Serotoninergic agonists increase plasma levels of β-endorphin and β-lipotropin in humans

A pharmacological approach was used to investigate the serotoninergic control of plasma levels on β-endorphin (0-EP) and β-lipotropin (β-LPH) in humans. Acute administration of L,5-OH-triptophan, the physiologic precursor of serotonin (SE), induced a significant rise in plasma β-EP and β-LPH levels both when injected iv (20 and 40 mg) (four normal men) and when adminitered orally (200 and 400 mg) (seven normal men) (P < 0.01 $$$vs. placebo). The iv route of administration induced a prompt (mean peak values after 150 min) dosedependent increase in β-EP and β-LPH levels. The responses evoked by oral administration (mean peak values after 130 and 240 min) were not dose dependent. Fluoxetine (15 and 30 mg orally) a blocker of SE reuptake, induced a significant doserelated rise in plasma β-EP and β-LPH levels in a group of seven normal men (P < 0.01) (mean peak values after 150 min). Pretreatment with methysergide, a SE receptor antagonist (3 × 2.8 mg orally, five men), did not induce any significant changes in plasma β-EP and β-LPH levels, but blocked the increase in the two hormones evoked by L,5-OH-triptophan (40 mg iv). Plasma cortisol levels changed similarly to those of (β-EP and β-LPH in all the experiments, indicating that putative serotoninergic drugs exert a positive role on the various corticotropinreleasing hormone-mediated secretions.