THE INFLUENCE OF OESTROGEN ADMINISTRATION IN VIVO ON IN VITRO PROLACTIN RELEASE

1979 ◽  
Vol 92 (3) ◽  
pp. 437-447 ◽  
Author(s):  
Sandford Jaques ◽  
Richard R. Gala
Keyword(s):  
Time Of Day ◽  
Ovariectomized Rat ◽  
Prolactin Release ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Stable Pool ◽  
Releasable Pool ◽  
Storage Pools

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.

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).

Tri-iodothyronine inhibition of thyrotrophin-releasing hormone-induced growth hormone release from the chicken adenohypophysis in vitro

1990 ◽  
Vol 126 (1) ◽  
pp. 75-81 ◽  
Author(s):  
S. Harvey
Keyword(s):  
Growth Hormone ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Direct Effects ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Site Of Action

ABSTRACT Tri-iodothyronine (T3) had no effect on the basal level of GH release from chicken hemipituitary glands perifused in vitro. The GH response to TRH was, however, markedly suppressed following exposure to T3. Suppression of TRH-stimulated GH secretion was observed after a 2-h preincubation with T3, and was induced, in a dose-related way, by 0·01–10 μmol T3/l. Exposure to T3 also reduced the effectiveness of TRH, at concentrations of 0·001–10 μg/ml, to stimulate GH release. These results demonstrate that, in addition to a hypothalamic site of action, T3 is likely to suppress GH secretion in vivo by direct effects on pituitary GH release. Journal of Endocrinology (1990) 126, 75–81

Thyrotrophin-releasing hormone responsiveness and degradation in children with chronic renal failure: effect of time of evolution

1982 ◽  
Vol 99 (4) ◽  
pp. 508-516 ◽  
Author(s):  
C. Marti Henneberg ◽  
J. M. Domenech ◽  
E. Montoya
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Normal Subjects ◽  
Serum Levels ◽  
Significant Negative Correlation ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Degradation Rates

Abstract. In order to study the hypothalamic-pituitarythyroid function in children with chronic renal failure (CRF), the serum levels of l-thyroxine (l-T4), l-triiodothyronine (l-T3), reverse T3 (rT3), thyrotrophin (TSH) and prolactin (Prl) were measured by radioimmunoassay (RIA). Values were compared with those of normal subjects. Low levels of l-T4 were present in CRF patients as compared to controls. l-T3 was also found to be low but less than l-T4, and rT3 was lower in patients with long evolution. No alterations were observed in TSH basal levels, whereas Prl values in patients were high. After thyrotrophin-releasing hormone (TRH) administration, TSH and Prl rose to similar levels in both groups, but high values were maintained throughout (120 min) in CRF. A significant negative correlation was found between the peak rise of the TSH response and the CRF evolution time. The l-T3 response to TRH administration (120 min) was similar in both CRF and controls. The rate of in vivo and in vitro exogenous TRH degradation was decreased in patients with CRF or by their sera, respectively. Our data seem to confirm that the hypothyroid syndrome described in CRF patients is of hypothalamic origin, and the low in vivo and in vitro TRH degradation rates are a consequence of this state.

Interaction of thyrotrophin releasing hormone with inhibin in male rats

1983 ◽  
Vol 98 (1) ◽  
pp. 1-6 ◽  
Author(s):  
A. R. Sheth ◽  
P. R. Sheth ◽  
R. Roy
Keyword(s):  
Pituitary Gland ◽  
Adult Male ◽  
Serum Levels ◽  
Male Rats ◽  
Prolactin Release ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone

Inhibin administered to adult male rats delayed the in-vivo pituitary responsiveness to thyrotrophin releasing hormone (TRH) as observed in terms of prolactin release in the serum. It also decreased the sensitivity of the pituitary gland to TRH, in terms of TSH release. However, inhibin alone did not alter the serum levels of prolactin and TSH, although it significantly suppressed serum FSH levels. In addition, the inhibin effect on FSH release was blocked by TRH.

Thyrotrophin-releasing hormone (TRH) and lung maturation

1995 ◽  
Vol 7 (3) ◽  
pp. 443 ◽  
Author(s):  
GC Liggins
Keyword(s):  
Fetal Lung ◽  
Lung Maturation ◽  
Rabbit Lung ◽  
Glucocorticoid Treatment ◽  
Fetal Sheep ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Fetal Plasma

Clinical trials of thyrotrophin-releasing hormone (TRH) in conjunction with antepartum glucocorticoid treatment in the prevention of respiratory distress syndrome is based on experimental evidence that fetal lung maturation is accelerated by exposure to raised concentrations of triiodothyronine (T3) in fetal plasma. Studies of fetal rat and rabbit lung in vitro show an inconsistent increase in surfactant synthesis in response to T3 and potentiation of the response to corticosteroid. Experiments with fetal rodents in vivo are difficult to interpret because of confounding effects of the procedures and the responses to T3 are variable. In fetal sheep, very high concentrations of T3 are without effect on lung maturation. These observations suggest that the action of TRH on the lung may be mediated at least in part by one of the numerous, non-hormonal pathways known to be stimulated by TRH, particularly the autonomic nervous system. Experiments in rats and sheep lend support to this possibility. It is concluded that available evidence is inadequate to determine the mechanism of action of TRH.

Feedback-inhibition of growth hormone (GH) secretion in fowl: GH-induced down-regulation of thyrotrophin-releasing hormone binding to pituitary membranes

1990 ◽  
Vol 4 (1) ◽  
pp. 13-21 ◽  
Author(s):  
S. Harvey ◽  
J. S. Baidwan
Keyword(s):  
Plasma Membranes ◽  
Feedback Inhibition ◽  
Inhibitory Effects ◽  
Thyrotrophin Releasing Hormone ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Gh Cells ◽  
Igf I

ABSTRACT Administration of ovine GH to immature domestic fowl blunted their subsequent GH response to thyrotrophin-releasing hormone (TRH), a GH secretagogue in birds. The in-vivo administration of GH also reduced the ability of radiolabelled TRH to bind to plasma membranes of the pituitary caudal lobe, in which GH cells predominate. These inhibitory effects of GH were mediated by extrapituitary actions, since GH had no direct inhibitory effects on TRH-induced GH release or on pituitary TRH binding in vitro. GH inhibition of GH secretion and TRH binding would not appear to be mediated by hypothalamic somatostatin (SRIF) or peripheral somatomedin (IGF-I), since SRIF and IGF-I had no direct effects in vitro.

ASSESSMENT OF GH RELEASING HORMONE ACTIVITY IN SEPHADEX-SEPARATED FRACTIONS OF PORCINE HYPOTHALAMIC EXTRACTS BY HYPOPHYSEAL PORTAL VESSEL INFUSION IN THE RAT

1975 ◽  
Vol 78 (3) ◽  
pp. 428-434 ◽  
Author(s):  
Jiro Takahara ◽  
Akira Arimura ◽  
Andrew V. Schally
Keyword(s):  
Growth Hormone ◽  
Growth Hormone Releasing Hormone ◽  
Hormone Activity ◽  
Prolactin Release ◽  
Releasing Hormone ◽  
Portal Vessel ◽  
Lh Rh ◽  
Lh Releasing Hormone

ABSTRACT Growth hormone-releasing hormone (GH-RH) activity in Sephadex G-25 fractions of porcine stalk median eminence (SME) extracts was examined in vivo by infusing these samples into a rat hypophyseal portal vessel. The increment of immunoreactive GH levels in the serum was used as the index for GH-RH activity. The GH-RH activities were found in two different locations: in the early fractions Nos. 3–4, and in somewhat retarded fraction No. 7. These GH-RH activities were not due to TRH, vasopressin, or potassium. The location of LH releasing hormone (LH-RH) and prolactin release-inhibiting hormone (PR-IH) determined in this in vivo system was in agreement with those found in other in vivo and in vitro assay systems for LH-RH and PR-IH, respectively. These results help validate this assay system.

Ontogeny of Angiotensin-II-Induced Prolactin Release in vivo and in vitro in Female and Male Rats

1994 ◽  
Vol 59 (1) ◽  
pp. 57-62 ◽  
Author(s):  
Graciela S. Díaz-Torga ◽  
Damasia Becú-Villalobos ◽  
Carlos Libertun
Keyword(s):  
Angiotensin Ii ◽  
Male Rats ◽  
Prolactin Release
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