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E Haug

Publications and source records attributed to E Haug.

At least 145 records · Page 8Linked to original sources
PubMed1987

Melatonin reduces the production and secretion of prolactin and growth hormone from rat pituitary cells in culture.

A culture of clonal tumour cells from rat pituitary gland that secrete both prolactin and growth hormone were used to investigate whether the pineal hormone melatonin can act directly on the pituitary gland to control prolactin production. Melatonin inhibition of prolactin and growth hormone production was significant but mild. Concentrations of between 10(-8) M and 10(-6) M reduced both prolactin and growth hormone production and prolactin secretion by 10-50%. 17 beta-oestradiol (OE) and thyrotrophin-releasing hormone (TRH) stimulated prolactin production but had no significant effect on growth hormone production. Melatonin reduced the effects of both of these compounds. Both TRH and vasoactive intestinal peptide (VIP) stimulated secretion of prolactin, and TRH also of growth hormone. Melatonin reduced these effects significantly. TRH and VIP increased cAMP production two- and 12-fold, respectively. Melatonin had no effect on basal or stimulated cAMP production. The melatonin-induced changes in prolactin and growth hormone production and secretion seen here do not approach the magnitude of the fluctuations seen in plasma in vivo. It is concluded that while melatonin does have a direct effect on the lactotroph in the regulation of prolactin production, its main physiological target must be elsewhere.

Animals↗
PubMed1987

Early postmenopausal bone loss is not associated with a decrease in circulating levels of 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, or vitamin D-binding protein.

To study changes in the rate of bone loss before and after the menopause, 19 normal premenopausal women of the same age were followed with annual measurements of appendicular bone mass for 8 yr. Their serum estrone, estradiol, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D, and vitamin D-binding protein levels also were measured annually. The serum estrogen levels declined before the menopause, and the rate of bone loss more than doubled at the time of the menopause. There were no significant changes in the serum 25-hydroxyvitamin D, 1,25-dihydroxyvitamin LD or vitamin D-binding protein levels from the pre- to the postmenopausal period. We conclude that changes in vitamin D metabolite levels are not associated with early postmenopausal bone loss.

Bone Diseases, Metabolic↗
PubMed1987

Effects of metabolic inhibitors on hormone release, cyclic AMP levels, and oxygen consumption in rat pituitary cells in culture.

The metabolic inhibitors antimycin A (2 mumol/l), dinitrophenol (0.5 mmol/l), and iodoacetate (6 mmol/l) were tested for their effects on hormone release, cAMP levels, and oxygen consumption in clonal strains of rat pituitary cells (GH3 cells). Basal release of growth hormone (GH) and prolactin (PRL) was reduced by all three inhibitors, and thyrotropin-releasing hormone (TRH) (1 mumol/l) and K+ (50 mmol/l) stimulated hormone release were blocked. Trifluoperazine, a calmodulin antagonist, inhibited basal GH and PRL release at concentrations up to 30 mumol/l and stimulated above 50 mumol/l. The stimulatory effect of 80 mumol/l trifluoperazine on basal hormone release was eliminated by antimycin A, dinitrophenol, and iodoacetate, whereas the inhibitory effect of antimycin A, dinitrophenol and iodoacetate on basal hormone was not affected by 30 mumol/l trifluoperazine. None of the inhibitors had any effect on the level of cellular cAMP (i.e. intracellular plus extracellular). Oxygen consumption of GH3 cells was blocked by antimycin A, reduced by 25% by iodoacetate and increased by about 100% by dinitrophenol. In contrast, hormone secretion stimulated by TRH and K+ was not accompanied by any measurable alteration in oxygen consumption. Trifluoperazine (greater than or equal to 80 mumol/l) reduced the basal oxygen consumption and blocked the stimulatory effect of dinitrophenol on oxygen consumption. In conclusion, inhibition of the energy generation of GH and PRL-producing cells severely affects the action of secretagogues, although stimulated hormone secretion may not be accompanied by any measurable increase in oxygen consumption. The cellular energy supporting hormone secretion is mostly generated via oxidative phosphorylation.

Animals↗
PubMed1987

Effects of trifluoperazine on prolactin release and cyclic AMP formation and degradation in GH4C1 pituitary cells.

In GH4C1 cells, the calmodulin antagonist trifluoperazine (TFP) showed a dose-dependent, biphasic effect on the basal release of PRL. An inhibition of PRL release was observed with 15-50 mumol/l TFP, whereas a concentration of 100 mumol/l and above had a stimulatory effect. The increase in basal hormone release evoked by TRH (1 mumol/l) and high extracellular concentration of K+ (50 mmol/l) was eliminated by 30 mumol/l TFP. The stimulatory effect of 100 mumol/l TFP on basal hormone release was not affected by addition of TRH (1 mumol/l) or K+ (50 mmol/l). The Ca2+ antagonists Co2+ (5 mmol/l) and verapamil (100 mumol/l), and the Ca2+ chelator EgTA (4 mmol/l) abolished the stimulatory effect of TRH (1 mumol/l) and of K+ (50 mmol/l) on PRL release, whereas only Co2+ inhibited the stimulation caused by 100 mumol/l TFP. TFP (75 mumol/l) caused a transient increase in the concentration of cellular cAMP. Incubation of intact GH4C1 cells with TFP (75 mumol/l), had an inhibitory effect on both the low and the high affinity form of cAMP phosphodiesterase. Basal as well as TRH-stimulated adenyl cyclase activity were inhibited by TFP, and this effect was counteracted by addition of calmodulin.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1986

Effects of hypersecretion of growth hormone and prolactin on plasma levels of glucagon and insulin in GH3-cell-tumor-bearing rats, and the influence of bromocriptine treatment.

Plasma levels of prolactin, growth hormone, glucagon insulin and glucose were measured in non-treated control rats, bromocriptine-treated control rats and GH3-cell-tumor-bearing rats with and without bromocriptine treatment. Bromocriptine treatment increased plasma levels of glucagon, insulin and glucose in control rats. Tumor-bearing rats had increased body weight and increased plasma levels of prolactin, growth hormone, glucagon, insulin and glucose. Bromocriptine treatment reduced body weight and decreased the plasma levels of prolactin, glucagon and insulin, as compared to non-treated tumor-bearing rats. The drug had no effect on plasma levels of growth hormone and glucose. These results indicate that, in GH3-cell-tumor-bearing rats, prolactin, glucagon and insulin are more sensitive to the action of bromocriptine than growth hormone.

Animals↗
PubMed1986

Metabolism of testosterone to 17 beta-hydroxy-5 alpha-androstane-3-one and 5 alpha-androstane-3 alpha, 17 beta-diol in alveolar macrophages from rat lung--II. Effects of intratracheal instillation of 3.4 mumol K2Cr2O7.

Activity of the steroid 5 alpha-reductase in pulmonary alveolar macrophages from adult male rats has been investigated in vitro. Intratracheal instillation of 3.4 mumol K2Cr2O7 lowered the enzyme activity within 6 h, and the reduction was significant on the subsequent 2, 4 and 7 days. The activity of this enzyme was significantly decreased only 6 and 24 h after instillation when measured in the 800 g supernatant fraction of whole lung. Instillation of 3.4 mumol K2Cr2O7 increased serum levels of corticosterone. Serum levels of triiodothyronine and thyroxine decreased except for a transient increase 3 h after the K2Cr2O7 instillation. Subcutaneous administration of 200 micrograms dexamethasone/100 g b.wt, 200 micrograms/100 g b.wt of testosterone, 17 beta-hydroxy-5 alpha-androstane-3-one (5 alpha-DHT), dehydroepiandrosterone or corticosterone had no effect on the 5 alpha-reductase activity of the pulmonary alveolar macrophages within 12 h. The combined treatment with dexamethasone s.c. and intratracheal instillation of 3.4 mumol K2Cr2O7 reduced the steroid 5 alpha-reductase activity in the pulmonary alveolar macrophages to about 25% of controls. Measurement of the steroid 5 alpha-reductase activity in pulmonary alveolar macrophages as an index of lung damage when exposed to toxic material is discussed.

5-alpha Reductase Inhibitors↗
PubMed1986

Gut peptides in lactation.

The circulating levels of prolactin (PRL), vasoactive intestinal polypeptide (VIP), somatostatin (SRIH), cholecystokinin (CCK), pancreatic polypeptide (PP), insulin, motilin and blood glucose were measured in nine nursing women 27-40 days after delivery to establish the possible role of some gastrointestinal regulatory peptides in human breast feeding. During the last 20 min of suckling a significant (P less than 0.05) increase in serum PRL was observed concomitantly with a significant decrease in plasma SRIH levels (P less than 0.05 at 20 min and P less than 0.01 at 30 min). There was a highly significant inverse correlation between mean PRL and SRIH levels during the first 30 min of breast feeding (r = -0.996, P less than 0.001). Pancreatic polypeptide (pp) also increased significantly (P less than 0.01) during nursing, while there were no changes in the plasma levels of the other gastrointestinal regulatory peptides studied.

Adult↗
PubMed1986

The phorbol ester TPA induces hormone release and electrical activity in clonal rat pituitary cells.

The phorbol ester TPA activates the protein kinase C in a similar way as 1,2-diacylglycerol. The effect of TPA on prolactin (PRL) secretion and electrical properties of rat pituitary cells in culture (GH4C1 cells) were compared with the effects of thyroliberin (TRH) on the corresponding parameters. The rate of hormone release was measured using a parafusion system optimized to give high time resolution. Samples for PRL measurements were taken every 4 s. The TRH evoked a biphasic PRL release, with a transient peak after about 30 s followed by a lower but sustained enhancement of the secretion. The TPA mimicked the late phase of the secretory response to TRH. The TPA analogue, 4 alpha-PDD, had no effect on the PRL release. The TRH also evoked biphasic membrane potential changes in the GH4C1 cells; the late phase consisting of membrane depolarisation associated with increased input resistance and enhanced firing of Ca2+ dependent action potentials. The TPA mimicked to a great extent these late phase effects of TRH, whereas the inactive analogue 4 alpha-PDD was ineffective. Continuous exposure to TPA masked the late phase of the electrophysiological response to TRH, suggesting that TPA and TRH share common mechanisms in their action on GH4C1 cells. We suggest that TRH enhances the electrical activity in these cells due to protein phosphorylation induced by diacylglycerol activation of protein kinase C, which in turn suppresses the membrane permeability to K+.

Animals↗
PubMed1986

On the functional relationship between 45Ca2+ release and prolactin secretion in cultured rat pituitary tumour (GH3) cells.

We have evaluated the role of cellular Ca2+ transport associated with stimulus-secretion coupling in prolactin (PRL) producing rat pituitary adenoma cells (GH3 cells). The action of different substances, known to modify PRL secretion, on release of 45Ca2+ from preloaded cells were examined. Surface-bound 45Ca2+ was removed by pretreatment with trypsin in EDTA buffer. During the first 6 min, basal efflux of 45Ca2+ occurred at a constant rate (0.24 min-1) at 37 degrees C. Addition of TRH (5 X 10(-7) M) resulted in an immediate enhancement of 45Ca2+ release representing about 20% of the remaining cellular 45Ca2+. In the same experiments PRL secretion increased by 45%. The EDTA in the external medium reduced the basal rate of 45Ca2+ release by 60%, but did not apparently affect the TRH-stimulated release. Somatostatin (10(-6) M) and verapamil (5 X 10(-5) M) inhibited both basal and TRH-stimulated PRL secretion, whereas high extracellular concentration of K+ (5 X 10(-2) M) had a stimulatory effect. However, neither of these treatments changed cellular 45Ca2+ release. Interference with energy-dependent Ca2+ transport by using metabolic inhibitors (iodoacetate, 6 X 10(-3) M; and antimycin, 2 X 10(-6) M) or by replacing Na+ in the medium by choline or by lowering the incubation temperature from 37 to 25 degrees C, had no effect on TRH-stimulated 45Ca2+ release although basal and TRH-stimulated PRL secretion were reduced. Thus, TRH apparently releases 45Ca2+ from calcium binding sites in the cell membrane.

Adenoma↗
PubMed1986

Effects of bromocriptine on prolactin release, electrical membrane properties and transmembrane Ca2+ fluxes in cultured rat pituitary adenoma cells.

The effects of the dopamine (DA) agonist bromocriptine on prolactin (Prl) release, electrical membrane properties and transmembrane Ca2+ fluxes have been studied in a clonal strain of rat pituitary adenoma cells (GH3). These cells generate Ca2+ dependent action potentials, and produce and secrete spontaneously both Prl and growth hormone. Prl release stimulated by thyroliberin (TRH) and elevated extracellular K+ concentration was completely blocked by bromocriptine, whereas the basal release was only moderately affected. The TRH and K+ evoked Prl release were half maximally inhibited by bromocriptine at 5-10 and 10-50 microM, respectively. The normal biphasic membrane response to TRH and the depolarizing effect of elevated K+ concentration were not altered by bromocriptine, whereas the Ca2+- spikes in Na+-free solution were suppressed by the drug. We therefore suggest that bromocriptine blocks the voltage sensitive Ca2+-channels of GH3 cell. In agreement with this notion, bromocriptine also suppressed the basal and TRH induced 45Ca2+ efflux from preloaded cells. We conclude that the inhibitory effect of bromocriptine on the voltage dependent Ca2+- channels is an important mechanism responsible for suppression of Prl release.

Action Potentials↗
PubMed1986

Short-term effects of mating on the accessory sex glands of the male rat.

Mating in the rat was associated with a significant reduction in the tissue concentrations of the presumptive secretory products of the male accessory sex glands: prostatein and the amines, putrescine, spermidine and spermine (ventral prostate lobe), zinc (lateral prostate lobe) and fructose (coagulating gland). The amount of secretory product discharged and the time taken to restore precopulatory levels differed for the different lobes. Within 12-24 h of the mating period, the activity of ornithine decarboxylase and cytosolic oestrogen binding in the ventral prostate lobe underwent a transient increase which lasted 2-3 days. No change was observed in prolactin binding. Circulating testosterone concentrations were significantly elevated above control values 12 h after the start of mating but were significantly lower than control values at 24 h. A gradual recovery to concentrations in controls occurred over the next 2-3 days. None of these changes could be explained by alterations in gonadotrophin or prolactin release.

Androgen-Binding Protein↗
PubMed1985

Human IgG subclass-specific rabbit antisera suitable for immunoprecipitation in gel, ELISA and multilayer haemagglutination techniques.

Antisera specific for human IgG subclasses were raised in rabbits by tolerance induction at birth followed by active immunization at 8 weeks of age. This procedure gave better antisera compared to tolerance/immunization of adult grown animals. Many animals gave antisera with subclass-specific precipitating activity without the need to use absorption procedures. However, for sensitive techniques such as ELISA and multilayer haemagglutination it was necessary to absorb the antisera to make them subclass-specific. Subclass specificity in ELISA and haemagglutination was verified by inhibition. We believe this is the first description of a procedure to prepare antisera specific for human IgG subclasses suitable for use in immunoprecipitation, ELISA and haemagglutination techniques.

Animals↗
PubMed1985

Circulating steroids in male rats following inhalation of n-alcohols.

The effect of inhaled methanol, ethanol, n-propanol and n-butanol on male reproductive function as measured by the serum concentration of circulating T (testosterone) and LH (luteinizing hormone) has been investigated. The animals were exposed to concentrations of these alcohols equal to the current threshold limit values in industry (methanol: 200 ppm, ethanol: 1000 ppm, n-propanol, n-butanol: 50 ppm) 6 h a day for up to 1 week. A significant depression in the concentration of circulating T was found after the first 6 h exposure to the respective alcohols with restoration after a recovery period of 18 h, except in rats exposed to n-butanol where a depression of 48% could still measured. The concentration of LH was within the normal range in all experimental groups whereas corticosterone was increased after exposure to n-butanol. Exposure for 1 week was not associated with any significant inability of the rat testis to produce T.

1-Butanol↗
PubMed1985

Demonstration and characterization of a 1 alpha,25-(OH)2D3 receptor-like macromolecule in cultured rat pituitary cells.

Recent studies have demonstrated the importance of prolactin (PRL) and growth hormone (GH) in the regulation of 25-hydroxycholecalciferol-1 alpha-hydroxylase activity. We have previously shown that 1 alpha,25-dihydroxycholecalciferol (1 alpha,25-(OH)2D3) reduces PRL and GH production by a clonal strain of rat pituitary tumour cells (GH3). The biologically active form of vitamin D3, 1 alpha,25-(OH)2D3, acts via an initial binding to cytoplasmic receptor proteins in target cells, and we demonstrate in this study the presence of specific receptors for 1 alpha,25-(OH)2D3 in the GH3 cells. GH3 cell cytosol was incubated with [3H]1 alpha,25-(OH)2D3 at 0-4 degrees C. Maximal binding was obtained between 2 and 6 h, and Scatchard analysis showed one single class of binding sites with Kd of 0.33 +/- 0.05 nM (mean + SD) and a Bmax of 103 +/- 26 fmol/mg cytosol protein. Competitive binding experiments revealed the following potency order: 1 alpha,25-(OH)2D3 greater than 25-OHD3 greater than 1 alpha-OHD3, 24,25-(OH)2D3. In contrast, corticosterone, testosterone, progesterone and oestradiol showed negligible ability to displace [3H]1 alpha,25-(OH)2D3 from its receptor. Sucrose gradient ultracentrifugation in high salt concentration revealed that GH3 cell cytosol possessed at 3.7S [3H]1 alpha,25-(OH)2D3 receptor protein which was inactivated by heating and protease treatment, but not after incubation with DNase or RNase. The receptor protein aggregated in salt-free sucrose gradients since the 3.7S complex was shifted reversibly to a approximately 6S form. Isoelectric focussing localized most of the [3H]1 alpha,25-(OH)2D3 to a protein peak with an isoelectric point of approximately 6 (pI 5.8-6.2). Since this 1 alpha,25-(OH)2D3 receptor protein has similar properties as the corresponding 1 alpha,25-(OH)2D3 receptors found in normal rat tissues, we suggest that lactotropes and somatotropes represent true target cells for 1 alpha,25-(OH)2D3.

Animals↗