Regulation of Urinary Bladder Capacity by Endogenous Opioid Peptides

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Abstract
Naloxone administered to chloralose or ketamine anesthetized cats reduced urinary bladder capacity. Successive cystometrograms revealed that naloxone in doses of 0.5 .mu.g/kg to 15 .mu.g/kg i.v. reduced the volume necessary to evoke micturition by 10-50%, respectively. The effect was maximal within a few min, returned to control values over the next 2-3 h. Following return to control, subsequent doses of naloxone produced no further effect on capacity. In chloralose anesthetized animals naloxone also increased the frequency and amplitude pressure waves on the tonus limb of the cystometogram. Intrathecal administration of naloxone to the sacral cord did not significantly reduce the volume necessary to evoke micturition even at large doses, but did increase the amplitude of micturition contractions. Mu receptors in the brainstem evidently alter urinary bladder capacity, while delta receptors in the spinal cord modulate the magnitude of bladder contractions. Pharmacological manipulation of these receptor systems could provide a tool for the management of neurogenic bladder dysfunction.