In order to evaluate the interaction between the opiate-like peptidergic pathways and the dopaminergic system in modulating prolactin (PRL) 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 sulpiride (a selective antidopaminergic agent, 25 mg i.v.) plus either placebo or three different doses of naloxone (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 naloxone (0.4 mg i.v.) plus either placebo or increasing doses of sulpiride (25, 50, 100 mg i.v.). In both groups, the drugs were injected simultaneously and blood samples for PRL determination were taken at various intervals during the 15 min preceding drug injections and then over the following 4 h. Naloxone (0.4 mg i.v.) per se did not induce any modification of plasma PRL levels, but reduced to a significant extent sulpiride-induced hyperprolactinaemia (P < 0.02). However, a higher dose of naloxone (0.8 mg i.v.) did not cause significant changes in sulpride-stimulated PRL levels. Increasing dosages of sulpiride (up to 100 mg i.v.) reversed the blunted response of PRL after sulpiride, 25 mg, in presence of naloxone. Our data show that naloxone, at a dose of 0.4 mg i.v. inactive per se on basal PRL levels, is able to blunt significantly sulpiride-induced hyperprolactinaemia. This suggests that, in man, opioid peptides are able to influence PRL release after antidopaminergic stimuli.
Naloxone inhibits sulpiride-induced hyperprolactinemia in men
BERNINI, GIAMPAOLO;PEDRINELLI, ROBERTO;SALVETTI, ANTONIO;
1985-01-01
Abstract
In order to evaluate the interaction between the opiate-like peptidergic pathways and the dopaminergic system in modulating prolactin (PRL) 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 sulpiride (a selective antidopaminergic agent, 25 mg i.v.) plus either placebo or three different doses of naloxone (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 naloxone (0.4 mg i.v.) plus either placebo or increasing doses of sulpiride (25, 50, 100 mg i.v.). In both groups, the drugs were injected simultaneously and blood samples for PRL determination were taken at various intervals during the 15 min preceding drug injections and then over the following 4 h. Naloxone (0.4 mg i.v.) per se did not induce any modification of plasma PRL levels, but reduced to a significant extent sulpiride-induced hyperprolactinaemia (P < 0.02). However, a higher dose of naloxone (0.8 mg i.v.) did not cause significant changes in sulpride-stimulated PRL levels. Increasing dosages of sulpiride (up to 100 mg i.v.) reversed the blunted response of PRL after sulpiride, 25 mg, in presence of naloxone. Our data show that naloxone, at a dose of 0.4 mg i.v. inactive per se on basal PRL levels, is able to blunt significantly sulpiride-induced hyperprolactinaemia. This suggests that, in man, opioid peptides are able to influence PRL release after antidopaminergic stimuli.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
