Kontani H, Kawabata Y
Department of Pharmacology, Hokuriku University, School of Pharmacy, Kanazawa, Japan.
Jpn J Pharmacol. 1988 Sep;48(1):31-6. doi: 10.1254/jjp.48.31.
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.
