Effects of Drugs That Modify Brain Biogenic Amine Concentrations on Thyroid Activation Induced by Exposure to Cold

Onaya, Toshimasa; Hashizume, Kazumoto

doi:10.1159/000122468

Cited by 35 publications

(14 citation statements)

References 15 publications

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“…There are many reports concerning the effects of amines, peptides and prostaglan dins (PGs) on thyrotoropin (TSH) secretion [1,2,4,7,9,10,12,13,19,21,23,[26][27][28][29][30][31][32][33], Substance P (SP), PG D2 and angiotensin II are found in the hypothalamus in rats [3,8,10,13,15], suggesting that they may affect thyrotropin-releasing hormone (TRH) and TSH secretion. A few studies have been made on the role of the cholinergic system in TSH secretion [1,10,12,21], Therefore, the authors investigated the effects of SP, angio tensin II, PG D2 and oxotremorine, a cholin ergic agonist, on TRH and TSH release in rats and have studied the possible mecha nism by which these substance exert their effect on TRH and TSH release.…”

Section: Introductionmentioning

confidence: 99%

Effects of Substance P, Angiotensin II, Oxotremorine and Prostaglandin D<sub>2</sub> on Thyrotropin Secretion in Rats

Mitsuma

Nogimori

1984

Horm Res

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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 µg/kg), angiotensin II (500 µg/kg), oxotremorine (1.0 mg/kg) or PGD2 (500 µg/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. In the haloperidol- or 5-HTP-pretreated group, the stimulatory effect of angiotensin II on TSH release was prevented. These drugs alone did not affect plasma TSH levels in terms of the dose used. The plasma thyroid hormone levels were not changed by SP, oxotremorine, angiotensin II or PG D₂. The inactivation of TRH immunoreactivity by hypothalamus or plasma in vitro after these injections did not differ from that of the control. These findings suggest that oxotremorine and PG D₂ act at the hypothalamus level by inhibiting TRH release, and that SP acts both on the hypothalamus and the pituitary to inhibit TRH and TSH release; angiotensin II, on the other hand, acts both at the hypothalamus and the pituitary levels to stimulate TRH and TSH release, and all of these effects are at least partially modified by amines of the central nervous system.

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Section: Introductionmentioning

confidence: 99%

Effects of Substance P, Angiotensin II, Oxotremorine and Prostaglandin D<sub>2</sub> on Thyrotropin Secretion in Rats

Mitsuma

Nogimori

1984

Horm Res

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“…Stimulation of TSH release by 5-HT has been suggested in studies em ploying intraventricular injection of 5-HT [17,18,39] and intraventricular and parenteral administration of the 5-HT precursor 5-hydroxytryptophan (5-HTP) [5,32] and the 5-HT synthesis inhibiting p-chlorophenylalanine [5,33], Con versely, inhibition of TSH release by 5-HT has been sugges ted in studies employing inirahypothalamic implants or in traventricular injection of 5-HT [15,23] and intraventricular or parenteral administration of the 5-HT agonist quipazine [19], the 5-HT-releasing ¿/-fenfluramine [8,9], the 5-HT pre cursor tryptophan [22,24,25], and p-chlorophenylalanine [31]. Further, studies employing 5-HTP suggest that 5-HT inhibits cold-induced activation of TSH [27,37].…”

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confidence: 99%

Central Serotoninergic Stimulation by Fenfluramine Challenge Does Not Affect Plasma Thyrotropin-Stimulating Hormone Levels in Man

et al. 1988

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Thyrotropin-stimulating hormone (TSH) and prolactin (PRL) responses to an acute oral challenge of fenfluramine (60 mg), a central serotoninergic (5-hydroxytryptamine) releasing/uptake inhibiting agent, were examined in 8 healthy males in order to assess the role of central serotoninergic stimulation in the release of TSH. Plasma PRL, but not TSH, was significantly elevated by fenfluramine. These data suggest that central serotoninergic activity does not play an important role in the physiologic release of plasma TSH in man. Further, thyrotropin-releasing hormone is unlikely to be the PRL-releasing factor involved in the fenfluramine-induced stimulation of PRL.

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“…Joseph-Bravo et al [4] reported that HA stimulated TRH release from rat mediobasal hypothalamus in vitro. Onaya and Hashizume [13] reported that bromoserine phosphate, a depletor of HA, inhibited increase in colloid droplet forma tion of mice thyroid under cold exposure. The present findings are in agreement with a report by Tuominen et al [ 15] and contrast to the reports of Joseph-Bravo et al [4] and Onaya and Hashizume [13].…”

Section: Discussionmentioning

confidence: 99%

“…Onaya and Hashizume [13] reported that bromoserine phosphate, a depletor of HA, inhibited increase in colloid droplet forma tion of mice thyroid under cold exposure. The present findings are in agreement with a report by Tuominen et al [ 15] and contrast to the reports of Joseph-Bravo et al [4] and Onaya and Hashizume [13]. The reason for this discrepancy is unclear, but it may be attributed to the differences in experimental conditions, i.e.…”

Section: Discussionmentioning

confidence: 99%

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Effects of Histamine and Related Compounds on Thyrotropin Secretion in Rats

Mitsuma¹,

Nogimori²,

Sun³

et al. 1986

Horm Res

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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 immunoreactivitiy 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.

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Effects of Drugs That Modify Brain Biogenic Amine Concentrations on Thyroid Activation Induced by Exposure to Cold

Cited by 35 publications

References 15 publications

Effects of Substance P, Angiotensin II, Oxotremorine and Prostaglandin D<sub>2</sub> on Thyrotropin Secretion in Rats

Effects of Substance P, Angiotensin II, Oxotremorine and Prostaglandin D<sub>2</sub> on Thyrotropin Secretion in Rats

Central Serotoninergic Stimulation by Fenfluramine Challenge Does Not Affect Plasma Thyrotropin-Stimulating Hormone Levels in Man

Effects of Histamine and Related Compounds on Thyrotropin Secretion in Rats

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