2-HYDROXYOESTRADIOL INHIBITS PROLACTIN RELEASE FROM THE SUPERFUSED RAT PITUITARY GLAND

1981 ◽  
Vol 90 (3) ◽  
pp. 315-322 ◽  
Author(s):  
ELIZABETH A. LINTON ◽  
NICKI WHITE ◽  
OFELIA LIRA DE TINEO ◽  
S. L. JEFFCOATE

The effects of 2-hydroxyoestradiol (2OH-OE2), dopamine, oestradiol-17β and 2OH-OE2 plus dopamine on prolactin and LH release from the male rat pituitary gland were examined in vitro. 2-Hydroxyoestradiol reduced prolactin secretion by 51% at 10−10 mol/l and by 34% at 10−7 mol/l, while oestradiol-17β had no effect at these doses. Dopamine alone (5 × 10−7 mol/l) decreased prolactin released by 58%, 2OH-OE2 plus dopamine produced a similar inhibition of 60%. No significant effect on LH release was observed throughout.

1977 ◽  
Vol 72 (1) ◽  
pp. 35-39 ◽  
Author(s):  
JOAN JACOBI ◽  
H. M. LLOYD ◽  
J. D. MEARES

SUMMARY The times of onset of oestrogen-induced prolactin secretion and DNA synthesis were studied in the pituitary gland of the male rat. At intervals from 3 to 96 h after injection of 10 mg diethylstilboestrol dipropionate, serum and pituitary prolactin concentrations were measured by radioimmunoassay and pituitary DNA synthesis by incorporation of [3H]thymidine in vitro. Serum prolactin was raised significantly from 6 h onwards and DNA synthesis was increased from 30 h onwards. Pituitary prolactin concentration began to increase at 30 h. Significant correlations were obtained between serum prolactin and DNA synthesis from 24 to 72 h but not during the period of prolactin secretion from 6 to 24 h.


1982 ◽  
Vol 94 (3) ◽  
pp. 347-NP ◽  
Author(s):  
M. J. Cronin ◽  
D. A. Keefer ◽  
C. A. Valdenegro ◽  
L. G. Dabney ◽  
R. M. MacLeod

The MtTW15 transplantable pituitary tumour grown in rats was tested in vitro for the ability of dopamine agonists to affect prolactin secretion and for the existence of dopamine receptors. Prolactin release from enzymatically dispersed cells and non-enzymatically treated tissue fragments of both the tumour and the anterior pituitary gland was determined in a cell perifusion column apparatus. Dopamine (0·1–5 μmol/l), bromocriptine (50 nmol/l) and the dopamine antagonist haloperidol (100 nmol/l) had no effect on prolactin release from the tumour cells. In contrast, dopamine (500 nmol/l) inhibited prolactin secretion from normal anterior pituitary cells in a parallel cell column and haloperidol blocked this inhibition. Although oestrogen treatment in vivo stimulated prolactin release in vitro when the tumour was removed and studied in the cell column, oestrogen had no effect on the inability of dopamine to modify the prolactin secretion. Growth hormone release from the tumour cells was not affected by dopamine. Although MtTW15 cells were refractory to dopaminergic inhibition of prolactin release, the dopamine receptors present in tumour homogenates were indistinguishable from the dopamine receptors previously defined in the normal anterior pituitary gland. The binding of the dopamine antagonist [3H]spiperone to the tumour was saturable (110 fmol/mg protein), of high affinity to one apparent class of sites (dissociation constant = 0·12 nmol/l), reversible and sensitive to guanine nucleotides. The pharmacology of the binding was defined in competition studies with a large number of agonists and antagonists. From the order of potency of these agents, a dopaminergic interaction was apparent. We conclude that the prolactin-secreting MtTW15 tumour cells appear to be completely unresponsive to dopamine or to the potent dopamine agonist bromocriptine, in spite of apparently normal dopamine receptors in the tumour.


1980 ◽  
Vol 87 (1) ◽  
pp. 95-103 ◽  
Author(s):  
G. DELITALA ◽  
T. YEO ◽  
ASHLEY GROSSMAN ◽  
N. R. HATHWAY ◽  
G. M. BESSER

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.


1969 ◽  
Vol 45 (2) ◽  
pp. 183-NP ◽  
Author(s):  
C. S. NICOLL ◽  
J. A. PARSONS ◽  
R. P. FIORINDO ◽  
C. W. NICHOLS

SUMMARY A procedure for estimating rat prolactin and growth hormone (somatotrophin, STH), by measuring the optical density of the electrophoretically isolated and stained hormone bands in polyacrylamide gel columns, is described and evaluated. A simple and inexpensive densitometer is also described. Prolactin levels in adenohypophyses and in medium from pituitary incubates were measured by electrophoresis-densitometry (ED) and by the pigeon crop-sac assay. The two methods showed a high degree of correlation. The validity of the ED method for estimating prolactin levels in adenohypophysial tissue and in incubation medium was demonstrated by comparing the prolactin content of adult male and female and of oestrogen-treated male glands and by experiments in vitro. The female pituitary contained about three times more prolactin than the male and the glands of oestrogen-treated males had levels about the same as those of females. It was also shown that the ED method could be used to demonstrate the inhibitory effects of extract of rat hypothalamic tissue on prolactin secretion in vitro by the rat pituitary. Levels of STH in adult male glands, as measured by this method, were comparable to results obtained by others using immunoassays. Propylthiouracil-induced hypothyroidism depressed the STH and prolactin levels in male rat pituitaries, in agreement with the observations of others. The stainability of the prolactin band in rat adenohypophyses was observed to decrease with time when the glands were stored on dry ice. No such change occurred in the staining characteristics of the STH band. Other aspects of the ED method are discussed, including its precision, efficiency, sensitivity, economy and utility.


2000 ◽  
Vol 166 (2) ◽  
pp. 373-380 ◽  
Author(s):  
BH Duvilanski ◽  
D Pisera ◽  
A Seilicovich ◽  
M del Carmen Diaz ◽  
M Lasaga ◽  
...  

Substance P (SP) may participate as a paracrine and/or autocrine factor in the regulation of anterior pituitary function. This project studied the effect of TRH on SP content and release from anterior pituitary and the role of SP in TRH-induced prolactin release. TRH (10(-7) M), but not vasoactive intestinal polypeptide (VIP), increased immunoreactive-SP (ir-SP) content and release from male rat anterior pituitary in vitro. An anti-prolactin serum also increased ir-SP release and content. In order to determine whether intrapituitary SP participates in TRH-induced prolactin release, anterior pituitaries were incubated with TRH (10(-7) M) and either WIN 62,577, a specific antagonist of the NK1 receptor, or a specific anti-SP serum. Both WIN 62,577 (10(-8) and 10(-7) M) and the anti-SP serum (1:250) blocked TRH-induced prolactin release. In order to study the interaction between TRH and SP on prolactin release, anterior pituitaries were incubated with either TRH (10(-7) M) or SP, or with both peptides. SP (10(-7) and 10(-6) M) by itself stimulated prolactin release. While 10(-7) M SP did not modify the TRH effect, 10(-6) M SP reduced TRH-stimulated prolactin release. SP (10(-5) M) alone failed to stimulate prolactin release and markedly decreased TRH-induced prolactin release. The present study shows that TRH stimulates ir-SP release and increases ir-SP content in the anterior pituitary. Our data also suggest that SP may act as a modulator of TRH effect on prolactin secretion by a paracrine mechanism.


1989 ◽  
Vol 120 (5) ◽  
pp. 682-688 ◽  
Author(s):  
G. Morel ◽  
J.-G. Chabot ◽  
A. Enjalbert ◽  
M. Priam ◽  
P. M. Dubois

Abstract. Classic concepts of calcitonin (CT) function have focused on the effects of CT on calcium homeostasis. More recently CT actions on brain and pituitary have been investigated. In order to evaluate the effects of CT on the anterior pituitary gland we studied the action(s) of CT in vitro and visualized endogenous CT in adult male rat pituitary gland by immunocytochemistry on ultrathin sections obtained by cryoultramicomy. In vitro study using dispersed anterior pituitary cells indicated that CT stimulated the secretion of PRL, whereas the secretion of GH, TSH and LH was not affected. CT-like immunoreactivity was observed in lactotropes only. The other pituitary cell types were not immunoreactive. In lactotropes, immunostaining was observed in the cytoplasm and in the nucleus. In the cytoplasm, CT-like immunoreactivity was visuzalized in the cytoplasmic matrix and in the secretory granules. In the nucleus, immunostaining was distributed primarly in the euchromatin, in the vincinity of heterochromatin region. CT-like immunoreactivity was also observed at the plasma membrane but was only scarce. No reaction product was found when anti-CT serum pre-incubated with CT was used. In conclusion, these results bring evidence for a direct action of CT on lactotrope regulation in vitro as well as in intact animals.


1984 ◽  
Vol 103 (1) ◽  
pp. 63-69 ◽  
Author(s):  
T. R. Hall ◽  
A. Chadwick

ABSTRACT Anterior pituitary glands from broiler fowl were incubated by themselves, with hypothalamic tissue or with thyrotrophin releasing hormone (TRH) in medium containing dopamine and its antagonist pimozide. The presence of hypothalamic tissue or TRH resulted in a stimulation of release of prolactin. Neither dopamine nor pimozide affected prolactin release directly from the pituitary gland. Dopamine inhibited the release of prolactin stimulated by hypothalamic tissue or TRH, in a concentration-dependent fashion. Pimozide diminished the response to dopamine. After pituitary glands were preincubated for 20 h in medium containing oestradiol-17β, the basal release of prolactin was enhanced as was the response to TRH. Both basal and TRH-stimulated release of prolactin from the oestrogen-primed pituitary glands was inhibited by dopamine, an effect blocked by pimozide. Hypothalami from broiler fowl were incubated for up to 8 h in medium containing dopaminergic drugs and pituitary glands were incubated in this medium, alone or with pimozide. As indicated by the prolactin released by the pituitary glands, the hypothalami appeared to secrete prolactin-releasing activity in a time-related fashion. Dopaminergic activity was also present in the hypothalami, since pimozide enhanced the prolactin-releasing activity of the medium. Dopamine apparently inhibited and pimozide stimulated the secretion of releasing activity from the hypothalamus. These results suggest that dopamine inhibits release of prolactin directly from the pituitary gland only when prolactin secretion is high. The hypothalamus secretes at least two factors regulating prolactin secretion, a prolactin-releasing factor and a dopaminergic prolactin-inhibiting factor. Dopamine may also play an inhibitory role in the regulation of secretion of the prolactin-releasing factor. J. Endocr. (1984) 103, 63–69


1982 ◽  
Vol 242 (4) ◽  
pp. E226-E233
Author(s):  
H. A. Zacur ◽  
W. E. Mitch ◽  
J. E. Tyson ◽  
P. T. Ostrow ◽  
G. V. Foster

Regulation of prolactin secretion was investigated by perfusing rat pituitaries in vitro. Two pituitary glands from inbred rats were transplanted beneath the renal capsule of a third recipient rat. Three weeks later, the transplanted kidney was removed and perfused in vitro with a defined cell-free medium. Normal renal function was maintained during perfusion, and cell morphology of the transplants remained unchanged as assessed by electron microscopy. Pituitary prolactin content did not change after 120 min of perfusion despite release of approximately 10 micrograms of hormone. Thyrotropin-releasing hormone (10 ng/ml) did not stimulate prolactin release; dopamine (20 ng/ml) rapidly, but transiently inhibited prolactin release; bromocriptine (20 ng/ml) rapidly and persistently inhibited prolactin release; haloperidol (100 ng/ml) blocked the inhibition by dopamine or bromocriptine, but when given alone inhibited prolactin release. Finally, prolactin release was also inhibited by the presence of 100 and 200 ng/ml, but not 50 ng/ml of NIAMDD RP-1 rat prolactin. It is concluded that in vitro perfusion of transplanted rat pituitaries provides a new model for studying the direct effect of agents on the secretion of prolactin from the pituitary and that rat prolactin and/or its metabolites directly inhibit pituitary prolactin secretion.


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