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.

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.

scholarly journals Intermedin/Adrenomedullin-2 Inhibits Growth Hormone Release from Cultured, Primary Anterior Pituitary Cells

Endocrinology ◽  
2006 ◽  
Vol 147 (2) ◽  
pp. 859-864 ◽  
Author(s):  
Meghan M. Taylor ◽  
Sara L. Bagley ◽  
Willis K. Samson
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Hormone Secretion ◽  
Prolactin Secretion ◽  
Anterior Pituitary Gland ◽  
Male Rats ◽  
Pituitary Cells ◽  
Anterior Pituitary Cells ◽  
Peptide Family

Intermedin (IMD), a novel member of the adrenomedullin (AM), calcitonin gene-related peptide (CGRP), amylin (AMY) peptide family, has been reported to act promiscuously at all the known receptors for these peptides. Like AM and CGRP, IMD acts in the circulation to decrease blood pressure and in the brain to inhibit food intake, effects that could be explained by activation of the known CGRP, AM, or AMY receptors. Because AM, CGRP, and AMY have been reported to affect hormone secretion from the anterior pituitary gland, we examined the effects of IMD on GH, ACTH, and prolactin secretion from dispersed anterior pituitary cells harvested from adult male rats. IMD, in log molar concentrations ranging from 1.0 pm to 100 nm, failed to significantly alter basal release of the three hormones. Similarly, IMD failed to significantly alter CRH-stimulated ACTH or TRH-stimulated prolactin secretion in vitro. However, IMD concentration-dependently inhibited GHRH-stimulated GH release from these cell cultures. The effects of IMD, although requiring higher concentrations, were as efficacious as those of somatostatin and, like somatostatin, may be mediated, at least in part, by decreasing cAMP accumulation. These actions of IMD were not shared by other members of the AM-CGRP-AMY family of peptides, suggesting the presence of a novel, unique IMD receptor in the anterior pituitary gland and a potential neuroendocrine action of IMD to interact with the hypothalamic mechanisms controlling growth and metabolism.

Evidence that angiotensin II is a paracrine agent mediating gonadotrophin-releasing hormone-stimulated inositol phosphate production and prolactin secretion in the rat

1988 ◽  
Vol 116 (3) ◽  
pp. 367-371 ◽  
Author(s):  
T. H. Jones ◽  
B. L. Brown ◽  
P. R. M. Dobson
Keyword(s):  
Angiotensin Ii ◽  
Inositol Phosphates ◽  
Inositol Phosphate ◽  
Prolactin Secretion ◽  
Male Rats ◽  
Pituitary Cells ◽  
Releasing Hormone ◽  
Phosphate Accumulation ◽  
Inositol Phosphate Accumulation ◽  
Gonadotrophin Releasing Hormone

ABSTRACT Gonadotrophin-releasing hormone (GnRH) stimulated the accumulation of inositol phosphates and prolactin secretion in anterior pituitary cells from young male rats. Saralasin ([Sar1,Ala8]-angiotensin II; a competitive antagonist of angiotensin II) inhibited the increase in both inositol phosphates and prolactin in a dose-dependent manner. Since angiotensin II has been shown to be a potent stimulus for inositol phosphate accumulation and prolactin secretion in the lactotroph, these findings suggest that angiotensin II acts as a paracrine agent, being released from the gonadotroph in response to GnRH and causing the lactotroph to release prolactin through an effect on phosphoinositide metabolism. The ability of GnRH to promote prolactin release was lost in pituitaries from older rats, and the increase in total inositol phosphate accumulation was less. These findings provide evidence of a physiological role for the presence of the renin–angiotensin system within the pituitary gland. J. Endocr. (1988) 116, 367–371

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.

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.

scholarly journals The hormonal status modulates the effect of neurokinin A on prolactin secretion in female rats

1998 ◽  
Vol 159 (3) ◽  
pp. 389-395 ◽  
Author(s):  
D Pisera ◽  
S Theas ◽  
A De Laurentiis ◽  
M Lasaga ◽  
B Duvilanski ◽  
...  
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
In Vitro Release ◽  
Anterior Pituitary Gland ◽  
Female Rats ◽  
Male Rats ◽  
Neurokinin A ◽  
Pituitary Cells ◽  
Anterior Pituitary Cells ◽  
Ovx Rats

We have previously reported that neurokinin A (NKA), a tachykinin closely related to substance P, increases the release of prolactin (PRL) from the anterior pituitary gland of male rats, but not from pituitaries of ovariectomized (OVX) female rats. In this study, we evaluated the influence of estrogens in the action of NKA on PRL secretion in female rats. NKA stimulated the in vitro release of PRL from pituitary glands of OVX-chronically estrogenized rats, and of proestrus and estrus rats, but had no effect in anterior pituitaries of diestrus rats. In addition, we observed that cultured anterior pituitary cells of OVX rats responded to NKA only when they were incubated for 3 days in the presence of estradiol 10(-9) M. This effect was blocked by L-659,877, an NK-2 receptor antagonist. We also studied the action of NKA on PRL release during lactation. The response of anterior pituitary cells to NKA was variable over this period. The maximal sensitivity to NKA was observed at day 10 of lactation. Furthermore, the blockade of endogenous NKA by the administration of an anti-NKA serum to lactating rats reduced the PRL surge induced by the suckling stimulus. These results show that the responsiveness of the anterior pituitary gland of female rats to NKA is modulated by the endocrine environment, and suggest that NKA may participate in the control of PRL secretion during the estrus cycle and lactation.

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