ABSTRACT
Objective To explore the myogenic basis of the increased excitability and contractile activity in detrusor instability (DI) and investigate the differences of spontaneous contractions by ryanodine receptor (RyR) channels regulation in sarcoplasmic reticulum (SR) between DI and normal bladder muscle and of the RyR channels protein expression. Methods DI model was confirmed by filling cystometry from rats that underwent partial bladder outlet obstruction (BOO) about 8 weeks ago. Muscle strips were dissected from fresh bladder under microscope and the isometric tension in DI and normal strips were detected. The contractions were recorded in these strips exposed to some agents. SR microsome protein was obtained from DI and normal bladder muscle preparations and was used for Western blot analysis to determinate RyR channels expression. Results Treated with RyR channels blocker ryanodine , the contractile frequence significantly increased in normal strips, but not in DI muscle. Western blot analysis showed that RyR channels expression in DI muscle was significantly less than that in normal preparations. Conclusion RyR channels act a negative role in spontaneous contractile activity and the presumed mechanism may involve in Ca 2+ release of RyR channels which causes activation of Ca 2+ -dependent K + channels to decrease contractility. But this crosstalk mechanism is weaken in DI muscle, which provides a chance for spontaneous contractile overactivity.