RESUMO
Activation of large conductance Ca2+-dependent potassium channels (BK channels) influences repolarization of the action potential and the level of the resting potential of detrusor smooth muscle cells (SMC). Overactive bladder syndrome (OBS) is one of the complications of diabetes. Here using whole-cell patch clamp technique we show sizable reduction of depolarization-evoked BK current (lBK) and decrease in the amplitude and frequency of spontaneous transient outward currents (STOCs) in isolated SMC from detrusor of rats with streptozocin-induced diabetes compared to control animals. Under the diabetes IBK density at step depolarization to +50 mV decreased from control value of 15.0+/-0.4 pA/pF to 10.0+/-0.5 pA/pF, whereas the mean values of the STOCs' frequency and amplitude at holding potential -20 mV were reduced from 12.0+/-1.5 Hz to 2.4+/-0.6 Hz and from 0.9+/-0.1 pA/pF to 0.510.1 pA/pF, respectively. Using real time RT-PCR it was found that the expression of mRNA for the BK-channel primary pore-forming KCa1.1-subunit increases under the diabetes, whilst that for the auxiliary BKCabeta1-subunit decreases. It is concluded that the observed changes in the BK-channel currents can enhance excitability of the detrusor SMCs thereby promoting myogenic OBS. However, further studies are needed to determine how the decrease in BKCabeta1 expression under the diabetes impairs functional properties of BK channels and to establish possible changes in calcium signals that modulate channel activation.