Title: Stimulation of growth hormone release by 5-hydroxytryptamine (5-HT) in cultured rat anterior pituitary cell aggregates: Evidence for mediation by 5-HT2B, 5-HT7, 5-HT1B, and ketanserin-sensitive receptors
Authors: Papageorgiou, Anna-Pia ×
Denef, Carl #
Issue Date: Sep-2007
Publisher: Endocrine soc
Series Title: Endocrinology vol:148 issue:9 pages:4509-4522
Abstract: 5-Hydroxytryptamine (5- HT) promotes the release of GH by a hypothalamic site of action. The present study explores a putative pituitary action in a perifused rat anterior pituitary aggregate cell culture system. In aggregates cultured with 1 nMestradiol for expression of the 5-HT4, -5, and -6 receptor ( R), 5- HT promptly stimulated GH secretion with a dose dependency between 1 and 10 nM. The effect of 5- HT was partially blocked by methiothepin and methysergide; by SB-206553, a 5- HTR2B/C antagonist; SB-269970, a 5- HTR7/5A antagonist; and SB-224289, a 5- HTR1B antagonist. The GH response was fully blocked by combined administration of SB-206553+SB-269970 and SB-206553+ketanserin but not by SB-206553+spiperone. Culturing the aggregates without estradiol diminished the magnitude of the GH response to 5- HT as well as the impact of 5- HTR7/5 blockade on the response. Basal GH release was stimulated by the 5-HTR2 agonists 1-(2,5-dimethoxy-4- iodophenyl)-2- aminopropane, m-chlorophenyl piperazine, and alpha- methyl 5-HT; 5-carboxytryptamine ( agonist at 5-HTR1, -5, and -7); tryptamine ( preferential 5-HTR7 agonist); and the selective 5-HTR1B agonist CP93129 but not the 5-HTR1A agonists 7-(dipropylamino)tetralin-1-ol-8-hydroxy-2-(di-n-propylamino) tetralin and the 5-HTR1B/D agonist sumatriptan. The selective 5-HTR2B agonist BW 723C86 stimulated GH release, and the selective 5-HTR2B antagonist SB-204741 attenuated the GH response to 5-HT. The present data suggest that 5-HT may release GH through a pituitary site of action, and that the 5-HTR2B, 5-HTR7 and 5-HTR1B mediate this response, with possibly an inhibitory component of the 5-HTR1D. The relative contribution of these receptors may be modulated by estrogen.
ISSN: 0013-7227
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Department of Cellular and Molecular Medicine - miscellaneous
Pharmacology Section (-)
Molecular and Vascular Biology
× corresponding author
# (joint) last author

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