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

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.

1980 ◽  
Vol 86 (3) ◽  
pp. 397-402 ◽  
Author(s):  
NICKI WHITE ◽  
E. C. GRIFFITHS ◽  
S. L. JEFFCOATE ◽  
R. D. G. MILNER ◽  
M. A. PREECE

Changes in the rate of in-vitro degradation of thyrotrophin releasing hormone (TRH) in serum as related to age have been investigated in the rat and man. In rats, no inactivation was found up to the age of 15 days but thereafter an age-related increase in inactivation was detected with approximately 75% inactivation in 60 min at 40 days and reaching a maximum of 88–93% inactivation in adult male and female animals. The human serum samples studied (both male and female) showed a similar but less clear-cut pattern of inactivation of TRH compared with that found in the rat. A physiological role for these age-related changes in the degradation of TRH remains to be established but it has been concluded that the changes observed in both rat and man may be associated with growth and development, possibly by facilitating feedback control of thyrotrophin secretion through the degradation of TRH.


1985 ◽  
Vol 108 (1) ◽  
pp. 79-84 ◽  
Author(s):  
Terunori Mitsuma ◽  
Tsuyoshi Nogimori ◽  
Masahiro Chaya

Abstract. The effects of peripheral administration of bombesin on thyrotrophin-releasing hormone (TRH) and thvrotrophin (TSH) secretion in rats were studied. Bombesin (200 μg/kg) was injected iv, and the rats were serially decapitated. TRH, TSH and thyroid hormone were measured by radioimmunoassay. The hypothalamic immunoreactive TRH (ir-TRH) content increased significantly after bombesin injection, whereas plasma concentrations tended to decrease, but not significantly. Plasma TSH levels decreased significantly in a dose-related manner with a nadir at 40 min after the injection. Plasma thyroid hormone levels did not change significantly. Plasma ir-TRH and TSH responses to cold were inhibited by bombesin, but the plasma TSH response to TRH was not affected. In the pimozide- or para-chlorophenylalanine pre-treated group, the inhibitory effect of bombesin on TSH levels was prevented, but not in the l-Dopa- or 5-hydroxytryptophan pre-treated group. These drugs alone had no effect on plasma TSH levels in terms of the dose used. The inactivation of TRH immunoreactivity in plasma or hypothalamus in vitro after bombesin injection did not differ from that of the controls. These findings suggest that bombesin acts on the hypothalamus to inhibit TRH release, and that its effects are at least partially modified by amines of the central nervous system.


1985 ◽  
Vol 110 (1) ◽  
pp. 90-94
Author(s):  
Terunori Mitsuma ◽  
Tsuyoshi Nogimori ◽  
De Heng Sun ◽  
Masahiro Chaya

Abstract. The effect of peripheral administration of eledoisin on thyrotrophin-releasing hormone (TRH) and thyrotrophin (TSH) secretion in rats were studied. Eledoisin (500 μg/kg) was injected iv, and the rats were serially decapitated. TRH, TSH and thyroid hormone were measured by radioimmunoassay. The hypothalamic immunoreactive TRH (ir-TRH) content increased significantly after eledoisin injection, whereas its plasma concentration tended to decrease, but not significantly. Plasma TSH levels decreased significantly in a dose-related manner with a nadir at 40 min after the injection. Plasma thyroid hormone levels did not change significantly. Plasma ir-TRH and TSH responses to cold were inhibited by eledoisin, but the plasma TSH response to TRH was not affected. In the pimozide- or para-chlorophenylalanine-pretreated group, the inhibitory effect of eledoisin on TSH levels was prevented, but not in the l-dopa- or 5-hydroxytryptophan-pretreated group. These drugs alone did not affect plasma TSH levels at the dose used. The inactivation of TRH immunoreactivity by plasma or hypothalamus in vitro after eledoisin injection did not differ from that of controls. These findings suggest that eledoisin acts on the hypothalamus to inhibit TRH release, and its effects are modified by amines of the central nervous system.


1983 ◽  
Vol 61 (2) ◽  
pp. 186-189 ◽  
Author(s):  
Noboru Fujihara ◽  
Masataka Shiino

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).


1984 ◽  
Vol 102 (2) ◽  
pp. 175-180 ◽  
Author(s):  
T. R. Hall ◽  
A. Chadwick

ABSTRACT Pituitary glands of grassfrog (Rana pipiens), bullfrog (Rana catesbeiana), clawed toad (Xenopus laevis) and two species of terrapin (Chrysemys picta and Pseudemys scripta) were incubated in medium containing hypothalamic extract (HE), thyrotrophin releasing hormone (TRH), somatostatin, dopamine, or combinations of these treatments. Prolactin and GH concentrations in the medium were determined by densitometry after polyacrylamide-gel electrophoretic separation. Hypothalamic extract stimulated secretion of both hormones in all species tested. Thyrotrophin releasing hormone stimulated secretion of prolactin and GH, showing a biphasic pattern of response. Dopamine had little effect alone, but inhibited HE-and TRH-stimulated release of prolactin, but not GH, in both amphibia and reptiles. Somatostatin by itself had no apparent effect on release of hormones, but it inhibited HE- and TRH-stimulated release of GH from both amphibian and reptilian pituitary glands. These results indicate that factors affecting mammals and birds also interact in the regulation of secretion of prolactin and GH in lower vertebrate species. J. Endocr. (1984) 102, 175–180


1984 ◽  
Vol 105 (1) ◽  
pp. 57-65 ◽  
Author(s):  
Ken Kubota ◽  
Hidemasa Uchimura ◽  
Tomoaki Mitsuhashi ◽  
Shoo Cheng Chiu ◽  
Nobuaki Kuzuya ◽  
...  

Abstract. Mice were infused continuously with graded doses of bovine TSH (bTSH) and changes in plasma concentrations of bTSH and T4 were measured. Then mice infused with 100 mU TSH per day were sacrificed on days 0, 1, 3 and 5 and their thyroids were excised to determine in vitro secretion of T4, T3 and rT3 during 3 h of incubation. At the end of the incubation, thyroidal contents of T4, T3 and rT3 were also determined after pronase digestion. Plasma bTSH levels were increased on day 1 to a level of 110 μU/ml and remained unchanged thereafter. Plasma T4 concentrations increased approximately 2-fold on day 1, but decreased to initial levels on days 3 and 5. Changes in T4 secretion in vitro paralleled those in plasma T4 concentrations; T4 secretion increased 2-fold on day 1, and decreased to the pre-TSH levels on days 3 and 5. In contrast, T3 secretion increased throughout the experimental period. The T3/T4 ratio in thyroidal secretion in vitro was the same as that in thyroidal contents on days 0 and 1 of TSH infusion, but the former was significantly greater than the latter on days 3 and 5. PTU (5.9 × 10−5 m), a known inhibitor of T4 deiodination, added to the incubation media did not affect T4 secretion on days 0 and 1, but increased T4 secretion on days 3 and 5 to the level of day 1, but did not affect T3 secretion. In the presence of PTU, the T3/T4 ratio in thyroidal secretion did not differ from that in thyroidal contents throughout the experimental period. Secretion of rT3 was increased on days 3 and 5 and PTU augmented this increase. Thyroidal content of rT3 was much increased on days 3 and 5. In contrast, methimazole (10−3 m), which does not inhibit in vitro T4 deiodination, added to the incubation media did not affect T4, T3 and rT3 secretion in vitro. When [125I]T4 was added to the media and incubated with mouse thyroid, no labelled products of T4-deiodination were observed to appear in the media even in mice infused with TSH for 5 days. These results suggest that intrathyroidal metabolism of T4 has physiological significance in controlling thyroid hormone secretion at least in TSH-stimulated thyroids.


1979 ◽  
Vol 92 (3) ◽  
pp. 437-447 ◽  
Author(s):  
Sandford Jaques ◽  
Richard R. Gala

ABSTRACT The influence of oestrogen administered to the ovariectomized rat on the interaction between dopamine (DA) and thyrotrophin releasing hormone (TRH) on the release of radioimmunoassayable (RIA) and [3H] leucine incorporated into prolactin ([3H]PRL) was examined in vitro. Dopamine had a more marked suppressing effect on newly synthetized PRL (80 %), as determined [3H]PRL, than on total PRL (50 %), as determined by RIA-PRL. The administration of 5 μg of oestradiolbenzoate (OeB) for 7 days resulted in blocking the suppressing effect of DA when RIA-PRL was measured but not when [3H]PRL was measured. The administration of 5 μg of OeB enabled TRH to partially override the suppressing effect of DA and the degree of response was more marked when RIA-PRL was measured than when [3H]PRL was measured. The administration of 50 μg of OeB for 3 days enabled TRH to override the DA blockade of prolactin release to levels comparable to that of the control when RIA-PRL was measured but had little to no effect on [3H]PRL. The results are discussed in relation to the two storage pools of PRL in the pituitary and the data suggest that DA acts predominantly to suppress the newly synthetized, rapidly releasable pool. Oestrogen acts to block DA action on the older more stable PRL pool. The ability of TRH to override the DA blockade of PRL release depends upon the presence of oestrogen; here TRH acts predominantly on the older more stable pool of PRL. Oestrogen's action on disrupting the DA suppression of PRL release appears to be related to the time of day the hormone is administered subsequent to when the pituitary is exposed to DA in vitro.


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