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.

Dynorphin (1–13) effects on thyrotrophin-releasing hormone and thyrotrophin secretion in rats

1983 ◽  
Vol 103 (3) ◽  
pp. 359-364 ◽  
Author(s):  
Terunori Mitsuma ◽  
Tsuyoshi Nogimori
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Inhibitory Effect ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Tsh Secretion ◽  
Pretreated Group ◽  
Basal Plasma ◽  
The Central Nervous System ◽  
Tsh Levels

Abstract. The effects of dynorphin (1-13) on thyrotrophin-releasing hormone (TRH) and thyrotrophin (TSH) secretion in rats were studied. Dynorphin (500 μg/kg) was injected iv, and the rats were serially decapitated. TRH and TSH, thyroxine (T4) and 3,3',5-triiodothyronine (T3) were measured by radioimmunoassay. The hypothalamic immunoreactive TRH did not change significantly after dynorphin injection. Basal plasma TSH levels significantly decreased in a dose-related manner with a nadir at 40 min after dynorphin injection. The effect of dynorphin on TSH release was partially prevented by naloxone. The plasma TSH response to cold was significantly inhibited by dynorphin. The plasma TSH response to TRH did not differ from that of the control. In the l-DOPA or 5-hydrotryptophan-pretreated group, the inhibitory effect of dynorphin on TSH release was prevented, but not in the haloperidolor para-chlorophenylalanine-pretreated group. These drugs alone did not affect plasma TSH levels. The plasma T4 and T3 levels did not change significantly after dynorphin injection. The findings suggest that dynorphin acts on the hypothalamus by inhibiting TRH release, which may be modified by amines of the central nervous system.

SERUM THYROTROPHIN AND THE RESPONSE TO THYROTROPHIN RELEASING HORMONE IN SYMPTOMLESS AUTOIMMUNE THYROIDITIS AND IN BORDERLINE AND OVERT HYPOTHYROIDISM

1974 ◽  
Vol 75 (2) ◽  
pp. 274-285 ◽  
Author(s):  
A. Gordin ◽  
P. Saarinen ◽  
R. Pelkonen ◽  
B.-A. Lamberg
Keyword(s):  
Autoimmune Thyroiditis ◽  
Elevated Serum ◽  
Mean Value ◽  
Primary Hypothyroidism ◽  
Overt Hypothyroidism ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
The Mean ◽  
The Individual ◽  
Serum Tsh

ABSTRACT Serum thyrotrophin (TSH) was determined by the double-antibody radioimmunoassay in 58 patients with primary hypothyroidism and was found to be elevated in all but 2 patients, one of whom had overt and one clinically borderline hypothyroidism. Six (29%) out of 21 subjects with symptomless autoimmune thyroiditis (SAT) had an elevated serum TSH level. There was little correlation between the severity of the disease and the serum TSH values in individual cases. However, the mean serum TSH value in overt hypothyroidism (93.4 μU/ml) was significantly higher than the mean value both in clinically borderline hypothyroidism (34.4 μU/ml) and in SAT (8.8 μU/ml). The response to the thyrotrophin-releasing hormone (TRH) was increased in all 39 patients with overt or borderline hypothyroidism and in 9 (43 %) of the 21 subjects with SAT. The individual TRH response in these two groups showed a marked overlap, but the mean response was significantly higher in overt (149.5 μU/ml) or clinically borderline hypothyroidism (99.9 μU/ml) than in SAT (35.3 μU/ml). Thus a normal basal TSH level in connection with a normal response to TRH excludes primary hypothyroidism, but nevertheless not all patients with elevated TSH values or increased responses to TRH are clinically hypothyroid.

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.

EFFECT OF THYROID STATUS ON THE THYROTROPHIN-RELEASING HORMONE-DEGRADING ACTIVITY OF RAT SERUM

1976 ◽  
Vol 71 (1) ◽  
pp. 13-19 ◽  
Author(s):  
N. WHITE ◽  
S. L. JEFFCOATE ◽  
E. C. GRIFFITHS ◽  
K. C. HOOPER
Keyword(s):  
Thyroid Hormone ◽  
Human Serum ◽  
Thyroid Function ◽  
Thyroid Status ◽  
Rat Serum ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Tsh Levels

SUMMARY The TRH-degrading activity of rat serum in vitro is five times more potent than that of human serum. In rats, it is significantly reduced in hypothyroidism (thiouracil-induced) and significantly increased in hyperthyroidism (T3 or T4-induced). This suggests a possible role in the regulation of adenohypophysial-thyroid function which is probably, in turn, dependent on thyroid hormone, rather than TSH, levels.

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.

β-Neoendorphin inhibits thyrotrophin secretion in rats

1983 ◽  
Vol 104 (4) ◽  
pp. 437-442 ◽  
Author(s):  
Terunori Mitsuma ◽  
Tsuyoshi Nogimori
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Plasma Concentrations ◽  
Inhibitory Effect ◽  
Thyrotrophin Releasing Hormone ◽  
Specific Radioimmunoassay ◽  
Tsh Secretion ◽  
Pretreated Group ◽  
The Central Nervous System ◽  
Tsh Levels

Abstract. The effects of β-neoendorphin on thyrotrophin-releasing hormone (TRH) and thyrotrophin (TSH) secretion in rats were studied. β-neoendorphin (500 μg/kg) was injected iv, and the rats were decapitated serially. TRH, TSH, thyroxine (T4) and 3,3',5-triiodothyronine (T3) were measured by means of a specific radioimmunoassay for each. Hypothalamic immunoreactive TRH (ir-TRH) content increased significantly after β-neoendorphin injection, and plasma concentrations tended to decrease, but not significantly so. Plasma TSH levels decreased significantly in a dose-related manner with a nadir at 40 min. Plasma T4 and T3 levels did not change after the injection. Plasma ir-TRH and TSH responses to cold were significantly inhibited by β-neoendorphin, but the plasma TSH response to TRH was not. Naloxone partially prevented the inhibitory effect of β-neoendorphin on TSH release. In the haloperidol- or 5-hydroxytryptophan-pretreated group, the inhibitory effect of β-neoendorphin on TSH release was prevented, but not in the l-dopa- or para-chlorophenylalanine-pretreated group. These drugs alone did not affect plasma TSH levels at the dose used. These findings suggest that β-neoendorphin acts on the hypothalamus by inhibiting TRH release, which may be modified by amines of the central nervous system.

PROGESTERONE AND HUMAN CHORIONIC GONADOTROPHIN (HCG) LEVELS IN PLASMA DURING DILATION OF THE UTERINE CERVIX IN EARLY HUMAN PREGNANCY

1970 ◽  
Vol 65 (2) ◽  
pp. 293-301 ◽  
Author(s):  
Petter Fylling ◽  
Nils Norman
Keyword(s):  
Plasma Level ◽  
Uterine Cervix ◽  
First Trimester ◽  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Control Group ◽  
Human Pregnancy ◽  
Medial Side ◽  
The Mean ◽  
Early Human

ABSTRACT Dilation of the uterine cervix for 16 hours as a preliminary to the induction of legal abortion during the first trimester of human pregnancy resulted in a marked increase in the plasma level of both progesterone and human chorionic gonadotrophin (HCG). In a control group (with the dilating instrument taped on the medial side of the upper thigh) no increase in progesterone occurred. The increase in the plasma level of HCG was more pronounced than that of progesterone, the mean increase being 80 and 50 per cent respectively. Following the termination of the pregnancy, the half life (t½) of endogenous HCG in peripheral plasma could be calculated, and was found to be about 7 hours.

EFFECT OF THYROTROPHIN RELEASING HORMONE AND THYROID-STIMULATING HORMONE ON SERUM PROTEIN-BOUND 131I

1972 ◽  
Vol 70 (3) ◽  
pp. 454-462 ◽  
Author(s):  
Egil Haug ◽  
Harald Frey ◽  
Terje Sand
Keyword(s):  
Oral Dose ◽  
Thyroid Stimulating Hormone ◽  
Significant Rise ◽  
Response Relationship ◽  
Dose Response Relationship ◽  
Thyrotrophin Releasing Hormone ◽  
Peak Response ◽  
Releasing Hormone ◽  
Clear Dose Response ◽  
The Mean

ABSTRACT Seventeen subjects without any clinical or laboratory evidence of thyroidal or pituitary disease were given 1.0 mg thyrotrophin-releasing hormone (TRH) as a rapid iv injection 48 hours after an oral dose of 50 μCi 131I-. In all subjects there was a clear rise in serum PB131I. The elevation in the mean serum PB131I was significant (P<0.01) one hour after TRH, and the mean peak response was noted at 4 hours. It is suggested that this elevation in serum PB131I following TRH administration reflects the effect of the TSH released. In order to find the most suitable method of administration, 1.0 mg TRH was given iv, im, or as a 1 hour infusion. The maximal responses seemed to be independent of the mode of administration. Six subjects were given 3.0 mg TRH iv and 4 others 6.0 mg TRH iv. It was not possible to demonstrate a clear dose-response relationship. In five subjects the serum PB127I and the serum PB131I were measured at the same times following administration of TRH. This showed that the serum PB131I was a more sensitive index of TSH release than the serum PB127I. Twenty-four hours after the TRH injection the same subjects were given 5 IU TSH as a rapid iv or im injection. All subjects responded with a significant rise in serum PB131I. In the subjects who did not respond to TRH the response to TSH allows the differentiation between pituitary and thyroid disease.

Physiological roles of thyrotrophin-releasing hormone and vasoactive intestinal peptide on the pulsatile secretory patterns of prolactin in pituitary-grafted female rats

1994 ◽  
Vol 142 (3) ◽  
pp. 581-586 ◽  
Author(s):  
A Lafuente ◽  
J Marcó ◽  
A I Esquifino
Keyword(s):  
Vasoactive Intestinal Peptide ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Thyrotrophin Releasing Hormone ◽  
Mean Values ◽  
Pulsatile Secretion ◽  
Releasing Hormone ◽  
Absolute Amplitude ◽  
The Mean ◽  
The Absolute

Abstract Much is known about the fact that thyrotrophin-releasing hormone (TRH) and vasoactive intestinal peptide (VIP) stimulate prolactin secretion but areas of uncertainty remain. This work was undertaken to describe the effects of TRH and VIP on the pulsatile secretion pattern of prolactin, in adult sham-operated and pituitary-grafted hyperprolactinaemic female rats. Two pulses of TRH (1 μg/rat) or one pulse of VIP (20 μg/rat) were given 60 or 120 min after the period of blood sampling. Pituitary grafting increased the mean values of prolactin, absolute amplitude and duration of the peaks and decreased their frequency, compared with control animals. In sham-operated rats, TRH elevated prolactin levels by increasing the absolute and relative amplitudes and duration of the pulses, along with a decrease in their frequency. No priming effects of TRH were observed in this study. Hyperprolactinaemia blunted TRH effects on the pulsatile secretion pattern of prolactin. In sham-operated rats, VIP administration increased the absolute and relative amplitudes of the prolactin peaks. None of the other parameters studied were changed. In pituitary-grafted animals, VIP administration increased the absolute and relative amplitudes of the prolactin peaks but to a lesser extent compared with controls. These data suggest that TRH and VIP affect prolactin pulsatility differentially. The effects of TRH and VIP were blunted to some extent by exposure to previously elevated circulating prolactin levels. Journal of Endocrinology (1994) 142, 581–586

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