. Application of either Ni²⁺ and mibefradil reduced the T current with an IC₅₀ = 7 ± 1 µM and ~40 nM respectively. To assess the contribution of T current to electrical activity we examined the effects of Ni²⁺ and mibefradil on spontaneous electrical activity recorded with intracellular electrodes from strips of rabbit urethra. The spontaneous electrical activity consisted of complexes comprising a series of spikes superimposed upon a slow spontaneous depolarisation (SD). Inhibition of T current reduced the frequency of these SD, but had no effect on either the number of spikes per complex or the amplitude of the spikes. In contrast, application of nifedipine failed to significantly alter the frequency of the SD but reduced the number and amplitude of the spikes in each complex.