PITUITARY HORMONE RESPONSES TO HYPOTHALAMIC RELEASING HORMONES IN ACROMEGALY

1976 ◽  
Vol 83 (4) ◽  
pp. 673-683 ◽  
Author(s):  
L. Cantalamessa ◽  
E. Reschini ◽  
A. Catania ◽  
G. Giustina
Keyword(s):  
Clinical Signs ◽  
Pituitary Function ◽  
Pituitary Hormone ◽  
Repeated Testing ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Prolactin Response ◽  
Plasma Gh ◽  
Lh Rh ◽  
Pituitary Irradiation

ABSTRACT The pituitary reserve of GH, prolactin, TSH, LH, and FSH has been studied in a group of 13 acromegalic patients with the aim of evaluating the pituitary function and the activity of the disease. Plasma GH, TSH and prolactin were determined after thyrotrophin releasing hormone (TRH) administration, plasma gonadotrophins and GH after luteinizing hormone releasing hormone (LH-RH) administration. The plasma TSH response to TRH was generally blunted in the patients treated with pituitary irradiation; however, none of the patients with diminished TSH reserve had signs of hypothyroidism. Six acromegalics showed prolactin basal levels higher than controls; none had galactorrhoea; 4 of them complained of impairment of the gonadal function. The prolactin response to TRH was variable and not related to prolactin basal levels. A subnormal LH reserve after LH-RH stimulation was observed in 5 out of 10 patients; 4 of them had also clinical signs of hypogonadism. A normal FSH response to LH-RH was present in all patients. A non-specific GH response to TRH and/or LH-RH was obtained in about half of the acromegalics studied. The GH responsiveness to TRH and/or LH-RH was not related to the activity of the disease or to a specific derangement of the hypothalamo-pituitary function. A concordant response was observed only between GH and prolactin response to TRH; the highest prolactin responses to TRH were obtained in the GH responsive patients. Each patient showed a constant GH pattern of response on repeated testing. Even after pituitary irradiation the pattern of GH response was unchanged in spite of lowered GH plasma levels.

INFLUENCE OF SUCKLING AND OF SUCKLING FOLLOWED BY TRH OR LH-RH ON PLASMA PROLACTIN, TSH, GH AND FSH

1976 ◽  
Vol 82 (1) ◽  
pp. 246-253 ◽  
Author(s):  
S. Jeppsson ◽  
K. O. Nilsson ◽  
G. Rannevik ◽  
L. Wide
Keyword(s):  
Limit Of Detection ◽  
Post Partum ◽  
Prolactin Secretion ◽  
Plasma Prolactin ◽  
Additional Increase ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Before And After ◽  
Plasma Gh ◽  
Lh Rh

ABSTRACT Ten women were studied during the first post-partum week. Suckling for 20 min induced a marked increase in plasma prolactin, reaching a maximum within 0–25 min after the end of suckling and then returning to pre-suckling levels after 120 min. Suckling induced no changes in plasma thyrotrophin (TSH), growth hormone (GH) or follicle stimulating hormone (FSH). The iv injection of 200 μg of thyrotrophin releasing hormone (TRH) immediately after suckling resulted in an additional increase in plasma prolactin and a rise in TSH. When given 120 min after suckling TRH was followed by increased plasma levels of prolactin and TSH, which for both hormones were of a magnitude comparable to the TRH induced increment seen immediately after suckling. Thus, suckling did not inhibit the effect of TRH on the release of TSH. These studies indicate that TRH is probably not involved in the suckling induced increase in prolactin secretion. The mean plasma FSH level was below the limit of detection before and after suckling. Neither plasma FSH nor prolactin showed any appearant changes following the iv injection of 25 μg of luteinizing hormone releasing hormone (LH-RH), when given immediately after and 120 min after suckling. When given after suckling as indicated above, TRH induced no changes in plasma GH or FSH and similarly LH-RH was without influence on plasma GH and TSH.

Effects of hypothyroidism on the growth hormone axis in sheep

1994 ◽  
Vol 140 (3) ◽  
pp. 495-502 ◽  
Author(s):  
T P Fletcher ◽  
I J Clarke
Keyword(s):  
Growth Hormone ◽  
Pulse Amplitude ◽  
Pulse Frequency ◽  
Pulse Interval ◽  
Short Term ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Prolactin Response ◽  
Plasma Gh

Abstract This study examined the effect of thyroidectomy (TX) on the GH axis in sheep. The secretion of GH was monitored 10 and 77 days after TX or sham-TX when the effects on plasma GH and prolactin levels of the injection of 0·5 μg GH-releasing factor (GRF)/kg and 1 μg thyrotrophin-releasing hormone (TRH)/kg were also assessed. There were no significant differences in GH pulse amplitude, pulse frequency, inter-pulse interval and GH secreted/h between sham-TX and TX animals at 10 or 77 days after TX. There was no difference in the GH response to GRF injection in sham-TX sheep at any time but in TX sheep the GH response was significantly (P<0·05) attenuated 10 days after TX. After 77 days the GH response was similar to the response before TX. There was no measurable GH response to injection of TRH in sham-operated or TX sheep at any time. The prolactin response to TRH was not affected by TX or sham-TX. These results suggest that TX in sheep does not affect GH secretion but paradoxically the response to GRF is attenuated in hypothyroid sheep in the short term. TRH causes release of prolactin but not GH in sheep. Journal of Endocrinology (1994) 140, 495–502

GROWTH HORMONE RELEASE FOLLOWING THYROTROPHIN-RELEASING HORMONE INJECTION INTO PATIENTS WITH ANOREXIA NERVOSA

1976 ◽  
Vol 81 (1) ◽  
pp. 1-8 ◽  
Author(s):  
K. Maeda ◽  
Y. Kato ◽  
N. Yamaguchi ◽  
K. Chihara ◽  
S. Ohgo ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Anorexia Nervosa ◽  
Luteinizing Hormone ◽  
Intravenous Injection ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Basal Plasma ◽  
Plasma Gh ◽  
Lh Rh ◽  
Plasma Prl

ABSTRACT The effect of thyrotrophin-releasing hormone (TRH) or luteinizing hormone-releasing hormone (LH-RH) on plasma levels of growth hormone (GH), prolactin (PRL), thyrotrophin (TSH), and luteinizing hormone (LH), were studied in patients with anorexia nervosa. The basal plasma GH levels were elevated in 6 of 11 patients studied. Intravenous injection of synthetic TRH (500 μg) significantly raised the plasma GH levels in 9 of 11 patients. The peak values of plasma GH after TRH ranged from 6.0 to 31.5 ng/ml. Plasma GH concentrations also increased following the administration of synthetic LH-RH (100μg) in 1 of 7 patients. The intravenous injection of saline solution caused no significant change in plasma GH in these patients. The plasma LH responses to LH-RH were significantly blunted in all patients, whereas the plasma PRL and TSH responses to TRH were almost normal in the patients examined. These results suggest that the hypothalamo-pituitary function regulating GH and LH secretion is altered in patients with anorexia nervosa.

Estimation of pituitary secretion rate during the reproductive cycle of sheep

1990 ◽  
Vol 114 (2) ◽  
pp. 213-218
Author(s):  
K. S. Lindsay ◽  
I. R. Fleet ◽  
D. E. Walters ◽  
R. B. Heap
Keyword(s):  
Blood Flow ◽  
Reproductive Cycle ◽  
Hormone Secretion ◽  
Pituitary Hormone ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Pituitary Secretion ◽  
Conscious Sheep ◽  
Cephalic Blood Flow ◽  
Secretion Rates

SUMMARYA technique has been developed for the measurement of pituitary hormone secretion rates in conscious sheep. The technique involves the continuous and simultaneous sampling of blood from the carotid artery and jugular vein and the measurement of cephalic blood flow by an indicator dilution technique. Veno-arterial differences in hormone concentrations multiplied by cephalic blood flow gave average secretion rates which were measured after single or repeated large doses of luteinizing hormone releasing hormone (LHRH) and thyrotrophin-releasing hormone (TRH) at various times in the reproductive cycle.

Stimulatory effect of thyrotrophin-releasing hormone (TRH) on the release of luteinizing hormone (LH) from rat anterior pituitary cells in vitro

1983 ◽  
Vol 61 (2) ◽  
pp. 186-189 ◽  
Author(s):  
Noboru Fujihara ◽  
Masataka Shiino
Keyword(s):  
Luteinizing Hormone ◽  
Anterior Pituitary ◽  
Pituitary Cells ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Anterior Pituitary Cells ◽  
Lh Release ◽  
Lh Rh

The effect of thyrotrophin-releasing hormone (TRH, 10−7 M) on luteinizing hormone (LH) release from rat anterior pituitary cells was examined using organ and primary cell culture. The addition of TRH to the culture medium resulted in a slightly enhanced release of LH from the cultured pituitary tissues. However, the amount of LH release stimulated by TRH was not greater than that produced by luteinizing hormone – releasing hormone (LH–RH, 10−7 M). Actinomycin D (2 × 10−5 M) and cycloheximide (10−4 M) had an inhibitory effect on the action of TRH on LH release. The inability of TRH to elicit gonadotrophin release from the anterior pituitary glands in vivo may partly be due to physiological inhibition of its action by other hypothalamic factor(s).

scholarly journals Evaluation of GnRH administration on the prolactin response to thyrotrophin-releasing hormone in normal women.

1986 ◽  
Vol 33 (4) ◽  
pp. 511-517 ◽  
Author(s):  
HISANORI MINAKAMI ◽  
KOZO KIMURA ◽  
KUNIHIKO IJIMA ◽  
AKIO AKABORI ◽  
TARO TAMADA
Keyword(s):  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Normal Women ◽  
Prolactin Response

Thyrotrophin and prolactin responses to thyrotrophin-releasing hormone in patients with Parkinson's disease

1982 ◽  
Vol 99 (3) ◽  
pp. 344-351 ◽  
Author(s):  
Abraham Martinez-Campos ◽  
Paolo Giovannini ◽  
Antonello Novelli ◽  
Daniela Cocchi ◽  
Tommaso Caraceni ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Growth Hormone ◽  
Parkinson's Disease ◽  
Chronic Treatment ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Marked Diminution ◽  
Dopaminergic Tone ◽  
Plasma Gh

Abstract. The thyrotrophin (TSH) and prolactin (Prl)-releasing effects of TSH-releasing hormone (TRH) were investigated in 20 subjects with Parkinson's disease (PD), unmedicated, on chronic treatment with a combination levodopa-benserazide (Madopar) or levodopa-carbidopa (Sinemet) or withdrawn from therapy. Administration of TRH (200 μg iv) induced in unmedicated patients TSH and Prl responses significantly lower than those of sex-and age-matched controls. In patients on Madopar therapy the TSH and Prl responses to TRH were greater than in unmedicated patients and comparable to those of controls, while in patients on Sinemet therapy the pituitary responses were undistinguishable from those of unmedicated subjects. Withdrawal of Madopar therapy resulted in a marked diminution of the TSH response but did not affect the Prl response to TRH. Withdrawal of Sinemet therapy did not alter the TSH and Prl responses to TRH. Concomitant evaluation of growth hormone (GH) levels, in none of the subjects evidenced non-specific changes in plasma GH following TRH. Since TSH and Prl responses to TRH are inhibited by an enhancement of the dopaminergic tone, it would appear that the latter is preserved in the tuberoinfundibular system of unmedicated subjects and subjects on chronic Sinemet therapy, but is defective in subjects on chronic Madopar therapy.

Hypothalamic hormones that release growth hormone stimulate hepatic 5′-monodeiodination activity in the chick embryo

1988 ◽  
Vol 118 (2) ◽  
pp. 233-236 ◽  
Author(s):  
E. R. Kühn ◽  
A. Vanderpooten ◽  
L. M. Huybrechts ◽  
E. Decuypere ◽  
V. Darras ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Plasma Concentration ◽  
Chick Embryo ◽  
Chick Embryos ◽  
Thyrotrophin Releasing Hormone ◽  
Growth Hormone Releasing Factor ◽  
Releasing Hormone ◽  
Pancreatic Growth ◽  
Hypothalamic Hormones ◽  
Plasma Gh

ABSTRACT Plasma GH, tri-iodothyronine (T3), thyroxine (T4) and liver 5′-monodeiodination (5′-D) activity were measured in 18-day-old chick embryos injected with thyrotrophin-releasing hormone (TRH) and human pancreatic growth hormone releasing factor (hpGRF). Injections of 0·1 and 1 μg TRH and 1·5 μg hpGRF increased the concentration of plasma GH while injection of 15 μg hpGRF had no effect. Concentrations of plasma T3 were raised after injection of TRH or hpGRF. Injections of TRH but not of hpGRF raised the concentration of plasma T4. The increases in concentration of plasma T3 after injection of TRH or hpGRF were parallelled by increases in liver 5′-D activity. An injection of 0·25 μg T4 significantly raised the concentration of T4 in plasma but had no effect on plasma T3 or liver 5′-D activity. It is concluded that the release of chicken GH by TRH or hpGRF is responsible for the observed increases in plasma concentration of T3 and liver 5′-D activity. J. Endocr. (1988) 118, 233–236

Combined pyridostigmine–thyrotrophin-releasing hormone test for the evaluation of hypothalamic somatostatinergic activity in healthy normal men

1995 ◽  
Vol 133 (4) ◽  
pp. 457-462 ◽  
Author(s):  
Inmyung Yang ◽  
Jeongtaek Woo ◽  
Sungwoon Kim ◽  
Jinwoo Kim ◽  
Youngseol Kim ◽  
...  
Keyword(s):  
Internal Medicine ◽  
Growth Hormone ◽  
Large Dose ◽  
Trh Test ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
School Of Medicine ◽  
Prolactin Response ◽  
Normal Men ◽  
Different Doses

Yang I, Woo J, Kim S, Kim J, Kim Y, Choi Y. Combined pyridostigmine–thyrotrophin-releasing hormone test for the evaluation of hypothalamic somatostatinergic activity in healthy normal men. Eur J Endocrinol 1995;133:457–62. ISSN 0804–4643 Pyridostigmine (PST), a cholinesterase inhibitor, induces a clear growth hormone (GH) release in man by suppression of hypothalamic somatostatin (SRIH). Somatostatin suppresses thyrotrophin (TSH) release in rats and men. Earlier studies showed that the thryotrophin-releasing hormone (TRH)-induced TSH response was not altered by 60–120 mg of PST. We studied whether a larger dose (180 mg) of PST can increase the TSH response to TRH. Six healthy young men were studied with the following six tests: (Test 1) 200 μg of TRH iv; (Test 2) 180 mg of PST po; (Test 3) three different doses of PST (60, 120, 180 mg) + TRH; (Test 4) 100 μg of octreotide (SMS) iv; (Test 5) SMS + TRH; (Test 6) PST + SMS + TRH. A large dose of PST (180 mg) significantly augmented GH, TSH and prolactin responses to TRH, while smaller doses of PST (60 and 120 mg) did not significantly increase the responses of GH and TSH. While the increased TRH-induced prolactin response by PST was not suppressed by SMS, the increased responses of GH and TSH were suppressed remarkably by SMS. Most of the subjects noticed a mild to moderate abdominal pain, nausea and muscular fasciculation after the administration of a large dose of PST administration. These data suggest that suppression of hypothalamic SRIH secretion by 180 mg of PST can augment the TSH response to TRH. However, the considerable side effects should be minimized before clinical application of the combined PST–TRH test. Inmyung Yang, Division of Endocrinology, Department of Internal Medicine, Kyunghee University School of Medicine, 1 Hoiki-dong, Dongdaemoon-ku, Seoul, 130–702, Korea

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