Naloxone induced micturition in unanesthetized paraplegic cats.

In chronic spinal cats 2 to 10 weeks after transection of the spinal cord at the lower thoracic level (T12-T13), the administration of naloxone, an opiate antagonist, (32-500 micrograms./kg. i.p.), stimulated micturition. The total quantity of urine released after administration of naloxone ranged from 10 to 70 per cent, (mean 39 per cent) of the initial bladder volume. The response to the drug occurred 5 to 10 minutes after injection and was characterized by repeated periodic expulsion of small quantities of urine (5 to 10 ml.) which coincided with a pattern of hind-limb movement which resembled walking behavior. The effects of naloxone persisted for about 1 hour. The motor activity following administration of naloxone was dependent upon activation of bladder afferents since it did not occur when the bladder was empty. Naloxone also facilitated the release of urine induced by stimulation of somatic afferents. With repeated administration of naloxone, tolerance developed which was evident for several days. These observations suggest that an endogenous opiate may have a tonic inhibitory role in regulation of micturition. Pharmacologic manipulation of this putative inhibitory mechanism may facilitate management of neurogenic bladder dysfunction.