Abstract
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)
JPET articles become freely available 12 months after publication, and remain freely available for 5 years.Non-open access articles that fall outside this five year window are available only to institutional subscribers and current ASPET members, or through the article purchase feature at the bottom of the page.
|