CHANGES IN ACTION-POTENTIAL KINETICS FOLLOWING EXPERIMENTAL BLADDER OUTFLOW OBSTRUCTION IN THE GUINEA-PIG

The effect of experimental bladder outflow obstruction on membrane electrical activity of guinea pig detrusor smooth muscle was studied. Using an intracellular microelectrode technique, action potentials were recorded from single smooth muscle cells to determine the effect of outflow obstruction on action potential (AP) kinetics. Bladder outflow obstruction resulted in smooth muscle hypertrophy with bladder weight gain to 2.7 times control levels after 8-12 weeks' obstruction. The changes in the AP kinetics noted with obstruction-induced bladder hypertrophy were a prolongation of the AP duration and a decrease in the maximum velocity of depolarization and repolarization. The AP amplitude, after hyperpolarization and overshoot potential in addition to the resting membrane potential (RMP) did not change significantly with bladder outflow obstruction. The values of these AP parameters were not affected significantly by the application of atropine and guanethidine in smooth muscle tissue from either control or obstructed bladders. These results suggest that the active electrical properties of the detrusor smooth muscle membrane are changed significantly by obstruction-induced bladder hypertrophy. Furthermore, the results suggest that adrenergic and cholinergic neurotransmitters do not contribute to these changes in AP kinetics following obstruction. The changes in AP properties with outflow obstruction-induced bladder hypertrophy were compared with those previously reported for the hypertrophic myocardium and were discussed in relation to the known impaired contractile properties of obstructed bladder smooth muscle.