DIFFERENT EFFECTS OF ORAL DOSES OF TRIIODOTHYRONINE OR THYROXINE ON THE INHIBITION OF THYROTROPHIN RELEASING HORMONE (TRH) MEDIATED THYROTROPHIN (TSH) RESPONSE IN MAN

1975 ◽  
Vol 80 (1) ◽  
pp. 42-48 ◽  
Author(s):  
K. W. Wenzel ◽  
H. Meinhold ◽  
H. Schleusener
Keyword(s):  
Oral Administration ◽  
Binding Sites ◽  
Direct Action ◽  
Normal Range ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Pituitary Tissue ◽  
Tsh Secretion ◽  
Inhibiting Protein ◽  
Oral Doses

ABSTRACT Since contradicting results about the existence of T3 or T3 and T4 receptors in pituitary tissue have been reported, the influence of L-triiodothyronine (L-T3) or L-thyroxine (L-T4) on TRH stimulated TSH release was investigated. Oral administration of 50 μg L-T3 caused an increasing inhibition of TSH response to 400 μg TRH from 64 % 2 h after L-T3 intake to 29% after 24 h, while serum T3 peaks up to 5.45 ng/ml occurred between 2 to 4 h after L-T3 ingestion and became normal after 8 to 10 h. This delay in the T3 action on TRH inhibition agrees with the postulate that T3 induces the synthesis of an inhibiting protein which is blocking TSH liberation. Oral administration of 1000 μg L-T4 induced increments of serum T4 up to 221 ng/ml between 6 to 24 h after intake; however, a TRH inhibition of 62 % did not become evident before 48 h. At this time T3 levels had risen to the upper normal range. These results support the theory that T3 is responsible for the regulation of TSH secretion. An intra-pituitary conversion from T4 to T3 seems more likely the cause of the TRH inhibition rather than the peripheral T4-T3 conversion or a direct action by T4 binding sites in the pituitary.

RESPONSE OF NORMAL, HYPOTHYROID AND HYPOTHALAMO-PITUITARY INSUFFICIENT CHILDREN TO SYNTHETIC THYROTROPHIN-RELEASING HORMONE

1971 ◽  
Vol 51 (3) ◽  
pp. 483-488 ◽  
Author(s):  
G. MILHAUD ◽  
P. RIVAILLE ◽  
M. S. MOUKHTAR ◽  
E. BINET ◽  
J. C. JOB
Keyword(s):  
Time Course ◽  
Solid Phase ◽  
Thyroid Stimulating Hormone ◽  
Normal Children ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Tsh Secretion ◽  
Course Changes ◽  
Serum Tsh ◽  
Tsh Deficiency

SUMMARY Thyrotrophin-releasing hormone (TRH) was synthesized by the solid phase technique, administered to 13 children, and the time-course changes in the serum level of thyroid-stimulating hormone (TSH) assessed. In eight normal children, peak levels of TSH occurred 20 min after the injection, and circulating TSH remained significantly raised for 60 min. In three hypothyroid children, the increase in serum TSH was much greater than in normal children, suggesting the existence of large pituitary TSH stores. In two hypopituitary children with TSH deficiency, TSH reserves seemed normal. One of these patients had a craniopharyngioma; after operation, the increase in serum TSH was reduced. These results show that assay of serum TSH after administration of synthetic TRH provides a test which distinguishes pituitary from hypothalamic defects affecting TSH secretion.

Role of naloxone and opioid peptides on thyrotrophin, alpha subunit and beta thyrotrophin by dispersed rat pituitary cells

1985 ◽  
Vol 110 (1) ◽  
pp. 101-106 ◽  
Author(s):  
L. Cacicedo ◽  
F. Sánchez Franco
Keyword(s):  
Opioid Peptides ◽  
Time Course ◽  
Direct Action ◽  
Opiate Receptors ◽  
Alpha Subunit ◽  
Pituitary Cells ◽  
Α Subunit ◽  
Thyrotrophin Releasing Hormone ◽  
Rat Pituitary ◽  
Tsh Secretion

Abstract. This study was undertaken to determine the effect of opioid peptides and naloxone on the secretion of thyrotrophin (TSH), alpha subunit (α subunit) and beta thyrotrophin (TSH-β) from rat pituitary dispersed cells in primary culture. Naloxone (NAL) 10−5m was found to increase basal TSH, α subunit and TSH-β secretion. This effect of NAL was not blocked by human β-endorphin (βh-End) 10−7 m. Concurrent treatment with triiodothyronine (T3) 10−7 m significantly decreased NAL stimulated secretion of TSH and its subunits. Thyrotrophin releasing hormone (TRH) stimulation of secretion of TSH and its subunits was not further augmented by NAL. In contrast, 10−7 m of βh-End, methionine-enkephaline (Met-Enk) and D-ala2-met-enkephalinamide (DALA) had no effect on secretion of TSH and subunits. A time course study confirmed no change in TSH secretion following pre-treatment with βh-End at 4, 10, 24 and 48 h. These findings go against a direct action of βh-End, Met-Enk and DALA on TSH secretion. The response of TSH and its subunits to NAL and the lack of interaction with βh-End might be explained by the existence of different types of opiate receptors. Counteraction of this effect by T3 suggests other possible mechanisms.

Decreased prolactin responsiveness to thyrotrophin-releasing hormone and metoclopramide in hyperthyroidism

1985 ◽  
Vol 110 (2) ◽  
pp. 221-226 ◽  
Author(s):  
Sven Röjdmark ◽  
Anders Carlsson
Keyword(s):  
Oral Administration ◽  
Normal Subjects ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Normal Individuals ◽  
Cytoplasmic Membranes ◽  
Before And After ◽  
The One

Abstract. To investigate whether prolactin (Prl) responsiveness to thyrotrophin-releasing hormone (TRH) differs in thyrotoxic and normal individuals, serum Prl was determined before and after iv injection of 200 μg TRH in 10 patients with untreated thyrotoxicosis and also in 9 normal subjects. Both the maximal Prl increment after TRH and the total Prl response, represented by the Prl incremental area, were significantly larger in the normal subjects compared with the thyrotoxic (max Prl increment 56 ± 11 vs 15 ± 3 ng/ml, P< 0.001; Prl incremental area 3071 ± 522 vs 579 ± 171, P <0.001; mean ± sem). The maximal Prl increase after 15 mg oral metoclopramide (MET) was also significantly larger in the normal (125 ± 13 ng/ml) than in the thyrotoxic subjects (60 ± 13 ng/ml, P < 0.01). When 200 μg TRH was injected iv 90 min after oral administration of 15 mg MET, an additional Prl increase was observed in normal individuals (21 ±6 ng/ml, P < 0.01). In thyrotoxic patients, however, iv TRH failed to induce a significant increase in Prl after oral priming with MET (0 ± 3 ng/ml). When 7 thyrotoxic patients, made euthyroid by 125I-treatment, were investigated according to the same protocol as the one mentioned above, they displayed normal Prl responses to iv TRH and to oral MET. Furthermore, they showed a significant Prl response to iv TRH after oral priming with MET (20 ± 8 ng/ml, P < 0.05). These findings imply that pituitary lactotrophs of untreated thyrotoxic patients might have cytoplasmic membranes with decreased permeability to Prl and/or reduced stores of releasable Prl which return to normal after oral 125I-therapy.

Specificity of gonadotrophin-releasing hormone binding sites of the human corpus luteum: comparison with receptors of rat pituitary gland

1986 ◽  
Vol 108 (3) ◽  
pp. 323-328 ◽  
Author(s):  
T. A. Bramley ◽  
G. S. Menzies ◽  
D. T. Baird
Keyword(s):  
Corpus Luteum ◽  
Binding Sites ◽  
Specific Binding ◽  
Similar Degree ◽  
Releasing Hormone ◽  
Pituitary Tissue ◽  
Rat Pituitary ◽  
Luteal Tissue ◽  
Gonadotrophin Releasing Hormone ◽  
Human Corpus Luteum

ABSTRACT The effects of a number of analogues of gonadotrophin-releasing hormone (GnRH) on the binding of a radiolabelled GnRH agonist (GnRH-A; d-Ser(But)6, des Gly10]GnRH-ethylamide) to homogenates of human corpus luteum (CL) and rat pituitary tissue were compared. Specific binding was inhibited by GnRH and GnRH-like peptides only. Both the C-terminal amide and N-terminal region of the GnRH molecule were required for binding in both tissues. However, amino acid substitutions at position 6 markedly enhanced, and at position 8 markedly reduced, binding potencies in rat pituitary tissue compared with human CL binding sites. These results indicate that GnRH-binding sites of rat pituitary and human luteal tissue have a similar degree of specificity for GnRH-like peptides, and a similar requirement for both N- and C-terminal regions of the peptide, but that differences in specificity related to the mid-chain region of GnRH exist between human luteal and rat pituitary binding sites. J. Endocr. (1985) 000, 000–000

INFLUENCE OF ANAESTHETICS ON BASAL, PERPHENAZINE-INDUCED AND THYROTROPHIN RELEASING HORMONE-INDUCED PROLACTIN SECRETION IN OVARIECTOMIZED, OESTROGEN-TREATED RATS

1975 ◽  
Vol 66 (2) ◽  
pp. 151-157 ◽  
Author(s):  
D. M. LAWSON ◽  
R. R. GALA
Keyword(s):  
Central Nervous System ◽  
Anterior Pituitary ◽  
Chloral Hydrate ◽  
Direct Action ◽  
Prolactin Secretion ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Site Of Action ◽  
The Central Nervous System ◽  
Normal Increase

SUMMARY Plasma levels of prolactin were determined, by radioimmunoassay, in ovariectomized, oestrogen-treated rats after administration of ether, sodium pentobarbitone, urethane, chloral hydrate or ketamine. These anaesthetics, when administered alone, induced sustained increases in the plasma level of prolactin (continuous ether inhalation), no change in prolactin secretion (urethane), or depressions in the level of prolactin (sodium pentobarbitone, chloral hydrate and ketamine). These same anaesthetics when given before perphenazine failed to alter the stimulatory effect of this phenothiazine on prolactin secretion. Sodium pentobarbitone did not alter the normal increase in prolactin concentration after intra-arterial administration of synthetic thyrotrophin releasing hormone (TRH). These results indicated that anaesthetics do not affect the response of either the central nervous system or the anterior pituitary to perphenazine or TRH although they affect prolactin secretion when administered alone. The site of action of anaesthetics must, therefore, be different from that of perphenazine or perphenazine must be capable of overcoming their influence by direct action on the pituitary.

Regulation of prolactin and thyrotrophin secretion during human pregnancy: effect of sulpiride and TRH administration

1981 ◽  
Vol 98 (3) ◽  
pp. 451-455 ◽  
Author(s):  
Olavi Ylikorkala ◽  
Seppo Kivinen ◽  
Lasse Viinikka
Keyword(s):  
Intramuscular Injection ◽  
Dopaminergic System ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Human Pregnancy ◽  
Healthy Women ◽  
Tsh Secretion ◽  
The Mean ◽  
Early Human ◽  
Tsh Levels

Abstract. The regulation of prolactin (Prl) and thyrotrophin (TSH) secretions during early human gestation was studied in 30 healthy women. Twelve women were treated with oral sulpiride, 150 mg daily for two weeks, and the Prl and TSH responses to 220 μg of iv thyrotrophin-releasing hormone (TRH) were measured before and at the end of sulpiride administration. Eight women were given 200 mg of sulpiride im, and 4 of them received 200 μg of TRH 30 min later. In 4 women the order of the TRH and sulpiride injections was reversed. Six women were studied as controls. Oral sulpiride treatment induced a significant Prl elevation from 14.6 ± 1.8 μg/l (mean ± sem) to 83.0 ± 4.0 μg/l, whereas the mean TSH levels did not change. Before sulpiride intake, TRH caused a mean maximal increment of 42.9 ± 4.7 μg/l in the Prl levels and an increment of 5.6 ± 0.9 IU/l in the TSH levels. During sulpiride administration, TRH caused a mean maximal increment of 16.5 ± 4.7 μg/l in the Prl levels and 3.5 ± 0.6 IU/l in the TSH levels. Both responses were significantly smaller (P < 0.001) during the sulpiride treatment than before. Intramuscular injection of sulpiride raised the mean Prl concentration by 282 ± 32 μg/l (P < 0.001) and the mean TSH concentration by 0.5 ± 0.1 IU/l (P < 0.05). The Prl elevation was 502 ± 109 μg/l when sulpiride was injected after TRH. A preceding im sulpiride injection caused no changes in Prl and TSH responses to TRH. These results show that in addition to Prl also TSH secretion is partially controlled by the dopaminergic system during early human pregnancy.

Dopaminergic regulation of pituitary gonadotrophin-releasing hormone receptor activity in the goldfish (Carassius auratus)

1989 ◽  
Vol 121 (2) ◽  
pp. 239-247 ◽  
Author(s):  
R. De Leeuw ◽  
H. R. Habibi ◽  
C. S. Nahorniak ◽  
R. E. Peter
Keyword(s):  
Binding Affinity ◽  
Binding Sites ◽  
Direct Action ◽  
High Capacity ◽  
Dopamine Antagonist ◽  
Releasing Hormone ◽  
Gnrh Receptors ◽  
Gonadotrophin Releasing Hormone

ABSTRACT In goldfish, dopamine acts as an endogenous inhibitor of basal and gonadotrophin-releasing hormone (GnRH)-stimulated gonadotrophin release. The purpose of the present study was to investigate the effects of dopamine on the pituitary GnRH receptors in vivo and in vitro in goldfish. The goldfish pituitary contains two classes of GnRH-binding sites, a high-affinity/low-capacity site and a low-affinity/high-capacity site. Injection of domperidone, a dopamine antagonist, resulted in a dose- and time-related increase in capacity of both the high- and low-affinity GnRH-binding sites; apomorphine, a dopamine agonist, completely reversed this effect. The effects on GnRH receptor capacity correlated very closely with changes in serum gonadotrophin concentrations. Domperidone was generally without effect on GnRH-binding affinity; however, a small but significant decrease in affinity was observed for the low- affinity binding site at 18 h after injection of the highest dose of domperidone used (40 μmol/kg body weight). Treatment with apomorphine of goldfish pituitary fragments in a perifusion system caused a decrease in the capacity of both the high- and low-affinity GnRH-binding sites without affecting binding affinity; domperidone reversed this effect. It is concluded that the dopaminergic inhibition of basal and GnRH-stimulated gonadotrophin release in goldfish might, in part, be the result of a down-regulation of the pituitary GnRH receptors; this effect of dopamine can be achieved by a direct action at the pituitary level. Journal of Endocrinology (1989) 121, 239–247

Oral administration of TRH in puerperal women: effect on insufficient lactation, thyroid hormones and on the responses of TSH and prolactin to intravenous TRH

1980 ◽  
Vol 93 (4) ◽  
pp. 413-418 ◽  
Author(s):  
O. Ylikorkala ◽  
S. Kivinen ◽  
A. Kauppila
Keyword(s):  
Oral Administration ◽  
Thyroid Hormones ◽  
Plasma Samples ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Trh Stimulation ◽  
Stimulation Tests ◽  
Tsh Levels

Abstract. Thirteen puerperal women with insufficient lactation were treated with thyrotrophin releasing hormone (TRH) 20 mg twice daily for two weeks. Intravenous (iv) TRH stimulation tests were done before the TRH therapy and within 3–5 h after the last dose of oral TRH. Plasma samples were assayed for prolactin (Prl), thyrotrophin (TSH), triiodothyronine (T3) and thyroxine (T4) by radioimmunoassays, and the lactational response was objectively monitored in 11 women. Oral TRH treatment was associated with significantly (P < 0.05) depressed Prl levels (23.0 ± 7.9 μg/l vs. 61.4 ± 26.2, mean ± sem), no change in TSH levels (3.7 ± 0.4 IU/1 vs. 4.0±0.4) but significantly (P<0.01) elevated T3 (2.17±1.14 nmol/l vs. 1.83 ± 0.09) and T4 (131.6 ± 7.9 nmol/l vs. 96.6 ± 5.8) levels. Oral TRH entirely blocked the TSH response and significantly (P<0.01) blunted the Prl response to iv TRH stimulation. No improvement in lactation was observed.

INHIBITION OF THYROTROPHIN-RELEASING HORMONE RESPONSIVENESS BY PHYSIOLOGICAL CONCENTRATIONS OF THYROID HORMONES IN THE CULTURED RAT PITUITARY GLAND

1977 ◽  
Vol 74 (3) ◽  
pp. 405-414 ◽  
Author(s):  
M. LEWIS ◽  
P. P. B. YEO ◽  
E. GREEN ◽  
D. C. EVERED
Keyword(s):  
Thyroid Hormone ◽  
Culture Media ◽  
Synthetic Medium ◽  
Mature Female ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Response Characteristics ◽  
Tsh Secretion ◽  
Female Wistar Rats ◽  
Hormone Binding Protein

SUMMARY Diced quarter anterior pituitaries from mature female Wistar rats were cultured in synthetic medium with or without added serum. Using each culture as its own control, the thyrotrophin-releasing hormone (TRH) dose–thyrotrophin (TSH) response characteristics of both media were similar; significant TSH secretion being stimulated at TRH doses around 1·5 × 10−9 mol/l. During days 1–3 of culture, basal TSH secretion fell significantly but TRH responsiveness was unchanged. Neither tri-iodothyronine (T3) nor thyroxine (T4) influenced basal TSH secretion. In both culture media inhibition of TRH responsiveness was demonstrated with concentrations of T3 and T4 within the ranges 1·5 × 10−12 to 1·5 × 10−9 mol/l for T3 and 6·5 × 10−10 to 6·5 × 10−7 mol/l for T4. Equivalent inhibition was accompanied by similar T3 concentrations whether T3 or T4 supplements were used, suggesting that T4 itself has no feedback action. The similar concentrations of T3 required to inhibit TRH responsiveness in media either with or without serum suggest that the pituitary is responsive not only to free but also to total thyroid hormone concentrations, since serum-free medium contains no thyroid hormone-binding protein.

Benzodiazepine antagonism of thyrotrophin-releasing hormone receptors: biphasic actions on growth hormone secretion in domestic fowl

1993 ◽  
Vol 137 (1) ◽  
pp. 35-42 ◽  
Author(s):  
S. Harvey
Keyword(s):  
Binding Sites ◽  
Domestic Fowl ◽  
Benzodiazepine Receptors ◽  
Growth Hormone Secretion ◽  
Thyrotrophin Releasing Hormone ◽  
Central Type ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Pituitary Glands

ABSTRACT Benzodiazepines are pharmacological agents widely used for their anxiolytic and anticonvulsant properties. However, as these drugs are known to antagonize the binding and action of thyrotrophin-releasing hormone (TRH) in pituitary tissue, the possibility that they may modulate GH secretion was investigated in domestic fowl, in which TRH is a GH-releasing factor. Chlordiazepoxide (an antagonist of central-type benzodiazepine receptors) had no significant effect on the basal release of GH from incubated chicken pituitary glands, but at concentrations > 10 μmol/l chlordiazepoxide suppressed somatotroph responsiveness and sensitivity to TRH stimulation. At this concentration, chlordiazepoxide competitively displaced the binding of [3H]3-methyl-histidine2-TRH ([3H]Me-TRH) to chicken pituitary membranes. The prior incubation of pituitary glands with chlordiazepoxide had no significant effect on the number of [3H]Me-TRH-binding sites, which were also unaffected by the administration of chlordiazepoxide in vivo. However, contrary to its effects in vitro, chlordiazepoxide reduced basal GH secretion in vivo, whilst potentiating the GH response to systemic TRH challenge. These results demonstrate benzodiazepine antagonism of TRH-binding sites in domestic fowl and a biphasic modulation of GH secretion, which may be mediated through opposing actions at pituitary and central sites. Journal of Endocrinology (1993) 137, 35–42

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