The effects of chronic ritanserin treatment on sleep and the neuroendocrine response to L-tryptophan.
A previous study has shown that acute administration of the 5-HT2 receptor antagonist ritanserin doubles Slow Wave Sleep (SWS) and increases the prolactin (PRL) response to L-tryptophan (LTP). The present study investigated the effect of repeated ritanserin treatment on sleep, neuroendocrine response to LTP and 5-HT2 platelet receptor binding. After 2 weeks, ritanserin administration SWS was persistently increased but the PRL response to LTP was unchanged. Platelet 5-HT receptor binding was undetectable at the end of ritanserin treatment but recovered 2 weeks after drug withdrawal. The results suggest that ritanserin causes a sustained effect on the 5-HT mechanisms mediating SWS and on platelet 5-HT2 receptors. However, adaptation occurs to its effect on 5-HT-mediated neuroendocrine responses.
D000328:Adult; D001667:Binding, Competitive / Q000187:drug effects; D013006:Growth Hormone / Q000097:blood; D006801:Humans; D008238:Lysergic Acid Diethylamide / Q000378:metabolism; D008297:Male; D009490:Neurosecretory Systems / Q000187:drug effects*; D010880:Piperidines / Q000494:pharmacology*; D011388:Prolactin / Q000097:blood; D011863:Radioimmunoassay; D016713:Ritanserin; D012890:Sleep / Q000187:drug effects*; D012894:Sleep Stages / Q000502:physiology; D014364:Tryptophan / Q000494:pharmacology*
D010880:Piperidines; D016713:Ritanserin; D014364:Tryptophan; D008238:Lysergic Acid Diethylamide; D011388:Prolactin; D013006:Growth Hormone