The acute effects of 17 beta-estradiol on bladder contractile function and on calcium currents were evaluated in vitro on isolated guinea pig bladder strips and detrusor myocytes, respectively. In the isolated bladder strip, 17 beta-estradiol inhibited KCl-induced contractions with an IC50 of 1.7 +/- 0.3 microM. In isolated detrusor myocytes, single cell capacitance was 52.9 +/- 2.2 pF. This corresponded to a mean cell surface area of 5297.5 +/- 214.8 micron2. The specific membrane resistance was 97.8 +/- 31.6 K omega cm2. The effects of 17 beta-estradiol (0.1 to 3 microM) on peak transmembrane calcium currents were evaluated using the whole cell voltage clamp technique. Peak calcium currents were decreased by approximately 50% (427.8 +/- 57.6 to 226.1 +/- 70.2 pA) at 1.0 microM. Additional analyses were performed at 1.0 microM. Evaluation of the current voltage relationship indicated a decrease in the maximum conductance from 12.31 +/- 1.85 to 7.29 +/- 1.91 nS. Current activations were reasonably fit to a Boltzmann logistic. After exposure to 17 beta-estradiol, the activation curve was shifted to the right by approximately 13 mV. The voltage-dependence of calcium current inactivation was U-shaped, but well described by a Boltzmann relation at membrane potentials between -80 and 0 mV. 17 beta-Estradiol had no effect on the voltage-dependence of calcium current inactivation. The combination of effects on peak current amplitude and voltage dependence of current activation produced a significant decrease in the calcium "window current." Quasi steady-state ramp currents were characteristically "N-shaped," and after exposure to 17 beta-estradiol became flattened.(ABSTRACT TRUNCATED AT 250 WORDS)