We previously reported that bladder overdistension led to denervation and subsequent supersensitivity of the detrusor muscle to acetylcholine. Therefore, to exclude the influence of bladder overdistension, we produced a low-pressure bladder in female mongrel dogs using an indwelling urethral catheter, and performed pelvic neurectomy (decentralization). We examined the effects of decentralization on the neuromuscular system of the bladder. The contraction response levels of bladder strips in dogs 1 and 2 weeks after neurectomy was low, and significantly different from that of bladder strips in the control group. The dose-response curves of dogs 4 and 8 weeks after neurectomy showed a shift to the left when compared to those of the control group, indicating a significant increase in sensitivity of the bladder strips. Many cholinergic terminal and varicosity profiles had a normal ultrastructure in all of the groups subjected to neurectomy, while some had degenerating profiles representing clear axoplasm without any recognizable organelles. Microphotographs of bladder obtained from dogs with spontaneous catheter loss showed degenerating axons, which were observed more frequently than in bladders kept empty with indwelling urethral catheters. Micturition in the dogs with spontaneous catheter loss was achieved by overflow incontinence without catheterization. These findings suggest that post-synaptic nerve degeneration may be augmented by impairment of micturition, followed by decentralization. Our observations also suggest that post-synaptic nerve degeneration (denervation) plays an important role in the increased sensitivity of the detrusor muscle to acetylcholine in the parasympathetically decentralized urinary bladder, whether denervation is due to trans-synaptic degeneration or impairment of micturition.