15-Lipoxygenase Products Stimulate Prolactin Secretion from a Cloned Strain of Rat Pituitary Cells

1988 ◽  
Vol 47 (4) ◽  
pp. 323-328 ◽  
Author(s):  
Mireille Rabier ◽  
Claude Chavis ◽  
André Crastes de Paulet ◽  
Marcelle Damon
Keyword(s):  
Prolactin Secretion ◽  
Pituitary Cells ◽  
Rat Pituitary ◽  
Lipoxygenase Products ◽  
Rat Pituitary Cells

Modulation of prolactin secretion by contraceptive progestins in cultured rat pituitary cells in vitro

1988 ◽  
Vol 117 (4_Suppl) ◽  
pp. S188-S189
Author(s):  
L. KIESEL ◽  
T. RABE ◽  
D. SCHOLZ ◽  
V. KIRSCHNER ◽  
B. RUNNEBAUM
Keyword(s):  
Prolactin Secretion ◽  
Pituitary Cells ◽  
Rat Pituitary ◽  
Rat Pituitary Cells

A COMPARISON OF THE EFFECTS OF FOUR ERGOT DERIVATIVES ON PROLACTIN SECRETION BY DISPERSED RAT PITUITARY CELLS

1980 ◽  
Vol 87 (1) ◽  
pp. 95-103 ◽  
Author(s):  
G. DELITALA ◽  
T. YEO ◽  
ASHLEY GROSSMAN ◽  
N. R. HATHWAY ◽  
G. M. BESSER
Keyword(s):  
Anterior Pituitary ◽  
Ergot Alkaloids ◽  
Prolactin Secretion ◽  
Pituitary Cells ◽  
Inhibitory Effects ◽  
Prolactin Release ◽  
Ergot Derivatives ◽  
Rat Pituitary ◽  
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.

Dihydropyridine Ca2+ antagonists: potent inhibitors of secretion from normal and transformed pituitary cells

1985 ◽  
Vol 248 (5) ◽  
pp. C510-C519 ◽  
Author(s):  
J. J. Enyeart ◽  
T. Aizawa ◽  
P. M. Hinkle
Keyword(s):  
Endocrine Cells ◽  
Hormone Secretion ◽  
Prolactin Secretion ◽  
Pituitary Cells ◽  
Excitable Cells ◽  
Rat Pituitary ◽  
Ic50 Values ◽  
Normal Rat ◽  
Rat Pituitary Cells ◽  
Ca2 Channels

Three dihydropyridine (DHP) Ca2+ antagonists were compared with several other organic Ca2+ antagonists with respect to their ability to inhibit depolarization-dependent hormone secretion from the GH4C1 pituitary cell line and from normal rat pituitary cells. The three DHP, nimodipine, nisoldipine, and nifedipine, potently and specifically inhibited KCl-stimulated prolactin secretion from GH4C1 cells (estimated IC50 values: 1.8, 1.8, and 6.0 nM, respectively). Both basal and thyrotropin-releasing hormone-stimulated secretion from GH4C1 cells were much less sensitive to inhibition by the DHP. The inhibition by the DHP was reversible, and their potency was independent of depolarizing concentrations of KCl between 18.8 and 53.8 mM. Other organic antagonists, including verapamil, cinnarizine, and diltiazem, blocked secretion from GH4C1 cells but at much higher concentrations. The estimated IC50 values for these three were 1,000, 1,100, and 3,500 nM, respectively. Depolarization-stimulated prolactin secretion from normal pituitaries was inhibited by the DHP and verapamil at the same concentrations found effective in GH4C1 cells. KCl-stimulated 45Ca2+ uptake by GH4C1 cells was also blocked by DHP at concentrations that inhibited secretion. Since depolarization-stimulated secretion and 45Ca2+ uptake are probably triggered by Ca2+ entering through voltage-sensitive channels, the above results suggest that DHP antagonists potently block these channels in both normal and transformed pituitary cells. These Ca2+ channels appear to be identical in this respect. These findings further suggest a similarity between the Ca2+ channels of endocrine cells and those of smooth muscle and other excitable cells.

Flunarizine, a calcium influx blocker, inhibits TRH- but not potassium-stimulated prolactin secretion

1984 ◽  
Vol 107 (1) ◽  
pp. 31-35 ◽  
Author(s):  
Janet E. Merritt ◽  
Stephen Tomlinson ◽  
Barry L. Brown
Keyword(s):  
Calcium Influx ◽  
Prolactin Secretion ◽  
Pituitary Cells ◽  
Monolayer Cultures ◽  
High K ◽  
Rat Pituitary ◽  
Normal Rat ◽  
Rat Pituitary Cells

Abstract. The effect of flunarizine on the secretion of prolactin from monolayer cultures of normal rat pituitary cells has been determined. Both basal and TRHstimulated secretion were found to be significantly inhibited by micromolar concentrations of flunarizine, whereas depolarization (high K+)-stimulated secretion was virtually unaffected. These results indicate that TRH-stimulated prolactin secretion probably involves calcium influx and that flunarizine may be useful as a probe for particular Ca2+ channels.

Agnus Castus Extracts Inhibit Prolactin Secretion of Rat Pituitary Cells

1993 ◽  
Vol 25 (05) ◽  
pp. 253-255 ◽  
Author(s):  
G. Sliutz ◽  
P. Speiser ◽  
A. Schultz ◽  
J. Spona ◽  
R. Zeillinger
Keyword(s):  
Prolactin Secretion ◽  
Pituitary Cells ◽  
Rat Pituitary ◽  
Agnus Castus ◽  
Rat Pituitary Cells

Mechanism of the prolactin rebound after dopamine withdrawal in rat pituitary cells

1993 ◽  
Vol 265 (1) ◽  
pp. E145-E152 ◽  
Author(s):  
C. Chen ◽  
J. Zhang ◽  
J. M. Israel ◽  
I. J. Clarke ◽  
J. D. Vincent
Keyword(s):  
Primary Cultures ◽  
Rebound Effect ◽  
Prolactin Secretion ◽  
Maximum Effect ◽  
Pituitary Cells ◽  
Channel Blockade ◽  
Short Term ◽  
Prolactin Release ◽  
Rat Pituitary ◽  
Rat Pituitary Cells

To study the mechanism underlying the effect of dopamine withdrawal on prolactin release, continuous perfusion experiments were performed on rat lactotroph-enriched primary cultures. Removal of dopamine (10(-7) M) after a short-term application (15 min) produced a rebound of prolactin secretion, which was enhanced by pretreatment of the cell culture with 17 beta-estradiol (10(-8) M for 48 h). Ca2+ channel blockade by Co2+ (1 mM) abolished the rebound in prolactin release. An increase in intracellular adenosine 3',5'-cyclic monophosphate by either forskolin (5 microM) or 3-isobutyl-1-methylxanthine (100 microM) enhanced the prolactin rebound after dopamine withdrawal. Application of thyrotropin-releasing hormone (10(-7) M) increased the prolactin rebound after dopamine withdrawal with a maximum effect obtained by commencing treatment immediately after removal of dopamine. Pretreatment of cell cultures with pertussis toxin (100 ng/ml, for 10 h) totally abolished the effects of dopamine on prolactin secretion. The dopamine agonist bromocriptine (10(-9) M) significantly decreased prolactin secretion, but no rebound effect was observed after its removal. We conclude that the rebound of prolactin release after dopamine treatment involves the influx of Ca2+.

Laminin induces formation of neurite-like processes and potentiates prolactin secretion by GH3 rat pituitary cells

1989 ◽  
Vol 40 (2) ◽  
pp. 106-118 ◽  
Author(s):  
Nicole Brunet-de Carvalho ◽  
Renée Picart ◽  
Solange Van de Moortele ◽  
Claude Tougard ◽  
Andrée Tixier-Vidal
Keyword(s):  
Prolactin Secretion ◽  
Pituitary Cells ◽  
Rat Pituitary ◽  
Rat Pituitary Cells
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