Changes in expression of neuroreceptor in unstable bladder and its functional role

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We investigated that whether the changes in expression of detrusor muscarinic and purinergic receptors of detrusor play a role in the pathogenic mechanism of detrusor instability (DI) secondary to bladder outlet obstruction. First, a model of secondary DI was established by partial urethral obstruction in rat. Atropine sulfate as a non-selective muscarinic receptor blocker and pyridoxal-phosphate-6-azophenil2 4-disulphonic acid tetrasodium salt (PPADS) as a P2X receptor biocker were administrated into common iliac artery. To estimate detrusor contractility, maximum detrusor contraction pressure (MCP) was measured in isovolumetric rhythmic contraction under urethane anesthesia. MCP and the bladder capacity were increased to 130% and 180% of control in 4 weeks obstructed group, respectively. MCP was inhibited to 50% in control and to 70% in obstructed group by atropine. PPADS administration after atropine did not altered MCP in the control group, but decreased MCP to 30% of pre-atfopine level in the obstructed group. These results suggest that purinergic transmission via P2X receptor does not influence the bladder contraction in intact micturition reflex, on the other hand, purinergic contraction occupies about 40% of bladder contraction strength in obstructed bladder.Detrusor could increase its contractility by expressing P2X receptor for the urethral resistance in benign prostatic hypertrophy. Purinergic receptor antagonist may be applied to the future treatment of secondary detrusor instability with prostatic hypertrophy.