XXXX inhibits @entity3216 -induced @entity4089 in @entity1 .

@entity1 @entity4089 @entity3216 @entity4090 @entity1510
In order to evaluate the interaction between the opiate-like peptidergic pathways and the dopaminergic system in modulating prolactin ( @entity4090 ) secretion, ten normal volunteers were studied according to a double-blind, cross-over, randomized experimental design. A group of five subjects was given a fixed dose of @entity3216 (a selective antidopaminergic agent, 25 mg i.v.) plus either placebo or three different doses of @entity1510 (a selective opioid antagonist, 0.2, 0.4, 0.8 mg i.v.) while a second group of five subjects received the same drugs in a 'reverse' protocol, i.e. a fixed dose of @entity1510 (0.4 mg i.v.) plus either placebo or increasing doses of @entity3216 (25, 50, 100 mg i.v.). In both groups, the drugs were injected simultaneously and blood samples for @entity4090 determination were taken at various intervals during the 15 min preceding drug injections and then over the following 4 h. @entity1510 (0.4 mg i.v.) per se did not induce any modification of plasma @entity4090 levels, but reduced to a significant extent @entity3216 -induced @entity4089 (P less than 0.02). However, a higher dose of @entity1510 (0.8 mg i.v.) did not cause significant changes in @entity3216 -stimulated @entity4090 levels. Increasing dosages of @entity3216 (up to 100 mg i.v.) reversed the blunted response of @entity4090 after @entity3216 , 25 mg, in presence of @entity1510 . Our data show that @entity1510 , at a dose of 0.4 mg i.v. inactive per se on basal @entity4090 levels, is able to blunt significantly @entity3216 -induced @entity4089 . This suggests that, in @entity1 , opioid peptides are able to influence @entity4090 release after antidopaminergic stimuli.
