scholarly journals Effects of dopamine on prolactin secretion and cyclic AMP accumulation in the rat anterior pituitary gland

1981 ◽  
Vol 194 (1) ◽  
pp. 119-128 ◽  
Author(s):  
Keith P. Ray ◽  
Michael Wallis
Keyword(s):  
Cyclic Amp ◽  
Cholera Toxin ◽  
Anterior Pituitary ◽  
Phosphodiesterase Inhibitors ◽  
Prolactin Secretion ◽  
Significant Inhibition ◽  
Female Rats ◽  
Control Value ◽  
Cyclic Amp Accumulation

The effects of dopamine on pituitary prolactin secretion and pituitary cyclic AMP accumulation were studied by using anterior pituitary glands from adult female rats, incubated in vitro. During 2h incubations, significant inhibition of prolactin secretion was achieved at concentrations between 1 and 10nm-dopamine. However, 0.1–1μm-dopamine was required before a significant decrease in pituitary cyclic AMP content was observed. In the presence of 1μm-dopamine, pituitary cyclic AMP content decreased rapidly to reach about 75% of the control value within 20min and there was no further decrease for at least 2h. Incubation with the phosphodiesterase inhibitors theophylline (8mm) or isobutylmethylxanthine (2mm) increased pituitary cyclic AMP concentrations 3- and 6-fold respectively. Dopamine (1μm) had no effect on the cyclic AMP accumulation measured in the presence of theophylline, but inhibited the isobutylmethylxanthine-induced increase by 50%. The dopamine inhibition of prolactin secretion was not affected by either inhibitor. Two derivatives of cyclic AMP (dibutyryl cyclic AMP and 8-bromo cyclic AMP) were unable to block the dopamine (1μm) inhibition of prolactin secretion, although 8-bromo cyclic AMP (2mm) significantly stimulated prolactin secretion and both compounds increased somatotropin (growth hormone) release. Cholera toxin (3μg/ml for 4h) increased pituitary cyclic AMP concentrations 4–5-fold, but had no effect on prolactin secretion. The inhibition of prolactin secretion by dopamine was unaffected by cholera toxin, despite the fact that dopamine had no effect on the raised pituitary cyclic AMP concentration caused by this factor. Dopamine had no significant effect on either basal or stimulated somatotropin secretion under any of the conditions tested. We conclude that the inhibitory effects of dopamine on prolactin secretion are probably not mediated by lowering of cyclic AMP concentration, although modulation of the concentration of this nucleotide in some other circumstances may alter the secretion of the hormone.

Characteristics of Action of Prostaglandins on Cyclic AMP Accumulation in Rat Anterior Pituitary Gland

1975 ◽  
Vol 53 (4) ◽  
pp. 455-460 ◽  
Author(s):  
Pierre Borgeat ◽  
Fernand Labrie ◽  
Pierre Garneau
Keyword(s):  
Cyclic Amp ◽  
Pituitary Gland ◽  
Incubation Medium ◽  
Anterior Pituitary ◽  
Complete Removal ◽  
Anterior Pituitary Gland ◽  
Pituitary Hormone ◽  
Maximal Effect ◽  
Cyclic Amp Accumulation

Prostaglandins (PGs) were found to lead to a marked stimulation of cyclic AMP accumulation in rat anterior pituitary gland in vitro in the following decreasing order of potency: [Formula: see text]. The effect of PGs is potentiated by theophylline. The stimulatory effect of PGs on cyclic AMP accumulation is already detected 2 min after the addition of 1 × 10−7 to 1 × 10−6 M PG E2 and its maximal effect is reached after approximately 30 min of incubation, with a progressive decrease toward basal cyclic AMP levels at later time intervals. Increased intracellular cyclic AMP concentrations are accompanied by an increased release of the nucleotide into the incubation medium. Complete removal of Ca2+ from the incubation medium by addition of EGTA was found to increase the stimulatory effect of PG E2 on cyclic AMP accumulation. The action of PGs on hormonal release and cyclic AMP accumulation support the hypothesis of a role of PGs in the mechanism of anterior pituitary hormone (particularly growth hormone) release.

Ontogeny of gonadotrophin receptors and gonadotrophin-stimulated cyclic AMP production in the neonatal rat ovary

1990 ◽  
Vol 127 (2) ◽  
pp. 297-303 ◽  
Author(s):  
T. Sokka ◽  
I. Huhtaniemi
Keyword(s):  
Cyclic Amp ◽  
Cholera Toxin ◽  
Specific Binding ◽  
The Body ◽  
Neonatal Rat ◽  
Female Rats ◽  
Fetal Life ◽  
Camp Production ◽  
Rat Ovary

ABSTRACT The sequence of appearance of FSH and LH receptors, and response of cyclic AMP (cAMP) production to these hormones and cholera toxin, were studied in the fetal and neonatal rat ovary. Specific binding of radio-labelled human (h)FSH and chorionic gonadotrophin (CG) to ovarian homogenates was first detectable on day 7 of life. The content of FSH receptors per ovary increased tenfold between days 7 and 16, and that of LH receptors 27-fold. A significant response of cAMP production in vitro to FSH appeared on day 4 of life, but no significant effect of hCG on cAMP was achieved until day 7. In contrast, cholera toxin had a marked effect on cAMP production by day 17 of fetal life. Although both FSH and LH receptors were detectable in the neonatal rat ovary by day 7, the present findings indicate that the FSH responsiveness of the ovary appears earlier than that of LH. The post-receptor machinery of cAMP production is already functional in the fetal ovary as shown by the experiments with cholera toxin. The appearance of the receptor may therefore be the last link in the ontogeny of the gonadotrophin signal transduction system in the ovary. To study the hormone dependence of the appearance of gonadotrophin responsiveness, neonatal female rats were treated on days 1–6 or 1–9 of life with a potent gonadotrophin-releasing hormone antagonist, and killed on the following day. In both treatment groups, the pituitary LH and FSH contents were suppressed. The body weights remained unaltered, but ovarian weights decreased significantly during both periods of treatment (days 1–6,26·1%, P < 0·05; days 1–9,54·0%, P <0·001). No difference in basal or FSH-stimulated cAMP production was achieved by antagonist treatment for the first 6 days of life. The basal and hCG-stimulated rates of cAMP production per ovary were reduced in animals treated for 9 days (P <0·01), but the FSH-stimulated cAMP production remained unaffected. Hence, whereas the responsiveness to FSH seems to develop in the absence of normal gonadotrophin secretion, a causal relationship between normal gonadotrophin levels and the appearance of LH/hCG responsiveness is apparent in the neonatal rat ovary. Journal of Endocrinology (1990) 127, 297–303

The effect of nifedipine on CRF-41 and AVP-induced ACTH release in vitro

1985 ◽  
Vol 109 (1) ◽  
pp. 32-36 ◽  
Author(s):  
Kazuharu Murakami ◽  
Kozo Hashimoto ◽  
Zensuke Ota
Keyword(s):  
Cyclic Amp ◽  
Calcium Ions ◽  
Anterior Pituitary ◽  
Inhibitory Effect ◽  
Extracellular Calcium ◽  
Pituitary Cells ◽  
Amp System ◽  
Cyclic Amp Accumulation ◽  
Acth Release

Abstract. The effect of nifedipine on CRF-41- and AVP-induced ACTH release was examined using monolayer cultured rat anterior pituitary cells and pituitary halves. Nifedipine inhibited ACTH release induced by synthetic rat CRF-41 in two systems. In pituitary halves, CRF-41 significantly stimulated both ACTH release and cyclic AMP accumulation. Nifedipine inhibited CRF-41-induced ACTH release and the inhibitory effect of nifedipine on CRF-41-induced ACTH release was accompanied by parallel decrease of cyclic AMP levels in pituitary halves. Nifedipine did not inhibit AVP-induced ACTH release in pituitary halves, and AVP did not significantly affect cyclic AMP accumulation in pituitary halves. These results suggest that CRF-41 stimulates ACTH release through the intracellular cyclic AMP system and calcium-calmodulin system which are accelerated by the influx of extracellular calcium ions. Moreover, it is suggested that the calcium required for AVP-induced ACTH release is derived primarily from intracellular rather than extracellular sources.

scholarly journals Pertussis toxin blocks the inhibitory effect of muscarinic cholinergic agonists on cyclic AMP accumulation and prolactin secretion in GH3 anterior-pituitary tumour cells

1984 ◽  
Vol 223 (1) ◽  
pp. 145-149 ◽  
Author(s):  
B L Brown ◽  
R J H Wojcikiewicz ◽  
P R M Dobson ◽  
A Robinson ◽  
L I Irons
Keyword(s):  
Cyclic Amp ◽  
Pertussis Toxin ◽  
Anterior Pituitary ◽  
Pituitary Tumour ◽  
Inhibitory Effect ◽  
Prolactin Secretion ◽  
Gh3 Cells ◽  
Muscarinic Agonists ◽  
Cyclic Amp Accumulation ◽  
Muscarinic Cholinergic

The inhibition of prolactin secretion and cyclic AMP accumulation in GH3 cells by muscarinic agonists was blocked by preincubation of the cells with pertussis toxin (islet-activating protein). There was a lag of approx. 80 min in the onset of the effect on secretion. These results suggest that muscarinic agonists decrease prolactin secretion by inhibiting adenylate cyclase activity.

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.

GnRH ACTION IN RAT ANTERIOR PITUITARY GLAND: REGULATION OF PROTEIN, GLYCOPROTEIN AND LH SYNTHESIS

1977 ◽  
Vol 86 (3) ◽  
pp. 473-488 ◽  
Author(s):  
K. M. J. Menon ◽  
K. P. Gunaga ◽  
S. Azhar
Keyword(s):  
Cyclic Amp ◽  
Anterior Pituitary ◽  
Amino Acid Mixture ◽  
Acid Mixture ◽  
Dependent Manner ◽  
Dibutyryl Cyclic Amp ◽  
Concomitant Increase ◽  
Cyclic Amp Accumulation ◽  
Dose Dependent

ABSTRACT The effect of synthetic GnRH on the synthesis of proteins and glycoproteins in the anterior pituitary and in vitro release of LH into the medium was studied. A maximal dose (25 ng/ml) of synthetic GnRH caused optimum release of radioimmunoassayable LH into the medium after 2 h of incubation. A concomitant increase in cyclic AMP accumulation in the tissue and LH in the incubation medium was also observed under the influence of GnRH during different periods of incubation time. Incubation of the rat anterior pituitary with GnRH stimulated the incorporation of [3H]proline into acid precipitable proteins in a time- and dose-dependent manner, similar to radioimmunoassayable LH released into the medium. Similar results were obtained when pituitary was incubated with dibutyryl cyclic AMP. LH, in addition, enhanced the incorporation of [3H]glucosamine and [3H]amine acids mixture into acidprecipitable proteins suggesting that proteins including glycoproteins are synthesized by the rat anterior pituitary under the influence of GnRH. Approximately 10 % of the radioactivity associated with proteins comigrated with radioimmunoassayable LH on the gels. GnRH also enhanced the incorporation of [3H]glucosamine and [3H]amino acid mixture into immunoprecipitable LH. The GnRH-induced incorporation of [3H]proline into anterior pituitary proteins was abolished by specific translation inhibitors.

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.

Effect of Cyclic AMP and Cyclic GMP on Thromboplastin (Factor III) Synthesis in Human Monocytes In Vitro

1983 ◽  
Vol 50 (04) ◽  
pp. 804-809 ◽  
Author(s):  
Torstein Lyberg
Keyword(s):  
Cyclic Amp ◽  
Cyclic Gmp ◽  
Immune Complexes ◽  
Phosphodiesterase Inhibitors ◽  
Inhibitory Effect ◽  
Intracellular Camp ◽  
Human Monocytes ◽  
Purified Protein Derivative ◽  
A 23187

SummaryHuman monocytes in vitro respond to various agents (immune complexes, lectins, endotoxin, the divalent ionophore A 23187, 12-0-tetradecanoyl-phorbol 13-acetate [TPA], purified protein derivative [PPD] of Bacille Calmette-Guerin) with an increased synthesis of the protein component of thromboplastin. The effect of cyclic AMP and cyclic GMP on this response has been studied. Dibutyryl-cyclic AMP, prostaglandin E1 and the phosphodiesterase inhibitors 3-butyl-1-methyl-xanthine (MIX) and rac -4-(3-butoxy-4-methoxybenzyl)-2-imidazolidinone (Ro 201724), separately and in combination have a pronounced inhibitory effect on the response to immune complexes and PPD, and a moderate effect on the response to endotoxin and lectins. The effect on TPA response and on the response to A 23187 was slight. Dibutyryl-cyclic GMP (1 mM) gave a slight inhibition of the TPA arid IC response, but had essentially no effect on the response to other inducers. The intracellular cAMP level increased when monocytes were incubated with IC, TPA or A 23187 followed by a decrease to basal levels within 1-2 hr, whereas lectin (PHA) and PPD did not induce such changes. The cAMP response to endotoxin varied. Stimulation with IC induced an increase in monocyte cGMP levels, whereas the other stimulants did not cause such changes.

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