Isometric recordings of mechanical activity in muscle strips from rat and human detrusor were performed and the effect of mu- and delta-opioid receptor stimulation and blockade on detrusor contraction induced by electrical field stimulation was tested. Stimulation of the opioid mu-receptor with morphine (10(-13)-10(-4) M) and DAGO (10(-13)-10(-6) M) had no significant effect on electrical field stimulation except at one concentration of morphine (10(-6) M). Naloxone (10(-10)-10(-5) M) caused a significant facilitation of the electrical field stimulation-induced contraction, which was counteracted by morphine (10(-8) M) and the delta-agonist DPDPE (10(-8) M) in both rat and human detrusor. Addition of atropine (10(-6) M) or hexamethonium chloride (10(-6) M) or spantide (10(-6) M) did not alter the facilitating effect of naloxone in the rat detrusor. Hexamethonium (10(-5) M) decreased the facilitating effect of naloxone on electrical field stimulation-induced contractions in the human detrusor, indicating involvement of ganglionic mechanisms. In human detrusor about 15% of the contractile response was found to be atropine-resistant (10(-6) M) and one third of this was found to be resistant to tetrodotoxin (1.5 x 10(-6) M). The atropine resistant-response in human detrusor was facilitated by naloxone to the same extent as the atropine-sensitive part. Adrenergic blockade per se, achieved with phentolamine mesylate (10(-6) M) and propranolol (10(-6) M), caused a significant facilitation of the electrical field stimulation-induced contraction in the rat detrusor but did not affect the facilitating effect of naloxone (10(-13)-10(-5) M).(ABSTRACT TRUNCATED AT 250 WORDS)