Effect of changes in thyroid state on metabolism of thyroxine by rat placenta

We studied the effect of the state of the thyroid on T4 monodeiodination in the rat placenta, and it was compared with those in the liver and kidney. The tissues, maternal serum, and amniotic fluid were obtained from pregnant rats. The tissues were homogenized in cold 50 mM Tris-HCl buffer, pH 7.5. The homogenate (1 mg protein) was incubated at 37 degrees C for 60 min with 1 microgram T4 in the presence of 5 mM DTT. The T3 and reverse T3 generated in the reaction mixture were extracted into cold ethanol and measured by RIAs. The conversion of T4 to reverse T3 in rat placenta was not significantly changed in MMI-induced hypothyroidism or T4 induced hyperthyroidism. On the other hand, conversion of T4 to T3 in the liver and kidney were changed in parallel with the thyroid state. The concentration of reverse T3 in the amniotic fluid was increased in accordance with the increase in the maternal serum T4 concentration. These results indicate that the placental T4 inner ring deiodination is not affected by the thyroid state, and that the change in the amniotic fluid reverse T3 concentration in this study is mainly dependent upon the change in maternal thyroid function.     

Morphine induced thyroxine release from rat thyroid gland in vitro

Male rat thyroid glands were incubated for two hours in Krebs-Ringer bicarbonate buffer with different amounts of morphine and/or naloxone. Five micrograms/ml morphine produced a significant increase in the T4 concentration of incubation medium, and resulted in an accumulation of cAMP in the tissue. Naloxone did not change the T4 release but its incubation with morphine prevented the morphine-induced changes. Similarly, naloxone inhibited the morphine-induced accumulation of cAMP in the thyroid tissue.     

Effect of arginine-vasopressin on the rat thyroid gland in vitro

The response of the rat thyroid gland to arginine-vasopressin in vitro was studied to clear a possibility of a direct regulation of this gland by hypothalamic nonapeptide neurohormones. The function of the thyroid gland was estimated by thyrocyte height and quantity of the autoradiographs on a thyrocyte. AVP makes more active hormone synthesis in thyrocytes after 30 min of incubation and it stimulates both synthesis and secretion of the thyroid hormones in 2 hours of incubation. The higher concentrations of AVP activate the thyroid hormone synthesis but not the secretion.     

The functional state of the thyroid gland following partial pancreatectomy]

In Wistar rats a study was made of a functional condition of the thyroid gland 1, 6 and 24 hours after partial pancreatectomy. The following signs-served as criteria of a functional condition of the gland: the amount of neutrone-activated iodine in iron, iodine-absorptive capacity of the gland by I131, the amount of protein-bound stable and radioactive iodine in the blood, a morphological condition of the gland structures. It was demonstrated that, despite the initial intensification of the process of synthesis and secretion in the thyroid gland, its secretory activity fell by the end of the experiment. This reduction is regarded as an adaptive response to partial insulin deficiency.     

Estimation of thyroid gland activity in the Snell dwarf mouse by ultrastructural observation of the thyroid gland, measurement of plasma thyroxine concentration and thyroid hormone binding capacity

An ultrastructural study of the thyroid gland of the Snell dwarf mouse showed cellular activity to be very low. Follicle cell diameters were significantly lower than in controls whilst the nucleocytoplasmic ratio was significantly higher. The observed cellular activity of the thyroid cells was associated with circulating levels of thyroxine which were found to be significantly lower than in controls. Measurement of the free thyroxine index showed very little free hormone available for tissue uptake. No differences in thyroid function due to age or sex in the dwarf mice were seen. Possible endocrine imbalances contributing to the low thyroid activity in the Snell dwarf mouse are discussed.     

Effect of hypercalcemia on parafollicular cells in the rat thyroid gland

Summary Hypercalcemia was induced in rats by the administration of A.T.10. We then determined the levels of total and ionized calcium and calcitonin in the serum, as well as performed ultrastructural observations and histochemical investigations of the calcitonin and neuron-specific enolase immunoreactivities in the stimulated parafollicular cells. The main aim of the study was to apply histochemical procedures to determine the immunoreactions of calcitonin gene-related peptide (CGRP), somatostatin and secretory protein-I in stimulated parafollicular cells. Immunoreactions of CGRP and calcitonin decreased strikingly in A.T.10-treated animals, whereas no visible changes were noted in somatostatin immunoreactivity. In the case of secretory protein-I, an insignificant increase of its immunoreactivity was observed in the treated animals. The cytophysiological significance of these results is discussed.Dedicated to Professor Dr. T.H. Schiebler on the occasion of his 65th birthday     

Effect of hypercalcemia on parafollicular cells in the rat thyroid gland

Hypercalcemia was induced in rats by the administration of A.T.10. We then determined the levels of total and ionized calcium and calcitonin in the serum, as well as performed ultrastructural observations and histochemical investigations of the calcitonin and neuron-specific enolase immunoreactivities in the stimulated parafollicular cells. The main aim of the study was to apply histochemical procedures to determine the immunoreactions of calcitonin gene-related peptide (CGRP), somatostatin and secretory protein-I in stimulated parafollicular cells. Immunoreactions of CGRP and calcitonin decreased strikingly in A.T.10-treated animals, whereas no visible changes were noted in somatostatin immunoreactivity. In the case of secretory protein-I, an insignificant increase of its immunoreactivity was observed in the treated animals. The cytophysiological significance of these results is discussed.     

Binding activities of thyroxine binding globulin versus thyroxine binding prealbumin in rat sera: differential modulation by thyroid hormone ligands, oleic acid and pharmacological drugs

We use gel equilibration and electrophoretic techniques to compare the binding properties of thyroxine binding globulin and thyroxine binding prealbumin in rat sera. The evidence indicates that TBG bears the serum lowest capacity highest affinity sites for thyroxine (T4) and triiodothyronine (T3) (Ka1 greater than or equal to 10(9) M-1) as well as weaker saturable T3 sites (Ka2 approximately 10(8) M-1). TBPA bears for T4 only Ka2 approximately 10(8) M-1 sites and for T3 only Ka approximately 10(6) M-1 sites. Consistent with these parameters are the specific responses of TBG and TBPA binding activities to varying serum concentrations of T4, T3, oleic acid, the drugs diphenylhydantoin or salicylate. The primary attack of these compounds is aimed at TBG. Small T4, oleate or DPH doses chase the TBG-bound T4 to TBPA, high doses of T4 or oleate but not of DPH inhibiting the T4 binding to both proteins. In the T3-serum interactions, all tested compounds displace the TBG-bound hormone without chasing it to TBPA. The high reactivity of TBG sites designates the protein as crucially involved in modulating the free vs bound serum levels of T4 and T3 against physiological or pathological variations of binding competitors.     

Effect of angiotensin on the ultrastructure of the rat thyroid gland

Four hours after administering angiotensin to rats accumulation of radioactive iodine by the thyroid glands is inhibited. Angiotensin produces the contraction of thyroid arterioles. The cytoplasm of endotheliocytes of the perifollicular exchange microvessels becomes dense and luminar surfaces very involuted. Administration of angiotensin also leads to the changes in the ultrastructure of thyrocytes. The cisternae of the granular endoplasmic network get enlarged, the number of membrane-associated ribosome and mitochondria diminishes, that of lysosomes increases.     

Evidence for a functional role of cholecystokinin receptors in the rat thyroid gland.

The aim of the present study was to examine the role of cholecystokinin (CCK) and/or cholecystokinin receptors subtypes (CCK1R and CCK2R) in the regulation of the thyroid gland structure and function. Animals were autopsied after 6 days of treatment with CCK or CCK receptor-specific antagonists (CCK1a--PD 140,548 or CCK2a--PD 135,158) solely or in combination with CCK. Results suggest that CCK exerts a stimulatory effect on follicular thyroid cells manifested by increased epithelium/colloid volume fraction ratio (E/C). Application of selective antagonists of CCK receptor subtypes has demonstrated that CCK acts through the CCK1 receptor subtype at the level of pituitary TSH. The model of endogenous hormone action reveals that thyroid CCK1 is responsible for the thyroid growth. It can be concluded that the physiological activity of CCK1 receptor plays a significant role in a complex interrelationship between TSH, vagal system and CCK1-dependent function of the thyroid gland.