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Serotoninergic agonists increase
plasma levels of beta-endorphin and beta-lipotropin in humans.
Petraglia F, Facchinetti F, Martignoni E, Nappi G, Volpe A, Genazzani AR.
A pharmacological approach was used to investigate the serotoninergic control
of plasma levels on beta-endorphin (beta-EP) and beta-lipotropin (beta-LPH) in
humans. Acute administration of L5-OH-triptophan, the physiologic precursor of
serotonin (SE), induced a significant rise in plasma beta-EP and beta-LPH
levels both when injected iv (20 and 40 mg) (four normal men) and when
administered orally (200 and 400 mg) (seven normal men) (P less than 0.01 vs.
placebo). The iv route of administration induced a prompt (mean peak values
after 150 min) dose-dependent increase in beta-EP and beta-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 dose-related rise in plasma beta-EP and
beta-LPH levels in a group of seven normal men (P less than 0.01) (mean peak
values after 150 min). Pretreatment with methysergide, a SE receptor antagonist
(3 X 2.8 mg orally, five men), did not induce any significant changes in plasma
beta-EP and beta-LPH levels, but blocked the increase in the two hormones
evoked by L5-OH-triptophan (40 mg iv). Plasma cortisol levels changed similarly
to those of beta-EP and beta-LPH in all the experiments, indicating that
putative serotoninergic drugs exert a positive role on the various
corticotropin-releasing hormone-mediated secretions.
Publication Types:
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Clinical Trial
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Controlled Clinical Trial
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