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PubMed1976

Prolactin and thyrotropin responses to thyrotropin-releasing hormone in patients with secondary amenorrhea: the effect of bromocriptine.

Prolactin (PRL) and thyrotropin (TSH) responses to a 200 mug intravenous thyrotropin-releasing hormone (TRH) bolus were measured by radioimmunoassay in 11 women with hyperprolactinemic amenorrhea and 9 with normoprolactinemic amenorrhea. In all cases, the tests were carried out under basal conditions and repeated during bromocriptine treatment. In women whose basal PRL level was normal; TRH caused a maximal PRL increment of 85 +/- 25.2 mug/l (mean +/- SE), while those women whose basal PRL level was raised showed a smaller increase (5.2 +/- 11.9 mug/l) (P=0.02). The peak levels were not significantly different in these two groups (95.0 +/- 26.7 and 134.6 +/- 35.9 mug/l) (P is greater than 0.1). During bromocriptine treatment, the raised PRL levels decreased in all cases, but levels over 30 mug/l remained in 3 patients, one of whom turned out to have a pituitary tumor. Prolactin responses to TRH were markedly inhibited in normoprolactinemic patients by the dose of bromocriptine used. The mean maximal net increase of PRL was 2.0 +/- 0.9 mug/l in normoprolactinemic patients and 11.0 +/- 8.1 mug/l in hyperprolactinemic patients taking bromocriptine. After TRH stimulation during bromocriptine, the peak PRL levels in hyperprolactinemic patients were higher (32.7 +/- 10.5 mug/l) than in normoprolactinemic patients (7.2 +/- 1.5 mug/l). Unlike what has been described for hypothyroid patients, the basal TSH level in euthyroid amenorrhea patients was not affected by bromocriptine, and we found that bromocriptine has no effect on the TRH-TSH response.

Adult↗
PubMed1976

Isolated thyrotropin deficiency with thyrotropin-releasing-hormone induced TSH secretion and thyroidal release.

A patient with isolated thyrotropin (TSH) deficiency was studied. Prior to treatment with thyroid hormone, administration of thyrotropin releasing hormone (TRH) produced no increment in serum TSH and a normal increase in plasma prolactin (PRL). In order to explore whether physiologic increases in serum TSH might be occurring below the limits of detectability of TSH by radioimmunoassay, a double isotope technique of assessing thyroidal secretion secondary to release of TSH was employed. The patient was restudied seven months later, after discontinuing thyroid hormone replacement therapy for two months, and on this occasion repeat TRH administration produced small increments in serum TSH. After administration of 125I and 131I-T4 to assess thyroid hormone secretion, TRH was infused continuously for 6 h. Small increases in serum TSH were again observed, along with significant increases in PG125I/PB131I and urinary 125I/131I, reflecting increased thyroidal iodine secretion, although serum T3 and T4 did not change. These studies indicate that: 1) isolated TSH deficiency need not be complete and may be associated with detectable levels of immunoassayable TSH; 2) the TSH released possesses in vivo biological activity; and 3) therapy with thyroid hormone may have facilitated TSH release.

Adult↗
PubMed1977

A radioimmunoassay for 3,3',5'-L-triiodothyronine (reverse T3): assessment of thyroid gland content and serum measurements in conditions of normal and altered thyroidal economy and following administration of thyrotropin releasing hormone (TRH) and thyrotropin (TSH).

The present report describes the development of a radioimmunoassay for 3,3',5'-L-triiodothyronine (reverse T3) which is performed on unextracted serum. Utilizing this radioimmunoassay, 21 normal subjects had a mean (+/-SD) serum reverse T3 level of 60 +/- 12 ng/100 ml, 17 of 19 hyperthyroid patients had elevated serum reverse T3 levels, and 10 of 11 hypothyroid subjects had decreased serum reverse T3 concentrations. Thyroidal secretion of reverse T3 was assessed by measurements in samples obtained from the internal carotid artery and jugular vein of sheep following the administration of thyrotropin releasing hormone (TRH) or bovine thyrotropin (TSH). Reverse T3 levels were increased 45-60 min after TRH administration, but TSH administration produced inconsistent alterations in reverse T3, although 18 of 27 samples obtained after TSH injection were higher than their average respective baseline concentration and the mean peak reverse T3 level was 14% higher than baseline. Following TRH administration to 10 normal human subjects, mean serum reverse T3 levels significantly increased from 53.6 ng/100 ml to 56.3ng/100 ml (P less than .05). The thyroid gland content of reverse T3 in human autopsy material was 6.5 +/- 1.5 microng/g tissue. Both pregnancy and estrogen administration were associated with increases in serum reverse T3 concentrations presumably because of their ability to augment thyroxine binding globulin synthesis.

Adult↗
PubMed1977

Response to thyrotropin releasing hormone: an objective criterion for the adequacy of thyrotropin suppression therapy.

Most serum thyrotropin (TSH) assays do not adequately discriminate between normal values and absent TSH. We therefore evaluated the TSH response to thyrotropin releasing hormone (TRH) as a criterion for the adequacy of TSH suppression therapy. Twenty-six outpatients with various thyroid disorders (cancer, 10; nodules, 9; miscellaneous, 4; hypothyroidism after 131I therapy for Graves' disease, 3) were studied. Using the frequent sampling technique (samples every 20 min) in two normal volunteers and one untreated patient who was TRH-responsive, we first confirmed the observation that TSH secretion occurred episodically throughout the 24-h period. In contrast, serum TSH was undetectable (less than 0.6 micronU/ml) throughout the 24-h period in 5 patients on TSH suppression therapy who were TRH-unresponsive and one who had a minimal response to TRH. Thus, TRH-unresponsive patients did not secrete measurable amounts of TSH throughout the 24-h period. To suppress TSH secretion, all patients were treated with L-thyroxine (T4) at doses which resulted in undetectable TSH values in random plasma samples. TRH tests were carried out only when random TSH concentrations were less than 0.6 micronU/ml. Seven of the twenty-six patients (27%) including two with thyroid cancer were TRH-responsive indicating a potential for TSH secretion. In these seven, the T4 dose was adjusted until they were TRH-unresponsive. The mean change in T4 dose of these 7 patients was 20+/-10 (SD) microng/day and this resulted in a mean increase of 1.5+/-1.1 microng/dl for T4 and 20+/-20 ng/dl for T3. For all patients, the mean T4 dose required for TSH suppression was 172+/-53 microng/day or 2.6+/-0.8 microng per day per kg body weight. Twenty-three of 26 patients required between 100-200 microng/day and the remaining 3, 250-300 microng/day. The T4 dose required to suppress TSH resulted in normal serum concentrations of T4. 9.1+/-2.0 MICRONG/DL, AND T3, 136.7+/-33.6 NG/DL. These T4 doses did not produce a rapid heart rate, either awake or asleep, arrhythmias, or electrocardiographic abnormalties as assessed by 24-h Holter monitor tracings in 11 patients. Our results thus show that the T4 dose which results in an unresponsive TRH test ensures that serum TSH will remain undetectable (less than 0.6 micronU/ml) throughout the 24-h period. An unresponsive TRH test, therefore, appears to be a very useful and reliable index of TSH suppression.

Adult↗
PubMed1985

Thyrotropin-releasing hormone provocative release of prolactin and thyrotropin in acute head injury.

The thyrotropin-releasing hormone (TRH) test was performed in 30 patients soon after trauma to evaluate the effects of acute head injury on hypothalamohypophyseal functions. Plasma prolactin (PRL) and thyrotropin (TSH) were measured before and after TRH loading. The basal level of the plasma PRL was elevated in patients with severe head injuries compared to those without. The patients with severe head injuries exhibited a lower PRL response to TRH. On the other hand, the basal level of plasma TSH and its response to TRH remained within the normal range. These findings suggest that the PRL data in the TRH test are significant in evaluating the severity of head injuries.

Adolescent↗
PubMed1978

Comparison between the thyrotropin response to thyrotropin-releasing hormone in summer and that in winter in normal subjects.

A comparison was made between the thyrotropin (TSH) response to 500 microgram thyrotropin-releasing hormone (TRH) in summer and that in winter in ten healthy normal adults living in Supporo. The serum resin triiodothyronine (T3) uptake (RT3U), thyroxine (T4) and T3 levels were also measured. While the TSH response to TRH in summer was similar to that in winter, serum T3 concentration and free T3 index were significantly higher in winter than in summer, associated with the similar values in RT3U and T4 levels in serum. Independently measured 86 specimens (43 in summer and 43 in winter) from normal adults living in the same district also showed a significant increase in serum free T3 index as well as a slight elevation of serum T3 concentration in winter but not in serum T4 level. These results indicate that the primary change in cold winter would be the stimulation of peripheral conversion of T4 to T3 rather than the activation of hypothalamo-pituitary-thyroid axis. The relevance of this interpretation was discussed.

Adult↗
PubMed1985

Growth hormone, thyrotropin and prolactin responses to simultaneous administration of human growth hormone-releasing factor and thyrotropin releasing hormone in the bovine.

The effects of intravenous injection of synthetic human pancreatic growth hormone-releasing factor-44-NH2 (hpGRF-44) and synthetic thyrotropin releasing hormone (TRH), or hpGRF-44 in combination with TRH on growth hormone (GH), thyrotropin (TSH), and prolactin (PRL) release in dairy female calves (6- and 12-month-old) were studied. When 0.25 microgram of hpGRF-44 per kg of body weight (bw) was injected in combination with TRH (1.0 microgram per kg of bw), the mean plasma GH concentration of the 12-month-old calves rose to a maximum level of 191.5 ng/ml (P less than 0.001) at 15 min from the value of 6.8 ng/ml before injection at 0 min. The maximum level was 3.1 and 6.1 times as high as the peak values obtained after injection of hpGRF-44 (0.25 microgram per kg of bw) and TRH (1.0 microgram per kg of bw), respectively (P less than 0.001). The area under the GH response curve for the 12-month-old calves for 3 hr after injection of hpGRF-44 in combination with TRH was 2.5 times as large as the sum of the areas obtained by hpGRF-44 and TRH injections. In contrast, the mean plasma GH level was unchanged in saline injected calves. The magnitudes of the first and the second plasma GH responses in the 6-month-old calves to two consecutive injections of hpGRF-44 in combination with TRH at a 3-hr interval were very similar. The peak values of plasma GH in the calves after hpGRF-44 injection were 2-4 times as high as those after TRH injection.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Serum free thyrotropin subunit in congenital isolated thyrotropin deficiency.

In two patients with congenital isolated thyrotropin (TSH) deficiency, serum TSH determined by a sensitive immunoradiometric assay (IRMA) was consistently undetectable. The basal levels of serum free TSH-alpha subunit (TSH-alpha) determined by a specific radioimmunoassay (RIA) were elevated in the hypothyroid state, and decreased to the undectable level during displacement therapy with thyroid hormone. The serum free TSH-alpha significantly increased following intravenous administration of thyrotropin releasing hormone (TRH). Serum free TSH-beta subunit (TSH-beta) was undectable. These findings suggest that TSH deficiency in this disease is not due to absence of thyrotroph in the pituitary gland or deficiency of TSH-alpha, but to abnormalities of the TSH-beta gene.

Adult↗
PubMed1985

Amniotic fluid thyrotropin (TSH) following maternal administration of thyrotropin releasing hormone.

Cord blood and amniotic fluid thyrotropin (TSH), T4, T3, and rT3 concentrations were measured in 49 women who received 400 micrograms thyrotropin releasing hormone (TRH) iv during labor and in 16 control women who received saline. Cord blood serum TSH concentrations were elevated for as long as 4 hours after TRH administration and peak values (38.0 +/- 4.2 microU/ml) were observed from 61-120 minutes after TSH as compared to control values of 5.0 +/- 0.3 microU/ml. The elevations in fetal TSH concentration stimulated the fetal thyroid, resulting in a progressive increase in cord blood T4 and T3 but not rT3 concentrations. These TRH induced elevations in fetal cord blood TSH concentrations were not accompanied by increases in unconcentrated and 4 fold concentrated amniotic fluid TSH concentrations which were almost always below 0.6 microU/ml, the limit of assay sensitivity. Unconcentrated amniotic fluid T4 concentrations were barely detectable and no variation was observed between the TRH treated and saline treated mothers; amniotic fluid T3 was not detectable in any of the groups; and amniotic fluid rT3 concentrations ranged between 46.4 and 55.6 ng/dl and did not differ between groups. These findings suggest that term amniotic fluid TSH values do not reflect transient but marked elevations in fetal serum TSH concentrations and that amniotic fluid TSH determination is probably not useful in the detection of primary fetal hypothyroidism. It is possible, but unlikely, that long-term and even greater elevations in fetal serum TSH concentrations would result in increased amniotic fluid TSH concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Amniotic Fluid↗
PubMed1991

Effects of triiodothyronine, triiodothyroacetic acid, iopanoic acid and iodide on the thyrotropin-releasing hormone-induced thyrotropin release from superfused rat pituitary fragments.

The effects of triiodothyronine, triiodothyroacetic acid, iopanoic acid and potassium iodide were investigated on basal and stimulated thyrotropin release in an in vitro experimental model. Rat pituitary fragments were superfused by Medium-199 with or without T3 (10(-7) mol/l), triiodothyroacetic acid (10(-8)-10(-6) mol/l), iopanoic acid (10(-7)-10(-5) mol/l) or potassium iodide (10(-7)-10(-4) mol/l). This was followed by a 6-min pulse of thyrotropin-releasing hormone (10(-8) mol/l). TSH was measured in 3-min fractions. The TRH-induced TSH release from the pituitary fragments was inhibited by T3 (10(-7) mol/l), by triiodothyroacetic acid (10(-7)-10(-6) mol/l), and by high concentrations of iodide (10(-4) or 10(-5) mol/l). Iopanoic acid had no significant effect at the concentrations tested. It is assumed that in vitro, and at similar concentrations, the inhibitory effect of triiodothyroacetic acid on the TRH-induced TSH secretion is comparable to that of T3, whereas iopanoic acid may have no direct detectable effect. In contrast, a direct inhibitory effect of inorganic iodide, at least in pharmacological concentrations in vivo, cannot be excluded.

Animals↗
PubMed1994

Thyrotropin-releasing hormone (TRH) binding sites and thyrotropin response to TRH are regulated by thyroid hormones in human thyrotropic adenomas.

In order to see whether, in thyrotropic adenomas with thyrotoxicosis, plasma thyroid hormones regulate the thyrotropin-releasing hormone (TRH) binding sites and the thyrotropin (TSH) response to TRH, we investigated: the presence of TRH binding sites in two cases of thyrotropic adenomas associated with hyperthyroidism and in one case of thyrotropic adenoma secondary to thyroid failure: and the in vitro effect, in a perifusion system, of triiodothyronine (T3) on the response of TSH to TRH in three cases of TSH-secreting adenomas associated with hyperthyroidism. The TRH binding sites were absent in the adenomas associated with high levels of circulating thyroid hormones, whereas they were present in the adenoma secondary to primary thyroid failure (Kd = 47 nmol/l, Bmax = 40 nmol/kg membrane proteins). In vitro, the three adenomas spontaneously released TSH in the perifusion medium (1.49 +/- 0.06 (mean +/- SEM), 7.25 +/- 0.12 and 16.73 +/- 0.36 mIU.l-1 x 10(6) cells-1 x 2 min-1) and exhibited an ample TSH response to 10(-7) mol/l TRH pulses. In two cases, tumoral secretion of fragments was compared with those of fragments maintained since the time of surgical removal in the presence of 10(-8) mol/lT3. The TSH responses to TRH were abolished in the presence of T3 in these two cases. We conclude that thyrotropic adenomas associated with hyperthyroidism are still controlled in vivo by T3. In particular, T3 regulates the TSH response to TRH, probably via a down-regulation of the TRH binding sites.

Adenoma↗
PubMed1995

Augmentation of thyrotropin-induced iodide uptake in FRTL-5 cells by immunoglobulins containing blocking thyrotropin-receptor antibodies under NaCl-depleted conditions.

We have found recently that Graves' immunoglobulins (Igs) are more active under NaCl-free conditions to increase iodide uptake in FRTL-5 thyroid cells. The present study was designed to examine the effect of blocking-type thyrotropin (TSH)-receptor antibodies (TR-abs) in the same assay. FRTL-5 cells were incubated with crude Ig fractions from 13 patients with primary hypothyroidism having blocking TR-abs and 100 mU/l bovine TSH in NaCl-free Hanks' balanced salt solution (HBSS) supplemented with 274 mmol/l sucrose (HBSS(-)-sucrose) to keep isotonicity for 3 days, followed by the determination of 60 min of 125I uptake in the cells. Thyrotropin alone increased the uptake to 3.3- to 5.2-fold of the basal. When the highest concentration (250 ml serum equivalent (eq.)/l) of the Ig was used, the TSH-stimulated 125I uptake was decreased to 0-42% in 11 of the 13 cases. When the lower concentrations (0.4-50 ml serum eq./l) were used, however, 125I uptake was enhanced (1.4- to 11.4-fold) unexpectedly in all 13 cases. Such an enhancement was specific to blocking TR-abs, because the effect was duplicated by the purified IgG but not by Igs from 10 healthy control subjects or from three TR-ab-negative hypothyroid patients. When Graves' Igs, instead of TSH, were used as a stimulator, the similar stimulatory effect of the Ig with blocking activity was observed on the 125I uptake induced by three Graves' Igs but not on the response to one Graves' Ig. These Igs alone displayed no stimulating activity. When isotonic 5H medium was used instead of HBSS(-)-sucrose, effects of these 13 Igs were only inhibitory on the TSH-stimulated 125I uptake.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1998

Modulation of human thyrotropin oligosaccharide structures--enhanced proportion of sialylated and terminally galactosylated serum thyrotropin isoforms in subclinical and overt primary hypothyroidism.

Enhanced sialylation of thyrotropin (TSH) prolongs its metabolic clearance rate and thus increases the hormone's in vivo bioactivity. This has been shown for hypothyroid rats and for recombinant human TSH, but there are few data on the sialylation of human serum TSH. The aim of this work was to further study sialylated human serum TSH, its precursors bearing terminal galactose residues, and the role of pharmacological doses of thyrotropin-releasing hormone (TRH) on their secretion under different degrees of primary hypothyroidism. We analyzed serum TSH in patients with subclinical (n = 9) and overt primary hypothyroidism (n = 13) compared with euthyroid individuals (n = 12) and human standard pituitary TSH (IRP 80/558). Blood was drawn before and 30 min after intravenous administration of 200 micrograms TRH, and TSH was purified by immunoaffinity concentration. The content of sialylated (sialo-) TSH and isoforms bearing terminal galactose (Gal-TSH, asialo-Gal-TSH) was measured by Ricinus communis (RCA 120) affinity chromatography in combination with enzymatic cleavage of sialic acid residues. TSH immunoreactivity was measured by an automated second generation TSH immunoassay. Pituitary TSH contained 16.5 +/- 0.8% Gal-TSH. In euthyroid individuals the proportion of Gal-TSH was 14.6 +/- 1.9%, whereas TSH in patients with subclinical and overt primary hypothyroidism contained 23.9 +/- 3.5% (P < 0.05 vs euthyroid individuals) and 21.1 +/- 1.7% Gal-TSH respectively. The mean ratio of asialo-Gal TSH was 23.8 +/- 0.6% for pituitary TSH, 35.7 +/- 4.2% in euthyroid individuals, 48.0 +/- 3.3% in patients with subclinical, and 61.5 +/- 3.8% (P < 0.001 vs euthyroid individuals) in patients with overt primary hypothyroidism. For pituitary TSH the calculated proportion of sialo-TSH was 6.5 +/- 0.2%, for euthyroid individuals 20.3 +/- 2.8%, for patients with subclinical hypothyroidism 24.1 +/- 3.0%, and for patients with overt primary hypothyroidism 40.7 +/- 3.0% (P < 0.001 vs euthyroid individuals). The proportions of Gal-TSH, asialo-Gal-TSH, and sialo-TSH did not differ significantly before and after TRH administration in the individuals studied. Our data show that patients with subclinical and overt primary hypothyroidism have a markedly increased proportion of serum TSH isoforms bearing terminal galactose and sialic acid residues, which may represent a mechanism for the further stimulation of thyroid function. Pharmacological doses of TRH cause an increased quantity of TSH to be released, but do not significantly alter the proportion of sialylated or terminally galactosylated TSH isoforms.

Adult↗
PubMed1996

Role of neuromedin B in the in vitro thyrotropin release in response to thyrotropin-releasing hormone from anterior pituitaries of eu-, hypo-, and hyperthyroid rats.

A role of neuromedin B (NB), a bombesin-like peptide, as an inhibitory paracrine/autocrine regulator of thyrotropin secretion has been suggested. We previously reported (10) that basal thyroid-stimulating hormone (TSH) release in vitro was decreased by NB and increased in the presence of a highly potent antiserum against NB (aNB). In these experiments, we studied the effects of NB (10(-11) - 10(-7) M) and antiserum against NB (aNB, 1:2000 dilution) on basal TSH release and the response to thyrotropin-releasing hormone (TRH) (0.5 x 10(-8) M) from incubated anterior pituitaries from eu-, hypo-, and hyperthyroid rats. As expected, in euthyroid rats NB decreased basal and TRH-stimulated TSH release, but only at the highest concentration tested (10(-7) M). Incubation of the pituitaries from euthyroid rats with the antiserum against NB increased basal TSH release above that from glands of normal rabbit serum-incubated controls, as anticipated based on the concept that NB inhibits TSH release from the pituitary glands of euthyroid animals. The antiserum did not augment the response to TRH, suggesting that NB released in this situation, although suppressing basal release, had no effort on the stimulated release induced by TRH. Glands from hypothyroid rats had a slightly lower basal TSH release and decreased response to TRH than glands from euthyroid rats. They responded with a decrease in basal TSH release at a much lower concentration of NB (10(-9) M) than pituitaries from euthyroid animals. Surprisingly, pituitaries from hypothyroid rats showed a paradoxical increased release of TSH in response to the lowest concentration of NB (10(-11) M), which decreased with increasing concentrations and was not distinguishable from control release in the presence of TRH at the highest concentration of NB (10(-7) M). We hypothesize that the increased responsiveness to the inhibition of basal TSH release by NB in the hypothyroid pituitaries may be related to an upregulation of NB receptors in this situation, in which the release of NB is diminished because of loss of feedback via thyroid hormones. The view that NB secretion was reduced in the hypothyroid situation was supported by the fact that there was no change in TSH release or the response to TRH following treatment with aNB in these animals. Remarkably, in the glands from the hyperthyroid rats, although basal TSH secretion was significantly lower than that from euthyroid pituitaries and response to TRH was also decreased, NB (10(-11)-10(-7) M) instead of decreasing TSH release augmented it significantly. Also, the response to TRH was significantly augmented but only at the lowest concentration of NB tested (10(-11 M). That NB was probably being secreted in vitro from the hyperthyroid pituitaries was indicated by an increased basal TSH release as well as a higher TSH medium concentration after TRH in the presence of the aNB. These results support the concept that the glands from the hyperthyroid animals secrete more NB because of positive feedback of thyroid hormones directly on the thyrotropes to increase NB synthesis and release which downregulates NB receptors on the gland. This downregulation of receptors in some manner reverses the inhibitory action of NB on basal and TRH-stimulated TSH release. In conclusion, the results provide further evidence for an important role of NB as an autocrine regulator of TSH release, which is modulated by increased release of NB induced by thyroid hormones.

Animals↗
PubMedDate not supplied

Comparison of thyrotropin-releasing hormone (TRH) to thyrotropin (TSH) stimulation for evaluating thyroid function in dogs.

Five normal dogs and 22 dogs with dermatological signs suggestive of hypothyroidism were evaluated using thyrotropin-releasing hormone (TRH) and thyrotropin (TSH) stimulation. Thyroxine (T4) concentration after TRH stimulation was significantly lower than that obtained by TSH stimulation. It was not possible to identify hypothyroid dogs with the TRH-stimulation test, because some euthyroid dogs had either decreases in T4 or only slight increases in T4 concentrations after TRH stimulation. In addition, dogs with pyoderma had decreased responses in serum T4 after TRH stimulation, which became normal following treatment with antibiotics. Six of the 22 dogs were diagnosed as hypothyroid based on TSH results and responses to thyroid hormone replacement. It was concluded that TRH stimulation is not a useful means of diagnosing hypothyroidism in dogs.

Animals↗
PubMed1998

Increase of thyrotropin response to thyrotropin-releasing hormone (TRH) and TRH release in rats during pregnancy.

Regulation of thyrotropin (TSH) release by thyrotropin releasing hormone (TRH) in the anterior pituitary gland (AP) of pregnant rats was studied. The pregnant (day 7, 14, and 21) and diestrous rats were decapitated. AP was divided into 2 halves, and then incubated with Locke's solution at 37 degrees C for 30 min following a preincubation. After replacing with media, APs were incubated with Locke's solution containing 0, or 10 nM TRH for 30 min. Both basal and TRH-stimulated media were collected at the end of incubation. Medial basal hypothalamus (MBH) was incubated with Locke's medium at 37 degrees C for 30 min. Concentrations of TSH in medium and plasma samples as well as the cyclic 3':5' adenosine monophosphate (cAMP) content in APs and the levels of TRH in MBH medium were measured by radioimmunoassay. The levels of plasma TSH were higher in pregnant rats of day 21 than in diestrous rats. The spontaneous release of TSH in vitro was unaltered by pregnancy. TRH increased the release of TSH by AP, which was higher in pregnant than in diestrous rats. Maternal serum concentration of total T3 was decreased during the pregnancy. The basal release of hypothalamic TRH in vitro was greater in late pregnant rats than in diestrous rats. After TRH stimulation, the increase of the content of pituitary cAMP was greater in late pregnant rats than in diestrus animals. These results suggest that the greater secretion of TSH in pregnant rats is in part due to an increase of spontaneous release of TRH by MBH and a decrease of plasma thyroid hormones. Moreover, the higher level of plasma TSH in rats during late pregnancy is associated with the greater response of pituitary cAMP and TSH to TRH.

1-Methyl-3-isobutylxanthine↗
PubMed1986

Transcriptional regulation of thyrotropin subunit genes by thyrotropin-releasing hormone and dopamine in pituitary cell culture.

Thyrotropin (TSH) is an anterior pituitary glycoprotein hormone which modulates thyroid hormone production by the thyroid gland. TSH and its two subunits, TSH beta and alpha-subunit, are in turn regulated by the thyroid hormones and several stimulatory and inhibitory factors produced by the hypothalamus. Hypothalamic hormones such as thyrotropin-releasing hormone (TRH) and dopamine have profound effects on TSH secretion and may also modulate TSH synthesis. We investigated the ability of these two hormones to directly influence the expression of the TSH subunit genes by measuring subunit mRNA synthesis rates in treated and untreated pituitary cell cultures from hypothyroid rats. In this system, basal rates of mRNA synthesis were similar for the two subunits, with 95 ppm for alpha-subunit and 85 ppm for TSH beta. Treatment with 10(-5) M dopamine, an inhibitor of TSH secretion, decreased both alpha-subunit and TSH beta mRNA synthesis within 15 min, and maximal decreases of approximately 75% for both subunits were obtained after 30 min. The inhibitory effects of dopamine were overcome by co-incubation of the cells with dopamine plus 5 X 10(-4) M dibutyryl cyclic AMP (cAMP), indicating that the actions of dopamine may have been mediated by decreasing intracellular cAMP levels. Treatment with 10(-7) M TRH, a potent stimulator of TSH secretion, increased transcription of both TSH subunit genes 3- to 5-fold. Maximal stimulation occurred after 30 min of treatment; however, 2-fold increases were maintained for up to 4 h and at 48 h. Cytoplasmic levels of TSH beta and alpha-subunit mRNA after 48 h were also depressed by dopamine (50-70%) and increased by TRH (200-280%) treatment. TRH-stimulated TSH beta and alpha-subunit mRNA synthesis was partially inhibited by dopamine. In a 4-h treatment period, TSH beta mRNA synthesis was decreased from 250 to 73% of control and alpha-subunit was decreased from 333 to 182% of control values. Thus, both dopamine and TRH can act to modulate TSH subunit gene transcription, although they differ in the direction of the response and the relative effects on TSH beta and alpha-subunit. The magnitude of the transcriptional response for either TRH (200 to 500%) or dopamine (75%) is similar to the observed changes in cytoplasmic levels of TSH subunit mRNAs and indicates that transcriptional control of the TSH genes may be an important component of hypothalamic regulation of TSH.

Animals↗
PubMed1987

Thyrotropin-releasing hormone and thyrotropin secretion.

Thyrotropin (TSH) secretion is regulated primarily by thyroid hormones and thyrotropin-releasing hormone (TRH). Normally, TSH secretion is exquisitely sensitive to small increases and decreases in serum thyroid hormone concentrations when they occur as a result of alterations in thyroid secretion. Serum TSH responses to TRH are altered by even smaller decreases and increases in serum thyroid hormone concentrations. This sensitivity explains the value of measurements of basal serum TSH concentrations and serum TSH responses to TRH in the diagnosis of hypothyroidism and hyperthyroidism, respectively. How TRH secretion is regulated is unknown, but the direct inhibitory effect of thyroid hormones on the thyrotrophs minimizes the stimulatory effect of any chronic changes in TRH secretion that may occur. In patients with nonthyroid illness, however, the normal relationships between serum thyroxine and triiodothyronine concentrations and TSH secretion are altered. Slightly or moderately ill patients have decreases in extrathyroidal triiodothyronine production that are not followed by an increase in TSH secretion, although the sensitivity of the thyrotrophs to further reduction or to an increase in triiodothyronine concentration is maintained. More severe illness may result in impaired TSH secretion and thus in decreased thyroidal as well as decreased extrathyroidal thyroid hormone production. These alterations in thyrotroph sensitivity and secretion, so that TSH secretion is not increased when extrathyroidal triiodothyronine production is decreased and thyroid secretion is decreased in more severe illness, suggest that decreased thyroid hormone production is a beneficial adaptation to nonthyroid illness.

Animals↗