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A study of morphine-induced urinary retention in anesthetized rats capable of micturition
1Department of Pharmacology, Hokuriku University, School of Pharmacy, Kanazawa, Japan.
Abstract:
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.
Insights
Morphine causes urinary retention by inhibiting bladder contractions through opioid receptors in the brain and spinal cord. Naloxone, an opioid antagonist, reverses this effect, indicating a central mechanism of action.
Area of Science:
- Neuropharmacology
- Urology
- Physiology
Background:
- Opioid analgesics like morphine are known to cause urinary retention, a common side effect.
- The precise mechanisms underlying morphine-induced urinary retention are not fully understood.
- Understanding these mechanisms is crucial for managing patient side effects and improving drug safety.
Purpose of the Study:
- To investigate the neuropharmacological mechanisms of morphine-induced urinary retention in a rat model.
- To determine the role of central opioid receptors in mediating the effects of morphine on bladder function.
Main Methods:
- Anesthetized rats were used to observe bladder contractions during micturition.
- Morphine was administered intravenously (i.v.), intracerebroventricularly (i.c.v.), and intrathecally (i.t.).
- Naloxone, an opioid antagonist, was used to assess the involvement of opioid receptors.
Main Results:
- Systemic and central administration of morphine prolonged the micturition interval and increased the micturition threshold.
- Morphine inhibited bladder contraction in a dose-dependent manner, an effect reversed by naloxone.
- Central administration (i.c.v. and i.t.) of morphine mimicked the effects of systemic administration, suggesting a central mechanism.
Conclusions:
- Morphine-induced urinary retention is mediated by the inhibition of bladder function via opioid receptors in the supraspinal and spinal micturition centers.
- These findings highlight the central nervous system's role in regulating micturition and the impact of opioids on this process.
- Targeting central opioid pathways may offer new strategies for managing opioid-induced urinary dysfunction.
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