Search Results
Search for other papers by R. GOLDSTEIN in
Google Scholar
PubMed
Search for other papers by S. PAVEL in
Google Scholar
PubMed
Institute of Endocrinology, Bucharest, Rumania
(Received 29 March 1977)
The mammalian pineal gland contains (Pavel, 1965) and synthesizes (Pavel, Goldstein, Ghinea & Calb, 1977) the nonapeptide arginine-vasotocin (AVT). Since luteinizing hormone releasing hormone (LH–RH), thyrotrophin releasing hormone (TRH) and growth hormone release-inhibiting hormone (somatostatin, SRIF) have now been localized not only in the brain, but also in the pineal gland (White, Hedlund, Weber, Rippel, Johnston & Wilber, 1974; Pelletier, Le Clerc, Dube, Labrie, Puviani, Arimura & Schally, 1975), we investigated the effects of these peptides on the release of AVT into the cerebrospinal fluid (CSF) of cats.
Intracarotid injections of 0·1 μg LH-RH, TRH (Hoechst, Frankfurt), SRIF (Serono, Rome) or oxytocin (Syntocinon, Sandoz Ltd, Basel) in 0·5 ml saline were given to urethane-anaesthetized male cats weighing 3–4 kg. Controls received an equal volume of saline only. The pineal glands were removed 60 min after the injections, quickly homogenized, and extracted
Search for other papers by J. R. REEL in
Google Scholar
PubMed
Search for other papers by CAROL A. PASTUSHOK in
Google Scholar
PubMed
Search for other papers by J. W. VAITKUS in
Google Scholar
PubMed
Search for other papers by R. SAKOWSKI in
Google Scholar
PubMed
Search for other papers by W. C. DERMODY in
Google Scholar
PubMed
Department of Pharmacology, Research and Medical Affairs Division, Parke, Davis & Company, Ann Arbor, Michigan 48106, U.S.A.
(Received 22 June 1976)
Leicht, Birò & Weinges (1974) recently reported that infusion of salmon calcitonin into 11 human subjects significantly inhibited luteinizing hormone (LH) and thyrotrophin (TSH) secretion induced by LH releasing hormone (LH-RH) and thyrotrophin releasing hormone (TRH) respectively. Basal secretion of these two pituitary hormones was unaffected. Since serum Ca2+ concentrations were not changed significantly, Leicht et al. (1974) postulated that calcitonin might act directly on the secretory cells of the pituitary gland, possibly by altering Ca2+ fluxes at the level of the cell membrane. To test the hypothesis of a direct action of calcitonin on pituitary cells, we examined the effect of synthetic salmon calcitonin on LH and TSH release in unstimulated, and LH-RH- and TRH-stimulated anterior pituitary cell cultures.
Pooled anterior pituitary glands from dioestrous Charles-River
Search for other papers by A. MASALA in
Google Scholar
PubMed
Search for other papers by G. DELITALA in
Google Scholar
PubMed
Search for other papers by G. LO DICO in
Google Scholar
PubMed
Search for other papers by S. ALAGNA in
Google Scholar
PubMed
Search for other papers by L. DEVILLA in
Google Scholar
PubMed
Cattedra di Semeiotica Medica 2 a and *Clinica Ostetrica e Ginecologica, University of Sassari, Viale San Pietro 12, 07100 Sassari, Italy
(Received 21 March 1977)
Recent evidence suggests that antioestrogens may interfere with secretion of prolactin. Tamoxifen inhibits oestrogen-induced release of prolactin in rats (Jordan, Koerner & Robison, 1975); furthermore, reduced levels of prolactin during fasting and blunted responses to synthetic thyrotrophin releasing hormone (TRH) have been reported in women with breast cancer undergoing treatment with tamoxifen (Willis, London & Butt, 1976). Another antioestrogen, clomiphene citrate, has been used with appreciable results to inhibit puerperal lactation (Zuckerman & Carmel, 1973; Weinstein, Ben-David & Polishuk, 1976), but it has no effect on the release of prolactin in normal man during fasting or hypoglycaemia, or after stimulation with synthetic TRH or sulpiride (Thomer, Besser, Hagen & McNeilly, 1974). We investigated the effect of clomiphene on the release of prolactin induced by mechanical
Search for other papers by G. MILHAUD in
Google Scholar
PubMed
Search for other papers by P. RIVAILLE in
Google Scholar
PubMed
Search for other papers by M. S. MOUKHTAR in
Google Scholar
PubMed
Search for other papers by E. BINET in
Google Scholar
PubMed
Search for other papers by J. C. JOB in
Google Scholar
PubMed
SUMMARY
Thyrotrophin-releasing hormone (TRH) was synthesized by the solid phase technique, administered to 13 children, and the time-course changes in the serum level of thyroid-stimulating hormone (TSH) assessed. In eight normal children, peak levels of TSH occurred 20 min after the injection, and circulating TSH remained significantly raised for 60 min. In three hypothyroid children, the increase in serum TSH was much greater than in normal children, suggesting the existence of large pituitary TSH stores. In two hypopituitary children with TSH deficiency, TSH reserves seemed normal. One of these patients had a craniopharyngioma; after operation, the increase in serum TSH was reduced. These results show that assay of serum TSH after administration of synthetic TRH provides a test which distinguishes pituitary from hypothalamic defects affecting TSH secretion.
Search for other papers by O. F. X. ALMEIDA in
Google Scholar
PubMed
Adult male Japanese quail held under short daily photoperiods (8 h light: 16 h darkness; 8L : 16D) had significantly higher plasma concentrations of thyroid-stimulating hormone (TSH), tri-iodothyronine (T3) and thyroxine (T4) than did those kept under long days (16L : 8D).
When given a single s.c. injection of 50 μg thyrotrophin releasing hormone (TRH) the birds held under both the 8L : 16D and 16L : 8D photoperiods showed rapid increases in their blood concentrations of TSH, T4 and T3, the amplitude of the TSH response of the birds exposed to 16L : 8D being particularly marked. These results suggest that, in the male quail, long daily photoperiods produce a hypothyroid state as a result of diminished TRH secretion. The synthetic and secretory capacities of the thyroid gland and pituitary thyrotrophs are apparently unimpaired by long days.
Search for other papers by D. M. LAWSON in
Google Scholar
PubMed
Search for other papers by R. R. GALA in
Google Scholar
PubMed
SUMMARY
Plasma levels of prolactin were determined, by radioimmunoassay, in ovariectomized, oestrogen-treated rats after administration of ether, sodium pentobarbitone, urethane, chloral hydrate or ketamine. These anaesthetics, when administered alone, induced sustained increases in the plasma level of prolactin (continuous ether inhalation), no change in prolactin secretion (urethane), or depressions in the level of prolactin (sodium pentobarbitone, chloral hydrate and ketamine). These same anaesthetics when given before perphenazine failed to alter the stimulatory effect of this phenothiazine on prolactin secretion. Sodium pentobarbitone did not alter the normal increase in prolactin concentration after intra-arterial administration of synthetic thyrotrophin releasing hormone (TRH). These results indicated that anaesthetics do not affect the response of either the central nervous system or the anterior pituitary to perphenazine or TRH although they affect prolactin secretion when administered alone. The site of action of anaesthetics must, therefore, be different from that of perphenazine or perphenazine must be capable of overcoming their influence by direct action on the pituitary.
Search for other papers by J.A. Franklyn in
Google Scholar
PubMed
Search for other papers by M. Wilson in
Google Scholar
PubMed
Search for other papers by J.R. Davis in
Google Scholar
PubMed
Search for other papers by D.B. Ramsden in
Google Scholar
PubMed
Search for other papers by K. Docherty in
Google Scholar
PubMed
Search for other papers by M.C. Sheppard in
Google Scholar
PubMed
ABSTRACT
We have reported previously the effect of thyroid status in vivo on pituitary cytoplasmic concentrations of messenger RNA (mRNA) encoding the thyrotrophin (TSH) β-subunit (Franklyn, Lynam, Docherty et al, 1985). Studies in vitro of the regulation of TSH β gene transcription have been confined to thyrotrophic tumour cells. We now report the demonstration of TSH β-subunit mRNA in non-tumorous rat pituitary cells in primary culture. Treatment of cells with thyrotrophin-releasing hormone (TRH) and with forskolin resulted in a marked increase in cellular concentration of TSH β-mRNA. These results suggest that TRH exerts a direct effect on the pretranslational events involved in TSH synthesis and further that the adenylate cyclase system may be involved in the regulation of synthesis. We have thus described a novel system for the study of TSH β-subunit gene expression in normal rat pituitary cells in vitro.
Search for other papers by L Schaaf in
Google Scholar
PubMed
Search for other papers by J Trojan in
Google Scholar
PubMed
Search for other papers by T E Helton in
Google Scholar
PubMed
Search for other papers by K H Usadel in
Google Scholar
PubMed
Search for other papers by J A Magner in
Google Scholar
PubMed
Abstract
The aims of the present study were to determine the influence of brief subclinical hypothyroidism on the isoforms of serum thyrotropin (TSH) and to examine the net charge of TSH in different metabolic states. Sera were obtained from euthyroid subjects (n=7) and from patients with subclinical hypothyroidism (n=8) before and 30 min after the intravenous administration of 200 μg thyrotropin-releasing hormone (TRH). The TSH from human pituitary extracts (IRP 68/38), basal and TRH-stimulated serum TSH was immunoconcentrated and further analysed by isoelectric focusing (IEF) and lentil lectin affinity chromatography. TSH immunoreactivity was determined in each specimen or fraction with an automated highly sensitive chemiluminometric TSH assay. We found that basal TSH in subclinical hypothyroidism, and TRH-released TSH in euthyroidism and in subclinical hypothyroidism is distributed in a similar neutral to acidic pattern, which significantly differs from the more alkaline to neutral isoform pattern of intrapituitary TSH (P<0·05). IEF analysis of pituitary standard TSH revealed 3 major peaks (pI values 7·5; 6·6; 5·8) whereas in most euthyroid or subclinically hypothyroid subjects 5 peaks were found. Lentil lectin affinity chromatography revealed that TRH-released TSH in euthyroid subjects has more core fucose residues than TSH from patients with subclinical hypothyroidism (64·6 ±6·7 vs 12·5 ±2·7%, P<0·0001).
Thus pituitary standard TSH seems to be less mature material than circulating TSH. Perhaps no alteration in the IEF pattern of TSH was detected during early hypothyroidism because sialylation of TSH was increasing as sulfatation was decreasing. Nevertheless, a change in the core fucose content of TSH was detectable by lentil analysis.
Journal of Endocrinology (1995) 144, 561–567
Search for other papers by N. WHITE in
Google Scholar
PubMed
Search for other papers by S. L. JEFFCOATE in
Google Scholar
PubMed
Search for other papers by E. C. GRIFFITHS in
Google Scholar
PubMed
Search for other papers by K. C. HOOPER in
Google Scholar
PubMed
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.
Search for other papers by M A Pavia Jr in
Google Scholar
PubMed
Search for other papers by B Paier in
Google Scholar
PubMed
Search for other papers by M I Noli in
Google Scholar
PubMed
Search for other papers by K Hagmüller in
Google Scholar
PubMed
Search for other papers by A A Zaninovich in
Google Scholar
PubMed
Abstract
The effect of in vivo administration of cadmium chloride on the pituitary-thyroidal axis was assessed in 200 g body weight Wistar rats. A dose of 2·5 mg/kg body weight was injected i.v. 24 h before the experiments were initiated. Plasma thyroxine (T4) and tri-iodothyronine (T3) concentrations in cadmium-treated rats were significantly (P<0·01) decreased, whereas plasma TSH failed to increase in response to low T4 and T3. However, the TSH response to TRH and the pituitary content of TSH in these rats were both normal. Cadmium induced a significant (P<0·01) decrease in 4-h thyroidal 131I uptake and in thyroid/plasma radioactivity ratio. The in vitro conversion of T4 to T3 in the pituitary was significantly (P<0·01) blocked by cadmium whereas there was no in vivo effect. Parameters of peripheral T4 kinetics in cadmium-treated rats, such as metabolic clearance rate (P<0·01), fractional turnover rate (P<0·01), absolute disposal rate (P<0·05), urinary clearance (P<0·05) and faecal clearance (P<0·05), were all decreased by cadmium. The lack of response of TSH to low plasma T4 and T3 and the normal response to exogenous TRH in this and in other non-thyroidal illness syndromes produced by other pathologies suggest a decreased stimulation of pituitary thyrotrophs by endogenous TRH.
Journal of Endocrinology (1997) 154, 113–117
