Involvement of opioid mechanisms in peripheral motor control of detrusor muscle

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)