Role of Vasoactive Intestinal Peptide and 5-HT<sub>2</sub> Receptor Subtype in Serotonin Stimulation of Basal and Thyrotropin-Releasing-Hormone- Induced Prolactin Release in vitro from Rat Pituitary Cells

The inhibitory effects of dopamine and various ergot alkaloids on prolactin secretion were studied using continuously perfused columns of dispersed rat anterior pituitary cells. Bromocriptine (5 nmol/l) and lisuride hydrogen maleate (5 nmol/l) both inhibited prolactin secretion, the effects persisting for more than 3 h after the end of the administration of the drugs. A similar although less long-lasting effect was observed with lergotrile (50 nmol/l) and the new ergoline derivative, pergolide (5 nmol/l). These effects contrasted with the rapid disappearance of the action of dopamine. The potency estimates of the ergots relative to that of dopamine were: lergotrile, 2·3; bromocriptine, 13; lisuride, 15; pergolide, 23. The dopamine-receptor blocking drugs, metoclopramide and haloperidol, antagonized the prolactin release-inhibiting activity of the compounds; bromocriptine and lisuride showed the highest resistance to this dopaminergic blockade. The results suggested that the direct effect of the ergot derivatives on dispersed pituitary cells was mediated through dopamine receptors and emphasized the long-lasting action of bromocriptine and lisuride in vitro.

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Extracellular ATP as an autocrine/paracrine regulator of prolactin release

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1997.272.6.e1117 ◽

1997 ◽

Vol 272 (6) ◽

pp. E1117-E1123 ◽

Cited By ~ 2

Author(s):

L. Nunez ◽

C. Villalobos ◽

L. S. Frawley

Keyword(s):

Secretory Granules ◽

Extracellular Atp ◽

Thyrotropin Releasing Hormone ◽

Pituitary Cells ◽

Prolactin Release ◽

Releasing Hormone ◽

Rat Pituitary ◽

Rat Pituitary Cells ◽

Cells Cultured ◽

Local Regulator

Recent evidence demonstrates that ATP, costored with a number of hormones and neurotransmitters in secretory granules, is coreleased during exocytosis of these agents. Here, we explored the possibility that extracellular ATP subserves an autocrine and/or paracrine role in the regulation of prolactin (PRL) release by subjecting rat pituitary cells to various experimental manipulations aimed at evaluating putative interactions between ATP and mammotropes. Our results strongly support the view that ATP functions as a local regulator of PRL secretion. To be more specific, we observed that ATP is released in a predictable manner by physiologically relevant secretagogues that are reasonably targeted to mammotropes. Moreover, we found that ATP can act directly on pituitary cells to stimulate the release of PRL from most (if not all) mammotropes. Finally, we determined that antagonism or removal of ATP leads to a diminution of PRL export from pituitary cells cultured under basal or thyrotropin-releasing hormone-stimulated conditions. On the basis of these results, we propose that ATP acts locally to amplify and prolong the PRL secretory response elicited by a more traditional hypophysiotropic signal.

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Vitamin D-enhanced thyrotrophin release from rat pituitary cells: effects of Ca2+, dihydropyridines and ionomycin

Journal of Endocrinology ◽

10.1677/joe.0.1210441 ◽

1989 ◽

Vol 121 (3) ◽

pp. 441-450 ◽

Cited By ~ 6

Author(s):

M. C. d'Emden ◽

J. D. Wark

Keyword(s):

Vitamin D ◽

Pituitary Tumour ◽

Prolactin Secretion ◽

Pituitary Cells ◽

Dihydroxyvitamin D ◽

Normal Pituitary Gland ◽

Rat Pituitary ◽

Rat Pituitary Cells

ABSTRACT Vitamin D may regulate pituitary function, as there are selective effects of 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) on gene expression in clonal pituitary tumour cells, and on TRH-induced TSH release in normal rat pituitary cells in vitro. The role of Ca2+ in 1,25-(OH)2D3-enhanced TSH release from primary rat pituitary cell cultures was investigated. Pretreatment with 10 nmol 1,25-(OH)2D3/l for 24 h augmented KCl (3–60 mmol/l)-induced TSH release over 1 h at all KCl concentrations greater than 7·5 mmol/l (P< 0·001), with a 76% enhancement of TSH release induced by 30 mmol KCl/l (P<0·001). The Ca2+ channel antagonist nifedipine (10 nmol/l–10 μmol/l) caused a concentration-dependent inhibition of KCl (60 mmol/l)-induced TSH secretion. Pretreatment with 1,25-(OH)2D3 enhanced KCl-induced release at all concentrations of nifedipine (P<0·001). The Ca2+ selective divalent cation ionophore ionomycin (1 nmol/l–1 μmol/l), and the Ca2+ channel agonist BAY K 8644 (10 nmol/l–1 μmol/l) increased prolactin secretion but did not increase TSH release, and 1,25-(OH)2D3 had no effect. At an extracellular Ca2+ concentration of less than 500 nmol/l, TRH-induced TSH release was observed only after treatment with 1,25-(OH)2D3 (P<0·01). As the extracellular Ca2+ concentration was increased, greater increments of TRH-induced TSH release were observed following pretreatment with 1,25-(OH)2D3 (P<0·01). However, the effect of 1,25-(OH)2D3 in the thyrotroph was independent of the pretreatment extracellular Ca2+ concentration. We have shown that 1,25-(OH)2D3 acts selectively on the thyrotroph to enhance in-vitro responsiveness to TRH and KCl. These data suggest that the action of 1,25-(OH)2D3 in the thyrotroph is to enhance intracellular signal transduction. They further support a permissive or regulatory role of vitamin D in the normal pituitary gland. Journal of Endocrinology (1989) 121, 441–450

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Rapid glucocorticoid inhibition of vasoactive intestinal peptide-induced cyclic AMP accumulation and prolactin release in rat pituitary cells in culture.

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.78.12.7584 ◽

1981 ◽

Vol 78 (12) ◽

pp. 7584-7588 ◽

Cited By ~ 31

Author(s):

W. H. Rotsztejn ◽

M. Dussaillant ◽

F. Nobou ◽

G. Rosselin

Keyword(s):

Cyclic Amp ◽

Vasoactive Intestinal Peptide ◽

Pituitary Cells ◽

Prolactin Release ◽

Cells In Culture ◽

Cyclic Amp Accumulation ◽

Rat Pituitary ◽

Rat Pituitary Cells

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

Journal of Endocrinology ◽

10.1677/joe.0.1360381 ◽

1993 ◽

Vol 136 (3) ◽

pp. 381-387 ◽

Cited By ~ 40

Author(s):

A. E. Calogero ◽

G. Bagdy ◽

M. L. Moncada ◽

R. D'Agata

Keyword(s):

Receptor Antagonist ◽

Receptor Agonist ◽

Receptor Subtype ◽

Pituitary Cells ◽

Releasing Hormone ◽

Rat Pituitary ◽

Rat Pituitary Cells ◽

Level 2 ◽

Acth Release

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-HT1A receptor agonist 8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT), the 5-HT1C receptor agonist metachloro-phenylpiperazine (m-CPP), which also binds to other 5-HT receptors with lower affinity, and the 5-HT2/1C 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 at 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-HT1A 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-HT1C 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-HT1A receptors; (3) serotonergic inhibition of CRH-stimulated ACTH release is mediated by 5-HT1A and 5-HT2 receptors; whereas (4) serotonergic potentiation of AVP-stimulated ACTH release is mediated mainly by 5-HT1C receptors. Journal of Endocrinology (1993) 136, 381–387

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