THE SEROTONIN RETAINING EFFECT OF LITHIUM IN THE RAT THYROID

1976 ◽  
Vol 82 (2) ◽  
pp. 530-534 ◽  
Author(s):  
H. Vejlsted ◽  
O. Korsgaard
Keyword(s):  
Thyroid Hormone ◽  
Inhibitory Action ◽  
Hormone Secretion ◽  
Serotonin Release ◽  
Hormone Release ◽  
Rat Thyroid ◽  
Stimulation Of

ABSTRACT The hypothesis of a lithium induced serotonin retention in the rat thyroid has been tested. It has been found that the thyroid in rats treated with lithium contains double the amount of serotonin compared with glands from untreated animals. The ability of TSH to stimulate serotonin release is inhibited by lithium. The ability of serotonin to stimulate thyroid hormone secretion in vitro is documented. The inhibitory action of lithium on both TSH and serotonin stimulation of hormone release is documented. The serotonin retaining effect of lithium as part of the goitrogenic effect of this ion is discussed.

scholarly journals In Vitro and In Vivo Refractoriness to Thyrotropin Stimulation of Iodine Organification and Thyroid Hormone Secretion

1979 ◽  
Vol 64 (1) ◽  
pp. 265-271 ◽  
Author(s):  
James B. Field ◽  
Andrew Dekker ◽  
Gail Titus ◽  
Mary Eleanor Kerins ◽  
William Worden ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Hormone Secretion ◽  
Stimulation Of

ACTION OF POTASSIUM IODIDE ON THYROID ACID PROTEASE

1973 ◽  
Vol 74 (4) ◽  
pp. 703-710 ◽  
Author(s):  
M. A. Pisarev ◽  
N. Altschuler
Keyword(s):  
Thyroid Hormone ◽  
Potassium Iodide ◽  
Enzyme Preparation ◽  
Specific Activity ◽  
Hormone Secretion ◽  
Enzyme Synthesis ◽  
Acid Protease ◽  
Rule Out ◽  
Stimulation Of

ABSTRACT Potassium iodide (KI) is known to inhibit thyroid hormone secretion. In the present studies its action on the proteolytic step of this process was investigated. Rats were treated with KI (200 μg/ml in the drinking water) for 30 days. This treatment caused a decrease of protease activity in total homogenate and in the specific activity of a 15 000 × g pellet. No alteration in the pattern of subcellular distribution was observed. In order to rule out an action of KI on enzyme activity its in vitro action was studied. KI concentrations around 103-–10−4 m were without effect, though 10−2 caused a stimulation of activity. Similar results were observed when a liver enzyme preparation was checked under the same conditions. Neither CL− nor F− had an effect on thyroid or liver protease at concentrations between 10−2 to 10−4 m. The present results suggest that KI inhibition of thyroid hormone secretion can be explained at least in part by its action on acid protease. Moreover, the lack of an in vitro inhibitory affect of KI would suggests that this drug affects enzyme synthesis and/or breakdown.

Ligand-dependent, Pit-1/growth hormone factor-1 (GHF-1)-independent transcriptional stimulation of rat growth hormone gene expression by thyroid hormone receptors in vitro

1993 ◽  
Vol 13 (3) ◽  
pp. 1719-1727
Author(s):  
C S Suen ◽  
W W Chin
Keyword(s):  
Gene Expression ◽  
Growth Hormone ◽  
Thyroid Hormone ◽  
Promoter Activity ◽  
Hormone Receptors ◽  
Nuclear Extract ◽  
In Vitro Transcription ◽  
Stimulation Of ◽  
Transcriptional Stimulation

The expression of the rat growth hormone (rGH) gene in the anterior pituitary gland is modulated by Pit-1/GHF-1, a pituitary-specific transcription factor, and by other more widely distributed factors, such as the thyroid hormone receptors (TRs), Sp1, and the glucocorticoid receptor. Thyroid hormone (T3)-mediated transcriptional stimulation of rGH gene expression has been extensively studied in vivo and in vitro including the measurements of (i) rGH mRNA by blot hybridization, (ii) transcriptional rate of rGH gene by nuclear run-on, and (iii) reporter gene expression in which a chimeric plasmid containing 5'-flanking sequences of the rGH gene linked to a reporter gene has been transfected either stably or transiently into pituitary and/or nonpituitary cells. From these studies, it has been suggested that the Pit-1/GHF-1 binding site is necessary for full T3 action. We developed a cell-free in vitro transcription system to examine further the roles of the TRs and Pit-1/GHF-1 in rGH gene activation. Using GH3 nuclear extract as a source of TRs and Pit-1/GHF-1, this in vitro transcription assay showed that T3 stimulation of rGH promoter activity is dependent on the addition of T3 to the GH3 nuclear extract. This transcriptional stimulation was augmented with increasing concentrations of ligand and was T3, but not T4 or reverse T3, specific. T3-mediated stimulation of rGH promoter activity was completely abolished by preincubation of the nuclear extract with rGH-thyroid hormone response element (-200 to -160) but not with Pit-1/GHF-1 (-137 to -65) oligonucleotides. Further, neither deletion of both Pit-1/GHF-1 binding sites nor mutation of the proximal Pit-1/GHF-1 binding site from the rGH promoter abrogated the T3 effect. These results provide evidence that T3-stimulated rGH promoter activity is independent of Pit-1/GHF-1 and raise the possibility that the stimulation of rGH gene expression by T3 might involve direct interaction of TRs with the general transcriptional apparatus.

Functional dedifferentiation of parathyroid cells results both from a defective regulation and action of cytoplasmic Ca2+

1986 ◽  
Vol 6 (12) ◽  
pp. 1057-1063 ◽  
Author(s):  
Peter Nygren
Keyword(s):  
Parathyroid Hormone ◽  
Inhibitory Action ◽  
Monolayer Culture ◽  
Hormone Secretion ◽  
Dose Effect ◽  
Parathyroid Cell ◽  
Hormone Release ◽  
Parathyroid Adenomas ◽  
Small Inhibition

Monolayer culture of bovine parathyroid cells for 24 hours resulted in a right-shift of the dose-effect relationships for Ca2+-inhibition of parathyroid hormone (PTH) release and the dependence of the cytoplasmic Ca2+ concentration (Ca2+) on extracellular Ca2+ as well as in a less suppressible hormone release. After 4 days of culture, hormone secretion was almost non-suppressible and Cai2+ increased poorly in response to a rise in extracelluiar Ca2+. Ionomycin, a Ca2+ ionophore, raised Cai2+, but there was only a small inhibition of PTH release and the correlation between Cai2+ and secretion was weak. A deteriorated Cai2+ regulation and a decreased inhibitory action of cytoplasmic Ca2+ on PTH release were also found in ceils from human parathyroid adenomas. Functional dedifferentiation of the parathyroid cell thus results from both defective regulation and action of cytoplasmic Ca2+.

Evidence for calcium inactivation during hormone release in the rat neurohypophysis

1976 ◽  
Vol 65 (3) ◽  
pp. 669-683
Author(s):  
J. J. Nordmann
Keyword(s):  
Hormone Secretion ◽  
Calcium Ionophore ◽  
High Rate ◽  
Hormone Release ◽  
45Ca Uptake ◽  
High K ◽  
K Concentration ◽  
The Relationship ◽  
Internal Calcium

1. A study has been made of the relationship between 45Ca uptake into and hormone release from isolated rat neurohypophyses incubated in vitro. 2. Hormone secretion is triggered by high-K (56 mM) but long exposure to the stimulus does not generate a maintained release of hormone. 3. When hormone release began to wane, addition of Ba of La increased hormone output which suggests that the decline in output did not result from depletion of the neurosecretory granules at the nerve terminals. 4. 45Ca uptake is enhanced in the presence of high-K concentration, but the initial high rate declines during long exposure to the potassium stimulus with a time constant similar to that of the decline in hormone release. 5. After a period of incubation in a K-rich, calcium-free medium, addition of calcium to the medium induced hormone release. The magnitude of this release was dependent on the time of exposure to excess potassium. 6. After inactivation of secretion, mobilization of internal calcium by means of a calcium ionophore increased hormone release.

In vivo effects of flavonoid EMD 21388 on thyroid hormone secretion and metabolism in rats

1991 ◽  
Vol 261 (2) ◽  
pp. E227-E232 ◽  
Author(s):  
J. P. Schroder-van der Elst ◽  
D. van der Heide ◽  
J. Kohrle
Keyword(s):  
Thyroid Hormone ◽  
Hormone Secretion ◽  
Male Rats ◽  
Intact Male ◽  
Hormone Production ◽  
Iodide Uptake ◽  
Brown Adipose ◽  
In Vivo Effects

In vitro, the synthetic flavonoid EMD 21388 appears to be a potent inhibitor of thyroxine (T4) 5'-deiodinase and diminishes binding of T4 to transthyretin. In this study, in vivo effects of long-term administration of EMD 21388 on thyroid hormone production and metabolism were investigated. Intact male rats received EMD 21388 (20 mumol.kg body wt-1.rat-1.day-1) for 14 days. [125I]T4 and 3,5,3'-[131I]triiodotyronine (T3) were infused continuously and intravenously in a double-isotope protocol for the last 10 and 7 days, respectively. EMD 21388 decreased plasma thyroid hormone concentrations, but thyrotropin levels in plasma and pituitary did not change. Plasma clearance rates for T4 and T3 increased. Thyroidal T4 secretion was diminished, but T3 secretion was elevated. Extrathyroidal T3 production by 5'-deiodination was lower. T4 concentrations were markedly lower in all tissues investigated. Total tissue T3 was lower in brown adipose tissue, brain, cerebellum, and pituitary, tissues that express the type II 5'-deiodinase isozyme due to decreased local T3 production. Most tissues showed increased tissue/plasma ratios for T4 and T3. These results indicate that this flavonoid diminished T4 and increased T3 secretion by the thyroid, probably in analogy with other natural flavonoids, by interference with one or several steps between iodide uptake, organification, and hormone synthesis.

Sign in / Sign up

Export Citation Format

Share Document