Previous studies have shown that 17 beta-estradiol (beta-E2) has a direct acute 
inhibitory effect on vascular smooth muscle (VSM) contraction. To investigate 
the mechanisms underlying this phenomenon, we utilized whole cell patch-clamping 
techniques to study effects of beta-E2 on voltage-dependent Ca2+ channels in 
cultured VSM cells (VSMC). T- and L-type Ca2+ currents were characterized with 
ramp and pulse protocols in A7r5 cultured VSMC. T-type current, inactivated in < 
100 ms, was reduced by Ba2+ and was comparatively little affected by isradipine. 
L-type current required higher voltages to activate, inactivated slowly, was 
greatly increased by Ba2+, and could be completely inhibited by 5 microM 
isradipine. beta-E2 (10 microM) significantly reduced peak L-type Ba2+ current 
and T-type Ca2+ current within 1-2 min, whereas alpha E2 (a hormonally inactive 
isomer of estradiol) caused significantly less reduction in both types of 
current. Vehicle (0.1% ethanol) had no significant effect on either current. The 
inhibitory effect of beta-E2 on voltage-dependent Ca2+ currents may contribute 
to previously demonstrated beta-E2 attenuation of VSM contraction.