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Department of Pharmacology, University of Pittsburgh, PA 15261.

1. Experiments were undertaken to examine the mechanisms involved in the reorganization of sympathetic efferent pathways to the urinary bladder of the cat following chronic unilateral, parasympathetic preganglionic denervation of the bladder. 2. Electrical stimulation (10-30 Hz) of the hypogastric nerve in cats with an intact bladder innervation or on the normally innervated side of the bladder in unilaterally denervated preparations elicited low-amplitude (10-25 cmH2O) transient (10-30 s) bladder contractions and non-synaptic axonal volleys on bladder postganglionic nerves. However, after chronic (3-22 months) sacral preganglionic denervation, hypogastric nerve stimulation on the side of the denervation elicited large (60-80 cmH2O) and more sustained (4-5 min) bladder contractions as well as synaptically mediated firing on bladder postganglionic nerves. 3. The vesicoexcitatory effects of hypogastric nerve stimulation on the chronically denervated side were not altered selectively by the adrenergic blocking agent, phenoxybenzamine, but were blocked by atropine and hexamethonium suggesting that the responses were mediated by muscarinic and nicotinic cholinergic synapses. These drugs did not influence the responses elicited by hypogastric nerve stimulation on the normally innervated side of the bladder. 4. Following more extensive chronic unilateral denervation (transection of the pelvic and hypogastric nerves on one side of the bladder) stimulation of the contralateral intact pelvic nerve elicited postganglionic firing in vesical postganglionic nerves on the denervated side. This crossed excitatory pathway was not observed in normal animals or following sacral preganglionic denervation. 5. It is concluded that parasympathetic preganglionic denervation of the bladder ganglia leads to a reinnervation of the denervated cholinergic ganglion cells by sympathetic preganglionic pathways in the ipsilateral hypogastric nerve. This reinnervation results in the conversion of sympathetic inhibitory pathways to excitatory pathways in the denervated bladder. This change may contribute to the development of the autonomous hyperactive bladder seen under conditions of peripheral nerve or conus medullaris lesions of the spinal cord.

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