Circulating beta-endorphin (beta EP) and beta-lipotropin (beta LPH) concentrations increase after the administration of acetylcholine or serotonin agonist drugs. In this study we examined the effect of dopamine receptor agonists and/or antagonists on plasma beta EP, beta LPH, cortisol, and PRL levels in normal subjects. Neither direct dopamine (DA) agonist drugs, DA (1 microgram/kg min for 120 min), bromocriptine (2.5 mg po), L-dopa (500 mg po) or an indirect DA agonist, nomifensine (200 mg po), significantly altered plasma beta EP and beta LPH levels. The administration of metoclopramide, a DA antagonist (10 mg iv), significantly increased plasma beta EP, beta LPH, PRL, and cortisol levels. This effect was completely reversed by pretreatment with L-dopa (500 mg po) and only partially antagonized by DA infusion. Domperidone (10 mg iv), a DA antagonist which does not cross the blood brain barrier, increased only plasma beta EP levels, an effect inhibited both by L-dopa and DA. After dexamethasone (2 mg/day for 2 days) domperidone still increased plasma beta EP and PRL levels. The concomitant increase of beta EP, beta LPH, and cortisol after metoclopramide suggests that endogenous DA inhibits the secretion of proopiomelanocortin-related peptides. Moreover, since domperidone increases only beta EP and this effect is not altered by dexamethasone, there may be a corticotropin-releasing hormone-independent source of circulating beta EP in humans, which is inhibited by DA.
The continuous and progressive rise of Β-endorphin (B-EP), Β-lipotropin (B-LPH) and cortisol plasma levels during labor in term-pregnant women represents one of the most relevant maternal hormonal responses to the stress of parturition. The aim of the present study was to evaluate the changes of these hormones, both in plasma and amniotic fluid (except cortisol), in a group of pregnant women undergoing prostaglandin-induced therapeutic abortion at the 2nd trimester of pregnancy. B-EP, B-LPH and cortisol were measured by radioimmunoassay. Both plasma and amniotic fluid samples were purified through extraction and chromatography (Sephadex G-75 columns). The prostaglandin derivative, 16-phenoxy-PGE2-methylsulfonylamide (sulprostone, Schering, Berlin) (500 µg, i.m., every 4 h), caused a rapid and significant rise of plasma B-EP, B-LPH and cortisol levels in all subjects. The relative increase of the 3 hormones was less relevant after the 2nd and absent after the 3rd injection of PGE2. The amniotic fluid concentrations of B-EP and B-LPH were also raised 2h after the 1st injection. These data indicate that sulprostone-induced abortion activates both maternal and fetoplacental release of opioids independently of the trend of uterine contractions. The pattern of pro-opiomelanocortin-related labor differs from spontaneous labor and can probably be linked to a direct effect of the drug.
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