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T Bjøro

Publications and source records attributed to T Bjøro.

45 records · Page 3Linked to original sources
PubMed1987

Bombesin stimulates prolactin secretion from cultured rat pituitary tumour cells (GH4C1) via activation of phospholipase C.

Bombesin (BBS) stimulated prolactin (PRL) secretion from monolayer cultures of rat pituitary tumour cells (GH4C1) in a dose-dependent manner with half maximal and maximal effect at 2 nM and 100 nM, respectively. No additional stimulatory effect on PRL secretion was seen when BBS was combined with thyroliberin (TRH) used in concentrations known to give maximal effects, while the effects of BBS and vasoactive intestinal peptide (VIP) were additive. Using a parafusion system, BBS (1 microM) was found to increase PRL secretion within 4 s and the secretion profiles elicited by BBS and TRH (1 microM) were similar. Both BBS and TRH increased inositoltrisphosphate (IP3) as well as inositolbisphosphate (IP2) formation within 2 s. BBS also induced the same biphasic changes in the electrical membrane properties of GH4C1 cells as TRH, and both peptides caused a rapid and sustained increase in intracellular [Ca2+]. These results suggest that BBS stimulates PRL secretion from the GH4C1 cells via a mechanism involving the immediate formation of IP3 thus resembling the action of TRH.

Animals↗
PubMed1987

Vasoactive intestinal peptide and peptide with N-terminal histidine and C-terminal isoleucine increase prolactin secretion in cultured rat pituitary cells (GH4C1) via a cAMP-dependent mechanism which involves transient elevation of intracellular Ca2+.

Vasoactive intestinal peptide (VIP) and peptide (P) with N-terminal histidine and C-terminal isoleucine (PHI) stimulated prolactin (PRL) secretion from GH4C1 cells equipotent with ED50 values of 30-50 nM. In a parafusion system optimized to give high time resolution both VIP and PHI increased PRL secretion with a delay of about 60 s and subsequent to the activation of the adenylate cyclase. Thyroliberin (TRH) increased PRL secretion within 4 s. The dose-response curves for VIP- and PHI-stimulated cAMP accumulation were superimposable on those for PRL secretion. At submaximal concentrations the effects of VIP and PHI on both cAMP accumulation and PRL secretion were additive, whereas the effects were not additive at concentrations giving maximal effects. VIP and PHI increased [Ca2+]i measured by quin-2 in a different way than TRH, without inducing changes in the electrophysiological membrane properties of the GH4C1 cells. We conclude that both VIP and PHI stimulate PRL secretion via a cAMP-dependent process involving an increase in [Ca2+]i.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1987

Binding and degradation of vasoactive intestinal peptide in prolactin-producing cultured rat pituitary tumour cells (GH4C1).

Vasoactive intestinal peptide (VIP) stimulates prolactin (PRL) secretion from cultured rat pituitary cells (GH cells) (Bjøro et al. 1984). This study demonstrates the presence of specific receptors for 125I-VIP on the GH4C1 cells. Specific binding was rapid and biphasic giving a transient plateau lasting from 7 to 30 min. Thereafter specific binding declined to about one-third after 90 min. This coincided with enhanced degradation of 125I-VIP. The degradation was mainly cell-mediated and only partly receptor dependent. Trichloroacetic acid precipitation and absorption chromatography indicated that the degradation products were either 125I- and/or small labelled peptide fragments. Bioassay, RIA and rebinding studies also demonstrated degradation of VIP. Pretreatment of GH4C1 cells with trypsin decreased the rate of degradation of 125I-VIP, but also reduced the amount of specific binding. Scatchard analysis of binding data indicated the existence of two independent classes of receptors, one with Kd = 2.2 nM and Bmax = 15 fmol per 10(6) cells and another with Kd = 180 nM and Bmax = 550 fmol per 10(6) cells. The IC50 for VIP, PHI and secretin were 4, 5 and 500 nM, respectively. We conclude that the high affinity receptor is the most probable mediator of VIP on PRL secretion. The effect of VIP and PHI on PRL secretion in GH4C1 cells is mediated through one common receptor.

Animals↗
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↗
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↗
PubMed1984

Vasoactive intestinal peptide causes a calcium-dependent stimulation of prolactin secretion in GH4C1 cells.

We have studied the effects of vasoactive intestinal peptide (VIP) on PRL secretion in a Bio-Gel column parafusion system containing rat pituitary tumour cells (GH4C1). A dose-dependent increase in PRL release was observed with half-maximal and maximal effect (2.1-fold) at 8 X 10(-8) and 5 X 10(-6) M, respectively. The PRL-stimulatory effect of VIP was instantaneous and maintained during the parafusion experiments (up to 60 min). On a molar basis VIP was always less effective than thyroliberin (THR), and the maximum stimulation of PRL release obtained with TRH was 1.2-3.0-fold higher (n = 12) than the maximum effect seen after VIP administration. The PRL-releasing effects of VIP, THR and high extracellular K+ were almost completely abolished in the presence of two inhibitors of voltage-sensitive Ca2+ channels, CoCl2 (10(-3) M) and verapamil (10(-4) M). In Ca2+-free buffer VIP, TRH and high extracellular K+ had only negligible effects, but the responses were fully restored in the presence of normal concentrations of extracellular Ca2+. In contrast to TRH, VIP had no demonstrable effect on the Ca2+-dependent action potentials of the GH4 cells.

Animals↗
PubMed1984

Thyroid antibodies in blood donors: prevalence and clinical significance.

In sera from 1643 randomly selected blood donors examined in 1979 thyroglobulin antibodies (TGA) were found in 3.4% and thyroid microsomal antibodies (TMA) in 7.0%. TMA, but not TGA, showed significant sex and age relationships. Eight-two donors with TMA titres greater than or equal to 1600 and/or TGA titres greater than or equal to 128 were available for a follow-up study in 1982. In 69 of these with TMA there was a significantly increased incidence of pathological thyroid function-test values (T4, T3 and TSH) as compared to age- and sexmatched donors without thyroid antibodies. In this group 9 individuals had overt and three latent hypothyroidism, two individuals were found with symptomless autoimmune thyroiditis and one with a non-toxic nodular goitre. Only 2 of these had been diagnosed before 1982, and none recognized before 1979. In addition, the group contained 9 individuals who had been treated because of hyperthyroidism, all except one before 1979. The likelihood of detecting a previously unrecognized hypothyroidism increased with increasing TMA titre. In contrast, the 24 donors with TGA did not show an increased frequency of pathological thyroid function-test-values in 1982.

Adult↗
PubMedDate not supplied

Changes in human skeletal muscle contractility and hormone status during 2 weeks of heavy strength training.

To examine neuromuscular and hormone changes during 2 weeks of heavy strength training, 18 weight-trained male students were recruited either into a heavy training group (HT, n = 11) or into a control group (Ctr, n = 7). The heavy training protocol consisted of leg-extensor workouts performed daily, while workouts were performed twice a week in the Ctr group. A test of one repetition maximum (1 RM) was performed before heavy training and on the 2nd day after heavy training. Isokinetic knee extensions, electrical stimulation, and squat jumps were performed before, on the 8th day of heavy training, and on the 4th day after heavy training. Morning blood samples (0800 hours) were drawn before, on the 8th day of heavy training, and on the 4th day after heavy training. Before, and on the 5th day after heavy training, 24 h urine samples were collected. The 1 RM leg press increased by 6 (SEM 2)% in the HT group. Testosterone and insulin-like growth factor-1 concentrations were respectively 12 (SEM 5)% and 11 (SEM 3)% lower than baseline on the 8th day of heavy training; however, hormone levels were back to baseline on the 4th day after heavy training. A significant correlation between individual changes in 1 RM leg press and changes in testosterone concentrations was observed in the HT group (r = 0.69). In the HT group, 24 h urinary catecholamine excretion increased by 26 (SEM 12)%, 3-methylhistidine excretion increased by 21 (SEM 6)% and creatinine excretion increased by 11 (SEM 5)%. There were no significant changes in the Ctr group. This work addresses the role of changes in basal hormone status (morning samples) for skeletal muscle adaptation to heavy strength training.

Adrenocorticotropic Hormone↗