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Title: Unexpected effects of peptide and nonpeptide substance P receptor antagonists on basal prolactin and growth hormone release in vitro
Authors: Houben, Herlinde ×
Denef, Carl #
Issue Date: Apr-1993
Series Title: Peptides. vol:14 issue:1 pages:109-15
Abstract: The effect of peptide and nonpeptide substance P antagonists on prolactin (PRL) and growth hormone (GH) secretion was evaluated in three-dimensional rat anterior pituitary cell aggregates. [D-Arg1,D-Phe5,D-Trp7,9,Leu11]Substance P inhibited basal growth hormone (GH) release at a concentration range of 1-10 microM. At higher concentrations (50 microM), the analogue inhibited basal prolactin (PRL) release but provoked a tenfold stimulation of GH release. However, these latter two effects could neither be mimicked nor antagonized by the tachykinins substance P (10 microM), neurokinin A (10 microM), and neurokinin B (3.3 microM). The effects could also not be explained by agonism or antagonism at the level of other receptors (e.g., vasopressin, bombesin, angiotensin II, thyroid hormone-releasing hormone, vasoactive intestinal peptide, dopamine, adrenaline, acetylcholine). Remarkably the nonpeptide substance P antagonists R 30732 (10 microM), R 32602 (10 microM), and CP-96,345 (10 microM) showed a similar inhibition of PRL release and a stimulation of GH release. At a one hundredfold lower concentration, sufficient to block substance P receptors in other tissues. CP-96,345 did not affect PRL or GH release. It is concluded that substance P antagonists, when used at high concentrations, have profound intrinsic activities on PRL and GH release that are not mediated by substance P receptors. The failure of the more potent substance P antagonist, CP-96,345, to influence basal PRL or GH release when used at lower concentrations suggests that endogenous substance P in the anterior pituitary does not play a tonic paracrine role on GH or PRL secretion.
ISSN: 0196-9781
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Pharmacology Section (-)
× corresponding author
# (joint) last author

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