DIE WIRKUNG VON SYNTHETISCHEM THYROTROPHIN RELEASING HORMONE AUF DIE ENTWICKLUNG EINES EXPERIMENTELLEN EXOPHTHALMUS BEIM GOLDFISCH

1971 ◽  
Vol 68 (2) ◽  
pp. 363-366 ◽  
Author(s):  
W. Wildmeister ◽  
F. A. Horster
Keyword(s):  
Carassius Auratus ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone

ABSTRACT Gold-fishes (carassius auratus) were injected with synthetic thyrotrophin releasing hormone (TRH) in concentrations of 25 μg to 1000 μg/fish. TRH did not provoke endocrine exophthalmos.

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.

THYROTROPHIN RELEASING HORMONE-INDUCED GROWTH HORMONE AND PROLACTIN RELEASE: PHYSIOLOGICAL STUDIES IN INTACT RATS AND IN HYPOPHYSECTOMIZED RATS BEARING AN ECTOPIC PITUITARY GLAND

1977 ◽  
Vol 72 (3) ◽  
pp. 301-311 ◽  
Author(s):  
A. E. PANERAI ◽  
IRIT GIL-AD ◽  
DANIELA COCCHI ◽  
V. LOCATELLI ◽  
G. L. ROSSI ◽  
...  
Keyword(s):  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Time Lapse ◽  
Anterior Pituitary Gland ◽  
Plasma Prolactin ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Clear Cut ◽  
Urethane Anaesthesia ◽  
Releasing Effect

SUMMARY To determine how the sensitivity of the ectopic anterior pituitary gland to the GH-releasing effect of thyrotrophin releasing hormone (TRH) might be affected by the time lapse from transplantation, TRH (0·15 and 0·6 μg) was injected i.v. into hypophysectomized (hypox)-transplanted rats under urethane anaesthesia 1,3, 8,15, 30 and 60 days after transplantation, and plasma samples were taken 5 and 10 min later. Baseline GH values gradually decreased with time from about 16·0 ng/ml (1 day) to about 3·0 ng/ml (30 and 60 days). The TRH-induced GH release was absent 1 day after transplantation, present only with the higher TRH dose 3 and 8 days after transplantation, and clearly elicitable, also with the lower TRH dose (0·15 μg), from 15 up to 60 days. Determination of plasma prolactin concentrations showed a decline from about 85·0 ng/ml (1 day) to about 32·0 ng/ml (8 days); subsequently (15–60 days) prolactin values stabilized. Plasma prolactin levels increased 15 and 60 days after transplantation only when a dose of 0·6 μg TRH was given. In intact weight-matched rats, TRH induced a GH response only at the dose of 1·2 μg while a short-lived but clear-cut prolactin response could be obtained even with the 0·3 μg dose. The present results indicate that: (1) disconnexion between the central nervous system and the anterior pituitary gland greatly enhances GH responsiveness while blunting prolactin responsiveness to TRH; (2) the sensitivity of the anterior pituitary gland to the GH-releasing effect of TRH increases with time from transplantation; (3) TRH is a more effective prolactin-than GH-releaser on the pituitary gland in situ.

scholarly journals An improved computational method to assess pituitary responsiveness to secretagogue stimuli

2002 ◽  
pp. 323-332 ◽  
Author(s):  
A Sartorio ◽  
G De Nicolao ◽  
D Liberati
Keyword(s):  
Measurement Error ◽  
Measurement Errors ◽  
Pituitary Hormones ◽  
Computational Method ◽  
Kinetics Parameters ◽  
Thyrotrophin Releasing Hormone ◽  
Deconvolution Analysis ◽  
Releasing Hormone ◽  
Sampling Protocols ◽  
Peak Value

OBJECTIVE: The quantitative assessment of gland responsiveness to exogenous stimuli is typically carried out using the peak value of the hormone concentrations in plasma, the area under its curve (AUC), or through deconvolution analysis. However, none of these methods is satisfactory, due to either sensitivity to measurement errors or various sources of bias. The objective was to introduce and validate an easy-to-compute responsiveness index, robust in the face of measurement errors and interindividual variability of kinetics parameters. DESIGN: The new method has been tested on responsiveness tests for the six pituitary hormones (using GH-releasing hormone, thyrotrophin-releasing hormone, gonadotrophin-releasing hormone and corticotrophin-releasing hormone as secretagogues), for a total of 174 tests. Hormone concentrations were assayed in six to eight samples between -30 min and 120 min from the stimulus. METHODS: An easy-to-compute direct formula has been worked out to assess the 'stimulated AUC', that is the part of the AUC of the response curve depending on the stimulus, as opposed to pre- and post-stimulus spontaneous secretion. The weights of the formula have been reported for the six pituitary hormones and some popular sampling protocols. RESULTS AND CONCLUSIONS: The new index is less sensitive to measurement error than the peak value. Moreover, it provides results that cannot be obtained from a simple scaling of either the peak value or the standard AUC. Future studies are needed to show whether the reduced sensitivity to measurement error and the proportionality to the amount of released hormone render the stimulated AUC indeed a valid alternative to the peak value for the diagnosis of the different pathophysiological states, such as, for instance, GH deficits.

THYROTROPHIN-RELEASING HORMONE IN DEPRESSION

The Lancet ◽  
1975 ◽  
Vol 305 (7899) ◽  
pp. 162 ◽  
Author(s):  
R. Hall ◽  
P.R. Hunter ◽  
J.S. Price ◽  
C.Q. Mountjoy
Keyword(s):  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone

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.

TRIIODOTHYRONINE RESPONSE TO THYROTROPHIN RELEASING HORMONE IN PATIENTS WITH HYPOTHALAMIC-PITUITARY DISORDERS

1975 ◽  
Vol 4 (6) ◽  
pp. 585-590 ◽  
Author(s):  
G. FAGLIA ◽  
C. FERRARI ◽  
ALESSANDRA PARACCHI ◽  
ANNA SPADA ◽  
P. BECK-PECCOZ
Keyword(s):  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone
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