Dopamine Inhibits Prolactin Secretion Stimulated by the Calcium Channel Agonist Bay-K-8644 through a Pertussis Toxin-Sensitive G Protein in Anterior Pituitary Cells*

Endocrinology ◽  
1988 ◽  
Vol 123 (1) ◽  
pp. 406-412 ◽  
Author(s):  
A. ENJALBERT ◽  
F. MUSSET ◽  
C. CHENARD ◽  
M. PRIAM ◽  
C. KORDON ◽  
...  
Keyword(s):  
Calcium Channel ◽  
G Protein ◽  
Pertussis Toxin ◽  
Anterior Pituitary ◽  
Prolactin Secretion ◽  
Bay K 8644 ◽  
Pituitary Cells ◽  
Anterior Pituitary Cells ◽  
Channel Agonist

Direct effect of adenosine on prolactin secretion at the level of the single rat lactotroph: involvement of pertussis toxin-sensitive and -insensitive transducing mechanisms

1993 ◽  
Vol 11 (3) ◽  
pp. 325-334 ◽  
Author(s):  
A Scorziello ◽  
E Landolfi ◽  
M Grimaldi ◽  
O Meucci ◽  
C Ventra ◽  
...  
Keyword(s):  
Adenylate Cyclase ◽  
Phospholipase C ◽  
G Protein ◽  
Pertussis Toxin ◽  
Anterior Pituitary ◽  
Prolactin Secretion ◽  
Catalytic Subunit ◽  
Pituitary Cells ◽  
Prolactin Release ◽  
Anterior Pituitary Cells

ABSTRACT We studied the effect of adenosine on prolactin secretion by the anterior pituitary, and the transduction mechanisms whereby the purine exerts its action. Adenosine inhibited prolactin release in basal and in vasoactive intestinal peptide (VIP)- or TRH-stimulated conditions. Pertussis toxin pretreatment reduced the inhibition of VIP-stimulated prolactin secretion which was induced by adenosine, while it completely abolished the effect of the purine on TRH-evoked prolactin release. In membrane preparations of anterior pituitary cells, adenosine reduced the adenylate cyclase activity stimulated by VIP. Such an inhibition was not blocked by pertussis toxin pretreatment. Furthermore, the purine reduced TRH-stimulated inositol phosphate production in cultured anterior pituitary cells, an effect that was reversed by pretreatment with pertussis toxin. In addition, the nucleoside did not significantly affect the TRH-induced rise in intracellular calcium. In conclusion, our data show that adenosine inhibits prolactin secretion, acting on purinergic receptors coupled to the adenylate cyclase enzyme and phospholipase C. The effect of the nucleoside on adenylate cyclase seems to be achieved either by the involvement of an adenosine receptor coupled to the catalytic subunit of the enzyme via a pertussis toxin-sensitive G protein, or by the activation of a site directly coupled to the catalytic subunit of the adenylate cyclase (the P site). Its effect on phospholipase C seems to be mediated by a purinergic receptor coupled to the intracellular effector via a pertussis toxin-sensitive G protein.

Hyperosmotic regulation of voltage-gated calcium currents in rat anterior pituitary cells

1996 ◽  
Vol 75 (5) ◽  
pp. 1894-1900 ◽  
Author(s):  
O. Matzner ◽  
S. Ben-Tabou ◽  
I. Nussinovitch
Keyword(s):  
Calcium Channel ◽  
Anterior Pituitary ◽  
Calcium Influx ◽  
Hormone Secretion ◽  
Bay K 8644 ◽  
Calcium Currents ◽  
Pituitary Cells ◽  
Activation Curve ◽  
Voltage Gated ◽  
Channel Agonist

1. The sensitivity of voltage-gated calcium currents to hyperosmotic media containing mannitol or sucrose (373-723 mOsm) and to the dihydropyridine (DHP) calcium channel agonist Bay K 8644 was examined in enriched populations of rat anterior pituitary somatotrophs by using the whole cell mode of the patch-clamp technique. 2. Hyperosmotic media reduced the amplitude of voltage-gated calcium currents. With a 61.9% increase in extracellular medium osmolarity (523 mOsm), low voltage-activated (LVA) calcium currents were reduced to 67.9 +/- 17.8% of control size and high voltage-activated (HVA) calcium currents were reduced to 57.0 +/- 5.7% (mean +/- SD) of control size. The hyperosmotic suppression of HVA calcium currents was usually accompanied with a negative shift of 6.0 +/- 2.9 mV (mean +/- SD) in the activation curve of HVA currents. 3. The DHP calcium-channel agonist Bay K 8644 (10 microM), which stimulates hormone secretion from somatotrophs, increased the amplitude of HVA calcium currents to 212.6 +/- 67.2% of their control size, prolonged their tail currents, and negatively shifted the activation curve of HVA calcium currents by 6.2 +/- 2.8 mV. 4. Hyperosmotic media reduced the amplitude of DHP-sensitive HVA calcium currents and their associated prolonged tail currents, thus providing direct evidence for hyperosmotic suppression of DHP-sensitive currents. 5. Hence, exposure of pituitary cells to hyperosmotic media reduced voltage-sensitive calcium influx through LVA and DHP-sensitive HVA calcium channels. The inhibition of calcium influx through DHP-sensitive channels, which are implicated in regulation of hormone secretion in these cells, suggests that inhibitory hyperosmotic effects on hormone secretion from pituitary cells may stem from inhibition of calcium influx, before the exocytotic process. These results may also be relevant to effects of hypertonicity on neurosecretion in the nervous system.

Modification by pertussis toxin of the responses of bovine anterior pituitary cells to acetylcholine and dopamine: effects on hormone secretion and 86Rb efflux

1988 ◽  
Vol 116 (3) ◽  
pp. 393-401 ◽  
Author(s):  
J. G. Schofield ◽  
A. I. Khan ◽  
A. Wood
Keyword(s):  
Growth Hormone ◽  
Pertussis Toxin ◽  
Anterior Pituitary ◽  
Hormone Secretion ◽  
Prolactin Secretion ◽  
Calcium Entry ◽  
Pituitary Cells ◽  
Cholinergic Stimulation ◽  
Anterior Pituitary Cells ◽  
Stimulation Of

ABSTRACT Acetylcholine is known to stimulate the secretion of growth hormone and prolactin and the efflux of 86Rb from bovine anterior pituitary cells: dopamine prevents the stimulation of 86Rb efflux and of prolactin but not growth hormone secretion. The sensitivity of these responses to pertussis toxin has been determined. Treatment of bovine anterior pituitary cells in primary culture with pertussis toxin (18 h, 100 ng/ml) did not modify the stimulation of prolactin secretion by acetylcholine, but prevented its inhibition by dopamine. In lactotrophs, dopamine but not acetylcholine receptors are therefore coupled to secretion through a pertussis toxin substrate. The stimulation of 86Rb efflux by acetylcholine was also unaffected by pertussis toxin and, again, its inhibition by dopamine was prevented. Treatment of the cells with pertussis toxin enhanced the secretion of growth hormone in response to acetylcholine. Nitrendepine (1 μmol/l) prevented the cholinergic stimulation of growth hormone but not prolactin secretion from these cells. Acetylcholine increased the cytoplasmic calcium concentration and this rise was enhanced by treatment of the cells with pertussis toxin. Nitrendepine partially inhibited the rise in calcium caused by acetylcholine, and prevented the enhancement of the rise following pertussis toxin treatment. Cholinergic stimulation of growth hormone therefore depends on calcium entry through nitrendepine-sensitive channels, whereas stimulation of prolactin secretion does not, and in somatotrophs a pertussis toxin substrate may limit calcium entry through these channels. These different sensitivities of somatotrophs and lactotrophs to pertussis toxin and nitrendepine may reflect differences in the properties of the predominant calcium currents in the two cell types. J. Endocr. (1988) 116, 393–401

Reserpine is a calcium channel antagonist in normal and GH3 rat pituitary cells

1985 ◽  
Vol 248 (1) ◽  
pp. E15-E19
Author(s):  
I. S. Login ◽  
A. M. Judd ◽  
M. J. Cronin ◽  
T. Yasumoto ◽  
R. M. MacLeod
Keyword(s):  
Calcium Channel ◽  
Calcium Channel Antagonist ◽  
Anterior Pituitary ◽  
Calcium Uptake ◽  
Calcium Ionophore ◽  
Gh3 Cells ◽  
Pituitary Cells ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Anterior Pituitary Cells

Reserpine exerts direct effects on several tissues, including inhibition of hormone release from rat anterior pituitary cells. To test the hypothesis that reserpine may be acting as a calcium channel antagonist, normal or GH3 rat anterior pituitary cells were preincubated in reserpine or the conventional calcium channel blocker, D-600, followed by exposure to 45Ca2+ together with stimulants of calcium uptake: maitotoxin, a potent calcium channel activator; A23187, a calcium ionophore; or 50 mMK+. After incubation, the cells were harvested by vacuum filtration and cell-associated radioactivity determined. In normal cells, reserpine blocked both basal and K+-stimulated calcium uptake. Reserpine selectively blocked maitotoxin but not A23187-induced calcium uptake. In GH3 cells 9 microM reserpine and 30 microM D-600 were equally effective in blocking maitotoxin-stimulated calcium uptake. Reserpine appears to block voltage-dependent calcium channels in pituitary cells in a concentration-dependent manner but not calcium uptake caused nonspecifically by A23187.

scholarly journals Cadmium Mimics Estrogen-Driven Cell Proliferation and Prolactin Secretion from Anterior Pituitary Cells

PLoS ONE ◽  
2013 ◽  
Vol 8 (11) ◽  
pp. e81101 ◽  
Author(s):  
Sonia A. Ronchetti ◽  
Eliana A. Miler ◽  
Beatriz H. Duvilanski ◽  
Jimena P. Cabilla
Keyword(s):  
Cell Proliferation ◽  
Anterior Pituitary ◽  
Prolactin Secretion ◽  
Pituitary Cells ◽  
Anterior Pituitary Cells

Bradykinin stimulates phosphoinositide metabolism and prolactin secretion in rat anterior pituitary cells

1989 ◽  
Vol 2 (1) ◽  
pp. 47-53 ◽  
Author(s):  
T.H. Jones ◽  
B. L. Brown ◽  
P. R. M. Dobson
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Inositol Phosphate ◽  
Prolactin Secretion ◽  
Male Rats ◽  
Pituitary Cells ◽  
Phosphoinositide Metabolism ◽  
Phosphate Accumulation ◽  
Anterior Pituitary Cells ◽  
Inositol Phosphate Accumulation

ABSTRACT Bradykinin stimulated prolactin secretion from monolayer cultures of rat anterior pituitary cells, the stimulation being greater from the cells of male rats. This stimulated secretion was accompanied by a rise in total inositol phosphate accumulation, suggesting that the action of bradykinin is mediated by phosphoinositide hydrolysis. The increase in inositol phosphate accumulation was biphasic; a further sharp rise occurred when the concentration of bradykinin exceeded 1 μmol/l. This may indicate that bradykinin acts on other cell types in the pituitary gland. Bradykinin had no effect on growth hormone secretion from cells of normal pituitary glands, or on prolactin secretion and phosphoinositide metabolism in GH3 rat pituitary tumour cells. Bradykinin receptor antagonists (both B1 and B2) had no effect on either bradykinin-stimulated inositol phosphate accumulation or prolactin secretion. Kallikreins, the enzymes responsible for the generation of kinins, are known to be present in the adenohypophysis. Therefore, the results presented here would suggest that kinins may have a role as paracrine agents in the pituitary gland.

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