Abstract
Intracerebroventricular (i.c.v.) administrations of the postulated μ 1 opioid receptor antagonist naloxonazine produced an increase in the frequency of urinary bladder contractions recorded isometrically in the anesthetized rat. This substance also antagonized the inhibition of spontaneous bladder contractions produced by submaximal i.c.v. doses of the highly selective μ opioid agonist [ D-Ala 2-MePhe 4,Gly-(ol) 5]enkephalin (DAGO) and the δ opioid agonist [ D-Pen 2, D-Pen 5]enkephalin (DPDPE). The antagonism of DAGO was reversible but that of DPDPE lasted up to 30 h. These data suggest that endogenous opioids are involved in the central control of bladder motility and that naloxonazine is a long-lasting δ opioid receptor antagonist.
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