These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Characterization of ergot and non-ergot serotonin antagonists by prolactin and growth hormone profiles during wakefulness and sleep. Author: Clarenbach P, Del Pozo E, Brownell J, Heredia E, Spiegel R, Cramer H. Journal: Brain Res; 1980 Dec 08; 202(2):357-63. PubMed ID: 7437907. Abstract: In order to further clarify the involvement of serotonin in the control of secretion of pituitary lactogens, diurnal and sleep prolactin (PRL) and growth hormone (GH) profiles were investigated in healthy subjects treated with ergot and non-ergot serotonin antagonists. A group of 10 subjects received a single oral dose of 2 mg each of pizotifen, methysergide, and the dopaminergic drug bromocriptine as reference substance, in comparison with placebo. Blood was collected at hourly intervals for 6 h. Another group of 10 individuals received either a placebo, 2.5 mg bromocriptine (n = 6) twice daily for 4 days or pizotifen (n = 10) 0.5 mg 3 times daily for 12 days before undergoing EEG recording and blood sampling during night sleep. The diurnal plasma profiles of PRL and GH were not modified by pizotifen, a non-ergot drug. Methysergide and bromocriptine, two ergot derivatives, significantly (P < 0.01 and P < 0.001 respectively) suppressed the basal secretion of PRL throughout the trial and increased plasma GH significantly (P < 0.01). The sleep profile of PRL was not modified by pizotifen but there was a moderate reduction in GH reaching the level of significance (P < 0.02) between hours 1 and 2 of sleep. Bromocriptine suppressed completely PRL secretion throughout the entire sleep period and significantly (P < 0.05) prolonged the secretory profile of GH. The results indicate the presence in the ergot molecule of a dopaminergic moiety responsible for PRL inhibition and GH stimulation. This effect is independent of the serotonin active component of the drug.[Abstract] [Full Text] [Related] [New Search]