Thyrotropin Secretion In Rats Research Articles

Effects of orexin A on thyrotropin-releasing hormone and thyrotropin secretion in rats.

Effects of orexin A on secretion of thyrotropin-releasing hormone (TRH) and thyrotropin (TSH) in rats were studied. Orexin A (50 microg/kg) was injected iv, and the rats were serially decapitated. The effects of orexin A on TRH release from the rat hypothalamus in vitro and on TSH release from the anterior pituitary in vitro were also investigated. TRH and thyroid hormone were measured by individual radioimmunoassays. TSH was determined by the enzyme-immunoassay method. The hypothalamic TRH contents increased significantly after orexin A injection, whereas its plasma concentrations tended to decrease, but not significantly. The plasma TSH levels decreased significantly in a dose-related manner with a nadir at 15 min after injection. The plasma thyroid hormone levels showed no changes. TRH release from the rat hypothalamus in vitro was inhibited significantly in a dose-related manner with the addition of orexin A. TSH release from the anterior pituitary in vitro was not affected with the addition of orexin A. The findings suggest that orexin A acts on the hypothalamus to inhibit TRH release.

The stimulatory effect of chronic lithium treatment on basal thyrotropin secretion in rats: in vivo antagonism by methylparaben.

Chronic treatment of rats with lithium chloride was examined in order to determine its effects on hypothalamic monoamine and metabolite content, basal thyrotropin (TSH) secretion and thyroid function. The hypothalamic concentrations of noradrenaline (NA), dopamine (DA) and its metabolites, dihydroxyphenylacetic acid. (DOPAC) and homovanillic acid (HVA) in the lithium treated rats remained unaltered when compared to control levels. NA turnover and the NA metabolite, 3-methoxy-4-hydroxyphenylglycol (total MHPG), were significantly lower (p < 0.01), whereas both serotonin (5-HT) and its metabolite, 5-hydroxyindole-3-acetic acid (5-HIAA), were significantly higher (p < 0.01 and p < 0.02, respectively) in the lithium treated rat hypothalami than in controls. Chronic lithium treatment significantly elevated basal TSH levels (p < 0.05). This effect was antagonized by methyl p-hydroxybenzoate (methylparaben, p < 0.01), which did not itself affect basal TSH levels. Free serum T3 and T4 levels were not significantly affected by chronic lithium treatment, although T4 tended to be slightly lower than control levels. The monoamine changes observed in the hypothalamus of lithium treated rats did not appear to account for the elevated TSH levels observed in these rats since NA activity which is generally regarded as stimulatory was decreased and 5-HT which has an inhibitory effect on TSH secretion, was increased. The elevated TSH levels may have been due to a reduced negative feedback inhibition of TSH release by the mildly reduced circulating T4 levels caused by chronic lithium treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Buspirone, ipsapirone and 1-(2-pyrimidinyl)-piperazine decrease cold-induced thyrotropin secretion in rats

The aim of this study was to analyse the effects of the 5-HT 1A receptor-related antidepressants/anxiolytics, buspirone and ipsapirone (1–10 mg/kg i.v.), and those of their common metabolite, the α-adrenoceptor antagonist, 1-(2-pyrimidinyl)-piperazine (1-PP, 1–10 mg/kg i.v.), on cold-induced thyrotropin (TSH) secretion in conscious catheterised rats. The effects of the centrally acting 5-HT 1A receptor agonist, 8-hydroxy-2-(d-n-propylamino)tetralin (8-OH-DPAT, 0.1–1 mg/kg i.v.), and of the peripherally acting 5-HT 1A receptor agonist, N,N-dipropyl-5-carboxamidotryptamine (DP-5-CT, 0.1–1 mg/kg i.v.), were also included in this study. Buspirone, ipsapirone, and 1-PP dose dependently decreased cold-induced TSH secretion throughout the 90 min of analysis. However, the preventive effect of 1-PP was reached with a lower dose (3 mg/kg) than that needed for the parent compound (10 mg/kg). 8-OH-DPAT administration diminished but did not prevent cold-induced TSH secretion, while only the highest dose of DP-5-CT diminished secretion (1 mg/kg). Lastly, the TSH-releasing hormone (TRH)-induced TSH secretion was left unaffected by either buspirone or ipsapirone pretreatment (10 mg/kg), but was diminished by 1-PP pretreatment (3 mg/kg). These data suggest that both central 5-HT 1A receptors and α 2-adrenoceptors mediate the effects of azapirones on cold-induced TSH secretion.

Effects of histamine and related compounds on thyrotropin secretion in rats.

The effects of histamine (HA) and related compounds on thyrotropin-releasing hormone (TRH) and thyrotropin (TSH) secretion in rats were studied. Histidine (1.0 g/kg), HA (5.0 mg/kg) or histamine antagonists mepyramine (MP) (100 mg/kg) or famotidine (FA) (5.0 mg/kg) were injected intraperitoneally, and the rats were decapitated at various intervals after the injection. The hypothalamic immunoreactive TRH (ir-TRH) content increased significantly after histidine or HA injection, decreased significantly after FA injection, but was not changed by MP. The plasma ir-TRH concentration did not change significantly after injection of these drugs. The plasma TSH levels decreased significantly in a dose-related manner after histidine or HA injection and increased significantly in a dose-related manner after FA injection. The plasma thyroid hormone levels showed no changes. In the FA-pretreated group, the inhibitory effect of histidine or HA on TSH levels was prevented, but not in the MP-pretreated group. The plasma ir-TRH and TSH responses to cold were inhibited by histidine or HA and enhanced by FA. The plasma TSH response to TRH was inhibited by histidine or HA and enhanced by FA. The inactivation of TRH immunoreactivity by hypothalamus or plasma in vitro after histidine, HA, MP or FA was not different from that of the control. These findings suggest that histamine may act both on the hypothalamus and the pituitary to inhibit TRH and TSH release, and that its effects may be mediated via H2-receptor.

Effects of various drugs on thyrotropin secretion in rats.

The effects of alpha-neoendorphin, kyotorphin, melatonin or diphenylhydantoin (DPH) on thyrotropin-releasing hormone (TRH) and thyrotropin (TSH) release in rats were studied. alpha-neoendorphin (1.0 mg/kg), kyotorphin (1.0 mg/kg), melatonin (2.5 mg/kg) or DPH (75 mg/kg) was injected iv or ip, and the rats were serially decapitated. TRH, TSH and thyroid hormone were determined by radioimmunoassay. The hypothalamic immunoreactive (ir-TRH) contents decreased significantly after melatonin injection, but not after alpha-neoendorphin, kyotorphin or DPH. The plasma ir-TRH concentrations decreased significantly after DPH injection, but not after alpha-neoendorphin, kyotorphin or melatonin. The plasma TSH levels decreased significantly in a dose-related manner with a nadir at 10 min. after melatonin, at 30 min. after DPH and at 40 min. after alpha-neoendorphin or kyotorphin injection. The plasma thyroid hormone levels did not change significantly after these drugs injection. The plasma ir-TRH and TSH responses to cold were inhibited by these drugs, but the plasma TSH response to TRH was not influenced. In the L-DOPA- or 5-hydroxy-tryptophan (5-HTP)-pretreated group, the inhibitory effect of alpha-neoendorphin or kyotorphin on TSH levels was prevented, but not in the haloperidol- or para-chloprophenylalanine (PCPA)- pretreated group. In the haloperidol- or PCPA-pretreated group, the inhibitory effect of melatonin on TSH levels was prevented, but not in the L-DOPA- or 5-HTP-pretreated group. These drugs alone did not affect plasma TSH levels in terms of the dose used. The inactivation of TRH immunoreactivity by hypothalamus or plasma in vitro after these drugs injection did not differ from that of the control.(ABSTRACT TRUNCATED AT 250 WORDS)

Tuftsin stimulates thyrotropin secretion in rats.

Tuftsin acts at the hypothalamus level to stimulate thyrotropin-releasing hormone and thyrotropin secretion in rats.

Effects of intraventricular administration of insulin on thyrotropin secretion in rats.

Intraventricular administration of insulin stimulates increases in the levels of thyrotropin-releasing hormone and thyrotropin in rats.

Peripheral administration of eel calcitonin inhibits thyrotropin secretion in rats

The effects of peripheral administration of eel calcitonin on thyrotropin (TSH) and thyrotropin-releasing hormone (TRH) secretion were studied in rats. Eel cacitonin (50 U/kg) was injected i.v. The hypothalamic immunoreactive TRH (ir-TRH) contents increased significantly after calcitonin injection. Plasma TSH levels decreased in a dose-related manner with a nadir at 30 min after the injection. The plasma ir-TRH and TSH responses to cold as well as the plasma TSH response to TRH were inhibited by calciton.n. The inhibitory effect of calcitonin on TSH levels was prevented in the haloperidol-, pimozide- or p-chlorophenylalanine-pretreated group, but not in the L-DOPA- or 5-hydroxytryptophan-pretreated group. The findings suggest that calcitonin acts on both the hypothalamus and the pituitary to inhibit TRH and TSH release, and that its effects may be modified by amines of the central nervous system.

Effects of substance P, angiotensin II, oxotremorine and prostaglandin D2 on thyrotropin secretion in rats.

The effects of substance P (SP), angiotensin II, oxotremorine and prostaglandin D2 (PG D2) on thyrotropin-releasing hormone (TRH) and thyrotropin (TSH) secretion in rats were studied. Either SP (100 micrograms/kg), angiotensin II (500 micrograms/kg), oxotremorine (1.0 mg/kg) or PGD2 (500 micrograms/kg) was injected intravenously or intraperitoneally, and the rats were serially decapitated. TRH, TSH and thyroid hormone were measured by means of a specific radioimmunoassay for each. The hypothalamic immunoreactive TRH (ir-TRH) contents were significantly increased by oxotremorine or SP and significantly decreased by angiotensin II, but no by PG D2. The plasma ir-TRH concentrations were significantly increased by angiotensin II, but not by oxotremorine, SP or PG D2. The plasma TSH levels were significantly increased by angiotensin II and significantly decreased by oxotremorine, SP or PG D2 in a dose-related manner. The plasma ir-TRH and TSH responses to cold were inhibited by oxotremorine, SP or PG D2, but enhanced by angiotensin II. The plasma TSH response to TRH was inhibited by SP, but enhanced by angiotensin II. The plasma TSH response to TRH did not differ from that of the control after PG D2 injection. In the haloperidol- or para-chlorophenylalanine (PCPA)-pretreated group, the inhibitory effect of PG D2 or oxotremorine on TSH release was prevented, while in the L-DOPA- or 5-hydroxytryptophan (5-HTP)-pretreated group, the inhibitory effect of SP on TSH release was prevented.(ABSTRACT TRUNCATED AT 250 WORDS)

Regulation of thyrotropin secretion in rats bearing the Walker 256 carcinoma.

Previous studies have shown that rats bearing transplantable Walker 256 carcinoma in the thigh have decreased serum total and free T4 and T3 concentrations as well as a decrease in the concentration of hepatic nuclear T3 receptors. Despite these findings, the tumor-bearing (T) rats appeared euthyroid, since the serum TSH concentration remained unchanged, and the induction of the thyroid hormone-sensitive hepatic enzymes a-glycerophosphate dehydrogenase and malic enzyme appeared normal. To evaluate the mechanisms whereby serum TSH was maintained in the normal range in T rats in association with decreased serum T4 and T3 concentrations, we studied the regulation of TSH secretion in groups of control (C) and T rats. The pituitary TSH contents were similar in the two groups of animals, and an iv injection of TRH (5 μg/100 g BW) resulted in a 10-fold increase in plasma TSH concentrations in the control group 15 min after injection. The TSH concentrations achieved after TRH injection were significantly greater ...

Pulsatile growth hormone, prolactin, and thyrotropin secretion in rats with hypothalamic deafferentation

Fifteen minute sequential blood sampling of male rats via right atrial cannulae was used to examine the patterns of anterior pituitary hormone secretion following hypothalamic deafferentations. Growth hormone (rGH) profiles from rats with complete hypothalamic deafferentation (CC) showed persistence of episodic rGH secretion with greatly increased frequency and elevated trough values, but without apparent entrainment to the light-dark cycle. Anterior (AC) and posterior (PC) deafferentation had no effect on the normal 3 h periodicity of rGH secretory episodes, but light-dark entrainment was lost in AC rats. Prolactin (rPRL) secretion in CC rats remained at normal low baseline levels without secretory episodes, while in AC and PC rats, as in normal rats, bursts of rPRL secretion occurred, often temporally related to rGH bursts. Thyrotropin (rTSH) levels in CC rats were less variable, and lower than in normal rats, while rTSH secretory profiles appeared normal in AC and PC rats. These results suggest that the isolated medial basal hypothalamus (MBH) contains neural substrates for episodic rGH secretion, and to a lesser extent, for rTSH. It is hypothesized that excessive rGH secretion in CC rats results from surgery damaging the rhythmicity of the rGH releasing factor (GRF) michanism, so that both sustained secretion and more frequent bursts of GRF occur. An effective rPRL inhibitory mechanism remains intact within complete hypothalamic deafferentations, while episodic rPRL and rTSH secretion require intact lateral afferents to the MBH. Visual pathway connections to the MBH, which mediate light-dark cycle entrainment of episodic rGH secretion, appear to pass through the region of the anterior hypothalamic and suprachiasmatic nuclei.

Thyrotropin secretion in rats after hypothalamic electrical stimulation or injection of synthetic TSH-releasing factor.

Plasma thyroid-stimulating hormone (TSH) levels, as measured by radioimmunoassay, begin to rise within 5 minutes after initiation of electrical stimulation of the medial-basal hypothalamus, become significantly elevated at 10 minutes, and reach a peak at 10 to 25 minutes. Intravenous administration of synthetic thyrotropin-releasing factor induces a marked rise in plasma thyroidstimulating hormone which is maximal within 5 minutes after administration. These data are interpreted to indicate that there are neuronal structures within the medial-basal hypothalamus which release preformed thyrotropin-releasing factor. The claim (based on bioassay data) that pyroglutamyl-histidyl-proline amide is a potent thyrotropin-releasing factor has also been confirmed by using a highly specific immunoassay system.