Inhibition of TSH-stimulated thyroid hormone release and potentiation of TRH-stimulated TSH release by indomethacin in perifusion systems of rat thyroids and pituitaries

Using indomethacin (Ind), a prostaglandin synthesis inhibitor, in vivo experiments in rats and in vitro experiments with perifusion systems of rat thyroids and pituitaries were conducted. After 35 days of intragastric infusion of Ind, serum TSH levels were markedly increased, the thyroid was swollen and, as a consequence, T3 and T4 levels were normal. The T3 release from perifused rat thyroids under continuous stimulation with 10 mU/ml TSH was inhibited significantly (p less than 0.01) by 1.0 X 10(-6) M Ind. On the other hand, the TSH release from perifused rat pituitaries under TRH stimulation was enhanced conspicuously by Ind. It was concluded that Ind decelerated thyroid hormone release from the thyroid and accelerated TSH release from the pituitary in perifusion systems.     

Inhibition of TSH-stimulated thyroid hormone release and potentiation of TRH-stimulated TSH release by indomethacin in perifusion systems of rat thyroids and pituitaries

Summary Using indomethacin (Ind), a prostaglandin, synthesis inhibitor, in vivo experiments in rats and in vitro experiments with perifusion systems of rat thyroids and pituitaries were conducted. After 35 days of intragastric infusion of Ind, serum TSH levels were markedly increased, the thyroid was swollen and, as a consequence, T₃ and T₄ levels were normal. The T₃ release from perifused rat thyroids under continuous stimulation with 10 mU/ml TSH was inhibited significantly (p<0.01) by 1.0×10^–6 M Ind. On the other hand, the TSH release from perifused rat pituitaries under TRH stimulation was enhanced conspicuously by Ind. It was concluded that Ind decelerated thyroid hormone release from the thyroid and accelerated TSH release from the pituitary in perifusion systems.     

Hormonal control of manganese transport in the mouse thyroid.

The present study deals with a possible mechanism controlling the transport of manganese (Mn), an essential trace element, from the circulation to the thyroid. Mice were pretreated with propylthiouracil (PTU) or triiodothyronine (T3), and a measurement of the thyroid:serum concentration ratio (T/S) of radioactive manganese (54Mn) was carried out. The T/S of 54Mn was greatly enhanced by PTU, but reduced by T3. Several methods were used to demonstrate that the T/S of 54Mn depends upon the level of thyroid-stimulating hormone (TSH) in the serum. First, bovine TSH was injected into mice; an increase in the T/S resulted. Secondly, serum thyroxine and T3 levels measured by radioimmunoassay (RIA) suggested that PTU produced an increase in serum TSH and T3 a decrease. However, direct measurement of mouse TSH by RIA for rat TSH failed to produce proof of any changes in TSH level, owing to poor cross-reactivity. Taking all the information into account, it is concluded that Mn-transport into the thyroid is controlled by the thyroid state.     

Hormonal control of manganese transport in the mouse thyroid

The present study deals with a possible mechanism controlling the transport of manganese (Mn), an essential trace element, from the circulation to the thyroid. Mice were pretreated with propylthiouracil (PTU) or triiodothyronine (T₃), and a measurement of the thyroid:serum concentration ratio (T/S) of radioactive manganese (⁵⁴Mn) was carried out. The T/S of⁵⁴Mn was greatly enhanced by PTU, but reduced by T₃. Several methods were used to demonstrate that the T/S of⁵⁴Mn depends upon the level of thyroid-stimulating hormone (TSH) in the serum. First, bovine TSH was injected into mice; an increase in the T/S resulted. Secondly, serum thyroxine and T₃ levels measured by radioimmunoassay (RIA) suggested that PTU produced an increase in serum TSH and T₃ a decrease. However, direct measurement of mouse TSH by RIA for rat TSH failed to produce proof of any changes in TSH level, owing to poor cross-reactivity. Taking all the information into account, it is concluded that Mn-transport into the thyroid is controlled by the thyroid state.     

Respective roles of circulating T4 and T3 in control of TSH secretion in severely iodide-deficient rats

Summary After a 6-month iodide deficiency, Wistar male rats were submitted to a normal iodine diet (20 and 50 g of¹²⁷I daily). Plasma T₃, T₄ and TSH were determined by RIA from 0 to 140 days of iodide refeeding. A highly significant correlation was found between plasma TSH and T₄ concentrations, but not between plasma TSH and T₃ levels. These data suggest that an increase in plasma T₃ alone, up to the normal value, is not able to inhibit TSH secretion. It is only when a certain plasma T₄ concentration is also reached, resulting in further T₃ formation through deiodination, that TSH secretion is inhibited.Dedicated to the memory of Prof. C. Simon.This work was supported by grants from the CNRS (Equipe de Recherche Associée no 234) and from the INSERM (A.T.P. 49.77.8).Acknowledgments. The authors wish to thank Mrs M. Chartier for valuable technical assistance. They are indebted to the rat pituitary distribution programme of NIAMDD, NIH, Bethesda, for their gift of rat TSH reagents.     

Radioimmunoassay of some hormones simultaneously measured in serum and breast cyst fluid

Blood and breast cyst fluid were drawn simultaneously for hormonal determination. There was no difference between serum and cyst fluid values of PRL and TSH. A significant difference was noted for LH (p less than 0.01) and FSH (p less than 0.05), serum concentrations being higher than cyst fluid concentrations.     

Fetal hypophysis as the main source of serum TSH in fetal rat

Decapitation performed at days 17-18 leads to a drastic drop (82%) in blood TSH of 19 and 21-day-old rat fetuses below the mother's level. 125I-TSH injected at 21 days into the mother's bloodstream is not found in fetal blood. The fetal hypophysis is the main source of fetal plasmatic TSH.     

Fetal hypophysis as the main source of serum TSH in fetal rat

Summary Decapitation performed at days 17–18 leads to a drastic drop (82%) in blood TSH of 19 and 21-day-old rat fetuses below the mother's level.¹²⁵I-TSH injected at 21 days into the mother's bloodstream is not found in fetal blood. The fetal hypophysis is the main source of fetal plasmatic TSH.     

Plasma triiodothyronine,thyroxine and thyrotrophin levels in germfree rats

Summary Plasma T₃, T₄ and TSH levels in developing germfree rats were high, low and normal as compared with those in conventional counterparts. The high T₃/T₄ ratio in germfree rat plasma was lowered by cholestyramine feeding.This work was supported in part by a grant from the Imanaga Foundation, Nagoya, Japan.     

Radioimmunoassay of some hormones simultaneously measured in serum and breast cyst fluid

Summary Blood and breast cyst fluid were drawn simultaneously for hormonal determination. There was no difference between serum and cyst fluid values of PRL and TSH. A significant difference was noted for LH (p<0.01) and FSH (p<0.05), serum concentrations being higher than cyst fluid concentrations.The authors are indebted to Miss J. Meister, E. Dullaert and J. Beck for their skillful technical help. We are also indebted to the National Institutes of Health, NIAMDD and the World Health Organization, International Laboratory for Biological Standards.     

Reciprocal changes in serum free thyroxine fraction and thyrotropin level after administration of thiocyanate to rats

Summary The administration of thiocyanate to rats caused a significant increase of serum free thyroxine fraction, which coincided with the significant decrease of TSH level. The other components (AFT₄, T₄, T₃) in serum at this time were decreased or unchanged. The finding suggests the role of free thyroxine fraction in feed-back regulation of TSH secretion.Acknowledgment. We thank Dr A. Parlow and the NIAMDD, Rat Pituitary Hormone Distribution Program, for material for rat TSH immunoassay; Dr J. Nauman (Inst. Postgrad. Med., Warsaw, Poland) for T₃ antibody, and to Ing. J. Sadlo, Mrs M. t'astná and Miss R Fajkoová for technical assistance.     

Influence of age on the plasma hormonal iodine response to thyrotropin injection in young calves]

The influence of age upon the increase in plasma hormonal iodine level following an intravenous injection of bovine TSH (0.2 USP units/kg) was studied in young jersey calves. The response to TSH increased between birth and the 7th day, then decreased regularly until the end of the third month. Reasons for these variations are discussed according to some results obtained following TSH injections.     

Plasma thyrotrophin concentration in the foetal calf

Résumé On a mesuré le taux de thyrotrophine (TSH), thyroxine et cortisol dans le plasma du foetus du veau pendant les 18 jours précédant la naissance. La diminution du TSH a précédé de 6 jours et s'est poursuivie en même temps que celle du taux de thyroxine.

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We are grateful to the Medical Research Council and the Milk Marketing Board for financial support.

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The TSH preparation used for iodination in these studies was kindly provided by Dr.J. Pierce, and the antiserum to Pierce bovine TSH was provided by Dr.G. D. Thorburn. Synacthen was kindly provided by Dr.D. M. Burley, CIBA Laboratories, Horsham, Sussex and Efcortelan by Dr.E. S. Snell, Glaxo Laboratories, Middx.     

Alternative methods of animal sacrifice: the effect on intestinal function in vitro.

The total fluid uptake of everted sacs of rat jejunum was compared in animals killed by stunning and decapitation, or anaesthetised with ether. Fluid transport was significantly higher in the tissue prepared from stunned and decapitated animals. It is suggested that etherization may have adverse effects on the physiological viability of subsequently isolated tissues.     

Plurihormonality in the secretory granules of the normal human pituitary. An immunoelectron microscopic study

Normal human autopsy anterior pituitary tissue from 5 cases was embedded in LR White resin and immunolabelled using silver-enhanced 5-nm protein A gold probes. Follicle stimulating hormone (FSH), thyroid stimulating hormone (TSH), luteinizing hormone (LH), adrenocorticotrophic hormone (ACTH), growth hormone (GH) and prolactin (PRL) were immunolocalised to the level of secretory granule. A two-sided double-labelling method was used to cross-react two hormones at a time with respect to their corresponding antibodies. All possible combinations of the six pituitary hormones were tested. Plurihormonal granules were found that contained LH + FSH, LH + TSH, and FSH + TSH. Each hormone was also found in monohormonal granules. Granule diameter was significantly larger in the pluri as opposed to monohormonal granules.     

Plurihormonality in the secretory granules of the normal human pituitary. An immunoelectron microscopic study

Summary Normal human autopsy anterior pituitary tissue from 5 cases was embedded in LR White resin and immunolabelled using silver-enhanced 5-nm protein A gold probes. Follicle stimulating hormone (FSH), thyroid stimulating hormone (TSH), luteinizing hormone (LH), adrenocorticotrophic hormone (ACTH), growth hormone (GH) and prolactin (PRL) were immunolocalised to the level of secretory granule.A two-sided double-labelling method was used to cross-react two hormones at a time with respect to their corresponding antibodies. All possible combinations of the six pituitary hormones were tested. Plurihormonal granules were found that contained LH+FSH, LH+TSH, and FSH+TSH. Each hormone was also found in monohormonal granules. Granule diameter was significantly larger in the pluri as opposed to monohormonal granules.     

Release of renal kallikrein to the perfusate by isolated rat kidney

Summary The addition of furosemide to the fluid used to perfuse isolated rat kidney increases the kallikrein activity found in the perfusion fluid. The experiments favour the concept that furosemide activates a kallikrein precursor or/and the synthesis and release of kallikrein in the kidneys.     

Regulation of sodium and body fluid homeostasis during development: Implications for the pathogenesis of hypertension

The spontaneously hypertensive rat (SHR) is an important animal model of human essential hypertension. During the first month of life, increased retention of sodium is present in the SHR which appears to be mediated by the renin-angiotensin system. The present review will discuss the role that increased activity of the renin-angiotensin system plays in sodium/body fluid regulation during early development. It is hypothesized that disordered regulation of sodium/body fluid homeostasis during this stage leads to pathological cardiovascular regulation in adulthood. Through an understanding of the relationship between sodium/body fluid balance in the young and cardiovascular function in the adult insights may be gained into both the pathological state of hypertension and the critical role played by early development in shaping homeostatic mechanisms in adulthood.     

Regulation of sodium and body fluid homeostasis during development: implications for the pathogenesis of hypertension.

The spontaneously hypertensive rat (SHR) is an important animal model of human essential hypertension. During the first month of life, increased retention of sodium is present in the SHR which appears to be mediated by the renin-angiotensin system. The present review will discuss the role that increased activity of the renin-angiotensin system plays in sodium/body fluid regulation during early development. It is hypothesized that disordered regulation of sodium/body fluid homeostasis during this stage leads to pathological cardiovascular regulation in adulthood. Through an understanding of the relationship between sodium/body fluid balance in the young and cardiovascular function in the adult insights may be gained into both the pathological state of hypertension and the critical role played by early development in shaping homeostatic mechanisms in adulthood.     

Effects of TSH and cyclic AMP on the human thyroid cells cultured in a chemically defined medium.

In a serum-free, chemically defined medium human thyroid cells elongated remarkably and resembled fibroblastic cells. They retained the cyclic AMP response to TSH and the supplement of medium with TSH or dibutyryl cyclic AMP permitted the preservation of epithelial nature by the cells. Cyclic AMP of the cells of epithelial nature was higher than those of fibroblastic appearance.