The supraspinal and spinal mechanisms of morphine-induced inhibition of isometrically recorded reflex urinary bladder contractions were studied in rats anesthetized with urethan. Chronic intracerebroventricular administration of 5,7-dihydroxytryptamine (200 micrograms) or 6-hydroxydopamine (150 micrograms), to selectively deplete central serotoninergic and noradrenergic systems, attenuated the intracerebroventricular effect but not the intrathecal effect of morphine. The intracerebroventricular effect of morphine was reversibly attenuated or abolished by an intrathecal injection of the novel delta-receptor antagonist ICI 174,864 (N,N-diallyl-Tyr-Arb-Aib-Phe-Leu-OH: Aib = alpha-aminoisobutyric acid) (1-3 micrograms) and by intrathecal methysergide (4-10 micrograms), phentolamine (5-10 micrograms), and yohimbine (5-10 micrograms) but not by intrathecal propranolol (10 micrograms), atropine (8 micrograms) or saline (2 micrograms) administered at similar molar concentrations and volumes respectively. These observations support the hypothesis that supraspinal and spinal mechanisms involved in morphine-induced inhibition of reflex urinary bladder contractions can be dissociated. The supraspinal actions of morphine were mediated indirectly via descending 5-hydroxytryptamine and noradrenergic pathways which activated specific 5-hydroxytryptamine and alpha-adrenergic but not beta-adrenergic receptor in the spinal cord. In addition, supraspinal morphine indirectly activated a spinal opioid system which could be directly activated by intrathecal morphine. The similarities between these observations and studies of central pathways mediating nociception and opioid analgesia suggest that similar physiological mechanisms control certain somatic and visceral activity.