The posterior pituitary: regulation of anterior pituitary prolactin secretion

Science ◽  
1981 ◽  
Vol 213 (4508) ◽  
pp. 659-661 ◽  
Author(s):  
L. Peters ◽  
M. Hoefer ◽  
N Ben-Jonathan
Keyword(s):  
Anterior Pituitary ◽  
Prolactin Secretion ◽  
Posterior Pituitary ◽  
Pituitary Prolactin

Ritonavir and Saquinavir Directly Stimulate Anterior Pituitary Prolactin Secretion, in Vitro

2002 ◽  
Vol 15 (1) ◽  
pp. 65-68 ◽  
Author(s):  
G. Orlando ◽  
L. Brunetti ◽  
M. Vacca
Keyword(s):  
Protease Inhibitors ◽  
Anterior Pituitary ◽  
Dopamine Release ◽  
Prolactin Secretion ◽  
Hiv Protease ◽  
Type I ◽  
Endogenous Dopamine ◽  
Pituitary Prolactin ◽  
Hiv 1

An association between human immunodeficiency virus type I (HIV-1) protease inhibitors (Pis) and galactorrhoea/hyperprolactinemia adverse effect has recently been reported in four HIV-1-infected women treated with Pis (indinavir, nelfinavir, ritonavir or saquinavir). This could be explained by a direct effect of ritonavir and saquinavir on anterior pituitary prolactin (PRL) release, and/or an indirect effect of Pis on the secretion of hypothalamic dopamine, which is the main PRL inhibitory factor. Anterior pituitaries were explanted from adult male Wistar rats, the cells were trypsin dispersed, plated into multiwell cultures and incubated for 1 h with either ritonavir or saquinavir (0.01 nM-1mM). PRL release into the incubation medium was evaluated by radioimmunoassay. Hypothalamic neuronal endings (synaptosomes) were prepared by tissue homogenization, incubated with [3H]dopamine, substituting for the endogenous dopamine pool, and perfused with ritonavir or saquinavir, both basally and during depolarization (K+ 15 mM)-induced dopamine release. Beta-emission from 2 min perfusate fractions, corresponding to [3H]dopamine release, was detected by liquid scintillation scanning. We found that both ritonavir and saquinavir are able to significantly stimulate PRL secretion, with saquinavir slightly more effective than ritonavir. On the contrary, both protease inhibitors do not modify either basal or depolarization-induced dopamine release. We can speculate that HIV Pis despite a high affinity for the catalytic site of HIV protease, could also bind to and inhibit homologous mammalian proteins in the anterior pituitary that are involved in PRL secretion.

Size heterogeneity of prolactin secreted from and stored in the rat anterior pituitary gland in vitro

1984 ◽  
Vol 4 (2) ◽  
pp. 129-137 ◽  
Author(s):  
Andrew M. Bentley ◽  
Teresa K. Surowy ◽  
Michael Wallis
Keyword(s):  
Anterior Pituitary ◽  
Relative Proportion ◽  
Gel Filtration ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Pituitary Glands ◽  
Dimeric Form ◽  
Size Heterogeneity ◽  
Pituitary Prolactin

The size heterogeneity of rat pituitary prolactin was investigated using anterior pituitary glands from female rats incubated in vitro and gel filtration on Sephadex G-100. Monomeric prolactin was preferentially secreted compared with dimeric and ‘trimeric” material. When glands were incubated with dopamine, prolactin secretion was inhibited and the relative proportion of dimer in the gland (but not the medium) was decreased. Morphine sulphate reversed the effect of dopamine on prolactin secretion and on the proportion of prolactin in the gland that was in the dimeric form. The results suggest that monomeric prolactin is more readily secreted than dimer, and that dopamine decreases the production or stability of the dimer.

Suppressed serum prolactin in sinoaortic-denervated rats

1987 ◽  
Vol 252 (2) ◽  
pp. R290-R293
Author(s):  
N. Alexander ◽  
S. Melmed ◽  
M. Morris
Keyword(s):  
Heart Rate ◽  
Anterior Pituitary ◽  
High Performance ◽  
Wistar Rats ◽  
Serum Prolactin ◽  
Posterior Pituitary ◽  
Before And After ◽  
Male Wistar Rats ◽  
Pituitary Prolactin ◽  
Arterial Baroreceptor

We investigated the effect of arterial baroreceptor deafferentation on serum and pituitary prolactin (PRL) and on catecholamines in median eminence (ME) and anterior and posterior pituitaries. Male Wistar rats were sinoaortic denervated (SAD) or sham operated (SO). Three days after surgery serum prolactin, measured by radioimmunoassay, was suppressed in SAD rats (-54%, P less than 0.05), and dopamine (DA) and norepinephrine (NE) concentrations, measured by radioenzymatic or high-performance liquid chromatography electron capture methods, were significantly reduced in ME of SAD rats (NE, -54% P less than 0.005 and DA, -56% P less than 0.001). Simultaneously, anterior pituitary of SAD rats had significant increases in both catecholamines, whereas posterior pituitary showed no changes. Four hours after surgery serum PRL was also reduced (-40%, P less than 0.05) in SAD rats, but no changes in ME catecholamines were found. Mean arterial pressure (MAP) and heart rate were measured before and after injection of bromocriptine (0.5 mg/kg ip) in SAD and SO rats 3 days after surgery. Bromocriptine markedly suppressed serum PRL in both groups and reduced MAP from 144 +/- 10 to 84 +/- 5 and from 116 +/- 2 to 99 +/- 3 in SAD and SO rats, respectively; heart rate was reduced in SAD rats. We conclude that the SAD rat is a model of hypertension with suppressed serum PRL and that interruption of arterial baroreceptor nerves suppresses PRL secretion probably by modulating tuberoinfundibular turnover of catecholamines.

Pertussis toxin uncouples dopamine agonist inhibition of prolactin release

1983 ◽  
Vol 244 (5) ◽  
pp. E499-E504 ◽  
Author(s):  
M. J. Cronin ◽  
G. A. Myers ◽  
R. M. MacLeod ◽  
E. L. Hewlett
Keyword(s):  
Cyclic Amp ◽  
Dopamine Agonist ◽  
Pertussis Toxin ◽  
Anterior Pituitary ◽  
Prolactin Secretion ◽  
Pituitary Cells ◽  
Prolactin Release ◽  
Pituitary Prolactin ◽  
Hormone System

Pertussis toxin, a protein exotoxin produced by Bordetella pertussis, markedly reduced or eliminated the ability of dopamine or the dopamine agonist bromocriptine to inhibit prolactin release from anterior pituitary cells in vitro. Toxin-mediated reversal of the effect on dopamine agonist inhibition of prolactin release occurred with a lag of greater than 6 h, was maximal by 24 h, and persisted for at least 6 days after removal of the toxin from the medium. The toxin reduced dopamine agonist efficacy without altering potency or directly modifying the dopamine receptor (as measured by [3H]spiperone binding). The ability of dopamine to reduce cellular cyclic AMP content was also antagonized by pertussis toxin, supporting the hypothesis that reduction of cellular cyclic AMP content and inhibition of prolactin secretion may be causally related. These data demonstrated that pertussis toxin can prevent the typical inhibitory action of dopamine agonists on anterior pituitary prolactin release and suggest that this receptor-mediated inhibitory hormone system is analogous to other inhibitory receptors coupled to adenylate cyclase.

Prolactin secretion and dopamine receptors of the MtTW15 transplantable pituitary tumour

1982 ◽  
Vol 94 (3) ◽  
pp. 347-NP ◽  
Author(s):  
M. J. Cronin ◽  
D. A. Keefer ◽  
C. A. Valdenegro ◽  
L. G. Dabney ◽  
R. M. MacLeod
Keyword(s):  
Pituitary Gland ◽  
Dopamine Receptors ◽  
Anterior Pituitary ◽  
Pituitary Tumour ◽  
Prolactin Secretion ◽  
Tumour Cells ◽  
Dopamine Antagonist ◽  
Cell Column ◽  
Prolactin Release

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.

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.

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