Thyrotropin-releasing hormone stimulates inositol phosphate production in normal anterior pituitary cells and GH3 tumour cells in the presence of lithium

1983 ◽  
Vol 3 (12) ◽  
pp. 1091-1099 ◽  
Author(s):  
John G. Baird ◽  
Pauline R. M. Dobson ◽  
Richard J. H. Wojcikiewicz ◽  
Barry L. Brown
Keyword(s):  
Dose Response ◽  
Anterior Pituitary ◽  
Inositol Phosphate ◽  
Thyrotropin Releasing Hormone ◽  
Pituitary Cells ◽  
Anterior Pituitary Cells ◽  
Trh Stimulation ◽  
Response Profile ◽  
Inositol Phosphate Accumulation ◽  
Stimulation Of

Phosphatidylinositol (Ptd Ins) breakdown in response to thyrotropin-releasing hormone (TRH) was measured after preincubation of both normal rat anterior pituitary cells and GH3 turnout cells with [3H]inositol by the determination of [3H]inositol phosphate accumulation in the presence of lithium (which inhibits myo-inositol phosphatase). The method employed, which was originally developed for use with tissue slices, was adapted for isolated cells in monolayer culture. In GH3 cells, TRH stimulated the breakdown of phosphoinositide in a manner similar to that reported previously using alternative methods. Furthermore, in normal male anterior pituitary cells the dose-response profile for TRH stimulation of inositol phosphate accumulation was found to correlate well with the dose-response profile for TRH stimulation of prolactin secretion. As this response was maintained in the absence of added calcium, the breakdown of phosphoinositide would appear to be implicated as an event preceding calcium mobilization.

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.

Cholinergic Stimulation of Inositol Phosphate Production in Cultured Anterior Pituitary Cells

1987 ◽  
Vol 46 (4) ◽  
pp. 306-311 ◽  
Author(s):  
P. Luigi Canonico ◽  
David Jarvis ◽  
Maria Angela Sortino ◽  
Umberto Scapagnini ◽  
Robert M. MacLeod
Keyword(s):  
Anterior Pituitary ◽  
Inositol Phosphate ◽  
Pituitary Cells ◽  
Cholinergic Stimulation ◽  
Anterior Pituitary Cells ◽  
Inositol Phosphate Production ◽  
Stimulation Of

Kallidin-induced stimulation of inositol phosphate production and prolactin release in rat anterior pituitary cells

1990 ◽  
Vol 123 (1) ◽  
pp. 37-42 ◽  
Author(s):  
T. Hugh Jones ◽  
Barry L. Brown ◽  
Pauline R. M. Dobson
Keyword(s):  
Anterior Pituitary ◽  
Inositol Phosphate ◽  
Prolactin Secretion ◽  
Male Rat ◽  
Pituitary Cells ◽  
Phosphoinositide Metabolism ◽  
Prolactin Release ◽  
Anterior Pituitary Cells ◽  
Inositol Phosphate Production ◽  
Stimulation Of

Abstract. The effect of the kinin, kallidin (lysyl-brady-kinin) on phosphoinositide metabolism and prolactin secretion was examined in male rat anterior pituitary cells in primary culture. Kallidin was found to stimulate both total inositol phosphate production and prolactin release. The stimulation of inositol phosphate was biphasic in nature, similar to that previously reported for bradykinin, although kallidin was approximately 10-fold more potent. Kallidin also stimulated prolactin secretion provoking a maximal stimulation of 193.0±11.1 (sem)% at 1 μmol/l. These findings suggest that kallidin-induced prolactin secretion may be mediated intracellularly by activation of phosphoinositide metabolism. The B2 receptor antagonists had no significant inhibitory effects on kallidin-stimulated phosphoinositide metabolism or prolactin release. The B1 agonist des-Arg9-bradykinin has previously been shown to have no effect on either parameter. As the effects of kinins on anterior pituitary cells do not appear to be mediated by either of the known kinin receptors, they may, therefore, act via a hitherto unrecognised kinin receptor.

Specific oxytocin agonist stimulates prolactin release but has no effect on inositol phosphate accumulation in isolated rat anterior pituitary cells

1993 ◽  
Vol 10 (2) ◽  
pp. 107-114 ◽  
Author(s):  
S E Chadio ◽  
F A Antoni
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Inositol Phosphates ◽  
Inositol Phosphate ◽  
Pituitary Cells ◽  
Uterine Tissue ◽  
Prolactin Release ◽  
Anterior Pituitary Cells ◽  
Oxytocin Receptors ◽  
Stimulation Of

ABSTRACT We have previously characterized specific oxytocin receptors in the rat anterior pituitary gland, using a highly selective oxytocin receptor antagonist as radio-ligand. The aim of the present study was to examine whether occupation of these receptors by oxytocin produces a stimulation of prolactin release and a rise in the accumulation of total inositol phosphates in the rat adenohypophysis. Anterior pituitary cells harvested from randomly cycling and diethylstilboestrol (100 μg s.c.)-treated rats were perifused with Dulbecco's minimal essential medium at a rate of 0·3 ml/min. Oxytocin and the specific oxytocin agonist [Thr4-Gly7]-oxytocin (TG-OT) both stimulated a significant prolactin release at concentrations of 10-6 and 10-7 m. Oestrogen treatment did not affect the response to oxytocin, indicating that there is no straightforward correlation between receptor number and prolactin secretory response in the rat pituitary gland. The involvement of phosphoinositide hydrolysis was investigated in dispersed anterior pituitary cells and uterine tissue from randomly cycling rats. Oxytocin and arginine-vasopressin stimulated a significant (P<0·05) and dose-related increase in total inositol phosphates, vasopressin being more potent. The specific oxytocin agonist TG-OT had no effect on total inositol phosphate production in pituitary cells, but when tested in uterine tissue it significantly (P< 0.05) stimulated the accumulation of total inositol phosphate at all concentrations tested (10-5 to 10-9 m). In conclusion, the data show that oxytocin has prolactin-releasing activity, acting on specific receptors in the anterior pituitary gland. Furthermore, although oxytocin receptors in the rat uterus are coupled to the inositol phospholipid cycle, it would appear that this is not a prerequisite for the stimulation of prolactin secretion when specific oxytocin receptors in the rat adenohypophysis are activated.

scholarly journals Thapsigargin, but not caffeine, blocks the ability of thyrotropin-releasing hormone to release Ca2+ from an intracellular store in GH4C1 pituitary cells

1990 ◽  
Vol 267 (2) ◽  
pp. 359-364 ◽  
Author(s):  
G J Law ◽  
J A Pachter ◽  
O Thastrup ◽  
M R Hanley ◽  
P S Dannies
Keyword(s):  
Channel Blocker ◽  
Inositol Phosphate ◽  
Cell Types ◽  
Thyrotropin Releasing Hormone ◽  
Pituitary Cells ◽  
Intracellular Store ◽  
Receptor Level ◽  
Releasing Hormone ◽  
Trh Stimulation ◽  
Stimulation Of

Thapsigargin stimulates an increase of cytosolic free Ca2+ concentration [( Ca2+]c) in, and 45Ca2+ efflux from, a clone of GH4C1 pituitary cells. This increase in [Ca2+]c was followed by a lower sustained elevation of [Ca2+]c, which required the presence of extracellular Ca2+, and was not inhibited by a Ca2(+)-channel blocker, nimodipine. Thapsigargin had no effect on inositol phosphate generation. We used thyrotropin-releasing hormone (TRH) to mobilize Ca2+ from an InsP3-sensitive store. Pretreatment with thapsigargin blocked the ability of TRH to cause a transient increase in both [Ca2+]c and 45Ca2+ efflux. The block of TRH-induced Ca2+ mobilization was not caused by a block at the receptor level, because TRH stimulation of InsP3 was not affected by thapsigargin. Rundown of the TRH-releasable store by Ca2(+)-induced Ca2+ release does not appear to account for the action of thapsigargin on the TRH-induced spike in [Ca2+]c, because BAY K 8644, which causes a sustained rise in [Ca2+]c, did not block Ca2+ release caused by TRH. In addition, caffeine, which releases Ca2+ from intracellular stores in other cell types, caused an increase in [Ca2+]c in GH4C1 cells, but had no effect on a subsequent spike in [Ca2+]c induced by TRH or thapsigargin. TRH caused a substantial decrease in the amount of intracellular Ca2+ released by thapsigargin. We conclude that in GH4C1 cells thapsigargin actively discharges an InsP3-releasable pool of Ca2+ and that this mechanism alone causes the block of the TRH-induced increase in [Ca2+]c.

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