The nature of
morphine-induced
urinary retention was studied in anesthetized rats in which the bladder contraction accompanying micturition could be observed.
Morphine (0.1 mg/kg, i.v.) prolonged the micturition interval and increased the level of micturition threshold.
Morphine (1 mg/kg, i.v.) completely inhibited bladder contraction and bladder pressure was elevated until
solution leaked from the penis, but the bladder pressure after inhibition by
morphine (1 and 5 mg/kg, i.v.) did not significantly rise over the peak pressure level during micturition before injection of
morphine. The inhibitory effect of
morphine (1 and 5 mg/kg, i.v.) was reversed by
naloxone (0.1 mg/kg, i.v.).
Morphine (5 mg/kg, i.v.) did not increase the pressure induced by infusion of
solution from near the bladder neck to the urethra. After intracerebroventricular (i.c.v.) and intrathecal (i.t.) administration of
morphine (1 microgram), the micturition interval was prolonged and the level of micturition threshold was increased.
Morphine (5 micrograms, i.c.v. and i.t.) inhibited bladder contraction and
naloxone (5 micrograms, i.c.v. and i.t.) reversed the inhibitory effect of
morphine injected by the same administration route. From these results,
urinary retention induced by systematically injected
morphine was considered to result from inhibition of bladder function mediated via
opioid receptors of the micturition centers in the supraspinal and spinal regions.