ROLE OF A CENTRAL MUSCARINIC CHOLINERGIC PATHWAY FOR RELAXATION OF THE PROXIMAL URETHRA DURING THE VOIDING PHASE IN RATS

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Abstract
We examined the role of a central muscarinic cholinergic pathway in proximal urethral function during the voiding phase. During isovolumetric bladder contraction we independently recorded proximal urethral pressure, external urethral sphincter activity, and hypogastric and pelvic nerve discharge in urethane anesthetized rats. We administered intravenous, intrathecal or intracerebral ventricular atropine sulfate and atropine methyl nitrate. Atropine sulfate crosses the blood-brain barrier, while atropine methyl nitrate does not. Filling the bladder with 0.5 ml. saline induced rhythmic urethral relaxation accompanied by efferent burst discharges from the pelvic nerve. When administered intravenously, only atropine sulfate caused the dose dependent inhibition of urethral relaxation and efferent pelvic nerve discharge. Neither atropine sulfate nor atropine methyl nitrate affected the maximum firing rate of the external urethral sphincter or hypogastric efferent discharge. Intrathecal and intracerebral ventricular atropine sulfate and atropine methyl nitrate similarly inhibited urethral relaxation. These results suggest that excitation of the central muscarinic cholinergic pathway at a supraspinal or spinal site promotes proximal urethral relaxation during the voiding phase through the activation of efferent pathways in the pelvic nerves.