Effect of selective serotonin agonists on basal, corticotrophin-releasing hormone- and vasopressin-induced ACTH release in vitro from rat pituitary cells

A. E. Calogero, G. Bagdy, M. L. Moncada, R. D'Agata

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Abstract

The present study was undertaken to evaluate the serotonin (5-HT) receptor subtype(s) by which 5-HT acts on the pituitary to stimulate ACTH secretion. We tested the effects of the 5-HT(1A) receptor agonist 8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT), the 5-HT(1C) receptor agonist metachloro-phenylpiperazine (m-CPP), which also binds to other 5-HT receptors with lower affinity, and the 5-HT(2/1C) receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) on basal, corticotrophin-releasing hormone (CRH) and arginine vasopressin (AVP)-stimulated ACTH release from primary rat anterior pituitary cell cultures. 5-HT, 8-OH-DPAT and DOI significantly increased basal ACTH release, an effect which was antagonized by 5-HT receptor antagonists. 5-HT and DOI were effective an nanomolar concentrations whereas 8-OH-DPAT was effective at higher concentrations. 5-HT, 8-OH-DPAT (both at 10 nmol/l) and DOI (at higher concentrations) blunted the stimulatory effect of CRH. The suppressive effects of 8-OH-DPAT and DOI on CRH-stimulated ACTH release were antagonized by (-)propranolol, a β-adrenergic receptor antagonist which binds the 5-HT(1A) receptor with elevated affinity, and ketanserin, a 5-HT2 receptor antagonist respectively. 5-HT, 8-OH-DPAT and DOI showed additive stimulatory effects with AVP but only at the highest concentration tested, whereas m-CPP potentiated AVP-induced ACTH release at concentrations of 1 nmol/l or more. This effect was antagonized by metergoline, a non-selective 5-HT receptor antagonist and mianserin, an antagonist which binds the 5-HT(1C) receptor with elevated affinity. Thus (1) 5-HT and selective 5-HT agonists such as 8-OH-DPAT, m-CPP and DOI modulate ACTH release by acting directly at the pituitary level; (2) serotonergic stimulation of basal ACTH release is mediated by both 5-HT2 and 5-HT(1A) receptors; (3) serotonergic inhibition of CRH-stimulated ACTH release is mediated by 5-HT(1A) and 5-HT2 receptors; whereas (4) serotonergic potentiation of AVP-stimulated ACTH release is mediated mainly by 5-HT(1C) receptors.

Original languageEnglish
Pages (from-to)381-387
Number of pages7
JournalJournal of Endocrinology
Volume136
Issue number3
Publication statusPublished - 1993

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Serotonin Receptor Agonists
8-Hydroxy-2-(di-n-propylamino)tetralin
Corticotropin-Releasing Hormone
Vasopressins
Adrenocorticotropic Hormone
Serotonin Receptors
Serotonin
Arginine Vasopressin
Receptor, Serotonin, 5-HT1A
Serotonin Antagonists
Metergoline
Serotonin 5-HT2 Receptors
Mianserin
Serotonin 5-HT2 Receptor Antagonists
In Vitro Techniques
Ketanserin
Adrenergic Antagonists
hydroxide ion
Propranolol
Cell Culture Techniques

ASJC Scopus subject areas

  • Endocrinology

Cite this

Effect of selective serotonin agonists on basal, corticotrophin-releasing hormone- and vasopressin-induced ACTH release in vitro from rat pituitary cells. / Calogero, A. E.; Bagdy, G.; Moncada, M. L.; D'Agata, R.

In: Journal of Endocrinology, Vol. 136, No. 3, 1993, p. 381-387.

Research output: Contribution to journalArticle

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AU - D'Agata, R.

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N2 - The present study was undertaken to evaluate the serotonin (5-HT) receptor subtype(s) by which 5-HT acts on the pituitary to stimulate ACTH secretion. We tested the effects of the 5-HT(1A) receptor agonist 8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT), the 5-HT(1C) receptor agonist metachloro-phenylpiperazine (m-CPP), which also binds to other 5-HT receptors with lower affinity, and the 5-HT(2/1C) receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) on basal, corticotrophin-releasing hormone (CRH) and arginine vasopressin (AVP)-stimulated ACTH release from primary rat anterior pituitary cell cultures. 5-HT, 8-OH-DPAT and DOI significantly increased basal ACTH release, an effect which was antagonized by 5-HT receptor antagonists. 5-HT and DOI were effective an nanomolar concentrations whereas 8-OH-DPAT was effective at higher concentrations. 5-HT, 8-OH-DPAT (both at 10 nmol/l) and DOI (at higher concentrations) blunted the stimulatory effect of CRH. The suppressive effects of 8-OH-DPAT and DOI on CRH-stimulated ACTH release were antagonized by (-)propranolol, a β-adrenergic receptor antagonist which binds the 5-HT(1A) receptor with elevated affinity, and ketanserin, a 5-HT2 receptor antagonist respectively. 5-HT, 8-OH-DPAT and DOI showed additive stimulatory effects with AVP but only at the highest concentration tested, whereas m-CPP potentiated AVP-induced ACTH release at concentrations of 1 nmol/l or more. This effect was antagonized by metergoline, a non-selective 5-HT receptor antagonist and mianserin, an antagonist which binds the 5-HT(1C) receptor with elevated affinity. Thus (1) 5-HT and selective 5-HT agonists such as 8-OH-DPAT, m-CPP and DOI modulate ACTH release by acting directly at the pituitary level; (2) serotonergic stimulation of basal ACTH release is mediated by both 5-HT2 and 5-HT(1A) receptors; (3) serotonergic inhibition of CRH-stimulated ACTH release is mediated by 5-HT(1A) and 5-HT2 receptors; whereas (4) serotonergic potentiation of AVP-stimulated ACTH release is mediated mainly by 5-HT(1C) receptors.

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