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Biomedical subjects

T Mitsuma

Publications and source records attributed to T Mitsuma.

At least 289 records · Page 16Linked to original sources
PubMed1985

Dermorphin inhibits basal and cold induced thyrotropin secretion in rats.

The effects of dermorphin on thyrotropin-releasing hormone (TRH) and thyrotropin (TSH) secretion in rats were studied. Dermorphin (400 micrograms kg-1) was injected i. v. and the rats were serially decapitated. TRH, TSH and thyroid hormones were measured by radioimmunoassay. The hypothalamic immunoreactive TRH (ir-TRH) content decreased significantly after dermorphin injection, whereas its plasma concentration tended to decrease, but not significantly. The plasma TSH levels decreased significantly in a dose-related manner with a nadir at 40 min after the injection. The plasma thyroid hormone levels were not changed significantly. The plasma ir-TRH and TSH responses to cold were inhibited by dermorphin, but the plasma TSH response to TRH was not. Naloxone partially blocked the inhibitory effect of dermorphin on TSH levels. In the para-chlorophenylalanine or pimozide pretreated groups the inhibitory effect of dermorphin on TSH levels was prevented, but not in the groups pretreated with 5-hydroxytryptophan or L-DOPA. These drugs alone did not affect plasma TSH levels in terms of the dose used. The inactivation of TRH immunoreactivity by plasma of hypothalamus in vitro after dermorphin injection did not differ from that of the control. These findings suggest that dermorphin acts on the hypothalamus to inhibit TRH release, and its effects are mediated via opioid receptor and modified by amines of the central nervous system.

Animals↗
PubMed1985

Stimulatory effect of PMRPamide (Phe-Met-Arg-Phe-NH2) on thyrotropin secretion in rats.

The effect of PMRPamide (Phe-Met-Arg-Phe-NH2) on thyrotropin (TSH) and thyrotropin-releasing hormone (TRH) secretion in rats was studied. PMRPamide (600 micrograms/kg) was injected i.v. and the rats were serially decapitated. TRH, TSH and thyroid hormone were measured by radioimmuassay. The content of immunoreactive TRH (ir-TRH) in hypothalamus significantly decreased after PMRPamide injection, whereas its plasma concentration tended to increase, but not significantly. The level of TSH in plasma increased significantly in a dose-related manner with a zenith at 40 min after the injection, while the level of thyroid hormone showed no changes. The plasma response of ir-TRH to cold was inhibited by PMRPamide. The response of plasma TSH level to TRH was not affected by PMRPamide. The stimulatory effect of PMRPamide on TSH levels was prevented in groups pretreated with L-DOPA or 5-hydroxytryptophan, but not in those pretreated with para-chlorophenylalanine or pimozide. 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 PMRPamide injection did not differ from that of the control. These findings suggest that PMRPamide may inhibit the release of TSH from the hypothalamus and that this effect may be modified by amines of the central nervous system.

Animals↗
PubMed1984

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 calcitonin (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 calcitonin. 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.

5-Hydroxytryptophan↗
PubMed1984

Beta-casomorphin inhibits thyrotropin secretion in rats.

The effects of beta-casomorphin on thyrotropin-releasing hormone (TRH) and thyrotropin (TSH) secretion in rats were studied. beta-casomorphin (300 micrograms/kg) was injected iv, and the rats were serially decapitated. TRH, TSH and thyroid hormone were measured by radioimmunoassay. The hypothalamic immunoreactive TRH (ir-TRH) contents increased significantly after beta-casomorphin 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 40 min. after the injection. The thyroid hormone levels showed no change. The plasma ir-TRH and TSH responses to cold were inhibited by beta-casomorphin, but the plasma TSH response to TRH was not. Naloxone partially blocked the inhibitory effect of beta-casomorphin on plasma TSH levels. In the haloperidol-pretreated group, the inhibitory effect of beta-casomorphin on plasma TSH levels was prevented, but not in the L-DOPA, para-chlorophenylalanine- or 5-hydroxytryptophan-pretreated group. These drugs alone did not affect plasma TSH levels in terms of the dose used. The findings suggest that beta-casomorphin acts at the hypothalamus to inhibit TRH release, and its effect are modified by a dopaminergic system.

Animals↗
PubMed1984

Effects of anti-thyrotropin-releasing hormone anti-serum treatment during the neonatal period on the development of rat thyroid function.

Effects of anti-thyrotropin-releasing hormone (TRH) anti-serum treatment during the neonatal period on the development of rat thyroid function were studied. On postnatal days 2 and 4, rats were administered anti-TRH anti-serum ip, and they were serially decapitated at the 4th, 8th and 12th week after birth. TRH, thyrotropin (TSH), thyroxine (T4) and 3,3',5-triiodothyronine (T3) were measured by radioimmunoassay. Immunoreactive TRH (ir-TRH) in the hypothalamus did not change significantly after anti-TRH anti-serum treatment, and plasma ir-TRH tended to decrease. The plasma ir-TRH and TSH responses to cold were significantly inhibited. The plasma TSH response to TRH was also significantly inhibited. The plasma basal TSH levels were significantly lower than in controls. The plasma T4 and T3 levels were found to be lower than those in the controls. Findings suggested that treatment with anti-TRH anti-serum during the neonatal period disturbed the development of rat thyroid function, inhibiting TRH release and altering thyrotroph sensitivity to TRH.

Animals↗
PubMed1984

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)

Angiotensin II↗
PubMed1984

Changes in plasma thyrotrophin-releasing hormone, thyrotrophin, prolactin and thyroid hormone levels after intravenous, intranasal or rectal administration of synthetic thyrotrophin-releasing hormone in man.

Changes in plasma thyrotrophin-releasing hormone (TRH), thyrotrophin (TSH), prolactin and thyroid hormone levels after iv, intranasal, or rectal administration of synthetic TRH were studied in man. The plasma TRH concentration increased with all three routes, but remained at higher levels for a longer time after intranasal or rectal administration, in contrast to the rapid decrease after iv administration. Plasma TSH, prolactin and thyroid hormone levels increased significantly after intranasal or rectal administration and also remained elevated for a longer period than iv administration. These findings suggest that TRH administered intranasally or rectally enters the blood stream and stimulates TSH, prolactin and thyroid hormone release in man.

Administration, Intranasal↗
PubMed1984

Prostaglandin I2 stimulates thyrotropin secretion in vivo and in vitro in rats.

Effects of prostaglandin I2 (PG I2) on secretion of thyrotropin (TSH) in vivo and in vitro in rats have been studied. Ten micrograms per kg of PG I2 were injected i. v. and the animals were serially decapitated. Thyrotropin releasing hormone (TRH), thyroxine (T4) and 3,3',5-triiodothyronine (T3) were determined by radioimmunoassay. Effects of PG I2 from anterior pituitary were also investigated by means of an in vitro experiment. Plasma and hypothalamic concentrations of immunoreactive (ir-TRH) did not change after PG I2 injection. Basal plasma TSH levels significantly increased with a peak at 20 min after PG I2 injection. The plasma ir-TRH response to cold did not differ from that of the control, while the plasma TSH response to cold was significantly enhanced by PG I2. The plasma TSH response to TRH was also significantly enhanced by PG I2. The plasma T4h and T3 levels did not change significantly after PG I2 injection. TSH release from anterior pituitary in vitro significantly increased after the addition of PG I2 to medium. These findings suggest that PG I2 stimulates TSH secretion from anterior pituitary in vivo and in vivo in rats.

Animals↗
PubMed1984

Effects of vasoactive intestinal polypeptide on hypothalamic-pituitary-thyroid axis in rats.

The effects of vasoactive intestinal polypeptide (VIP) on the hypothalamic-pituitary-thyroid axis in rats were studied. VIP (250 micrograms kg-1) was injected i.v. and the rats were serially decapitated. Thyrotropin-releasing hormone (TRH), thyrotropin (TSH) and thyroid hormone were measured by radioimmunoassay. The hypothalamic immunoreactive TRH (ir-TRH) content significantly decreased after VIP injection, whereas its plasma concentration significantly increased. The plasma TSH level increased significantly in a dose-related manner with a zenith at 20 min after the injection. The plasma thyroid hormone level also increased significantly. The plasma ir-TRH and TSH responses to cold as well as the plasma TSH response to TRH were significantly enhanced by VIP. Naloxone partially blocked VIP induced TSH release. In 5-hydroxytryptophan pretreated group the stimulatory effect of VIP on TSH release was prevented, but not in that pretreated with para-chlorophenylalanine, L-DOPA or haloperidol. These drugs alone did not affect plasma TSH levels in terms of the dose used. The inactivation of TRH immunoreactivity by plasma or hypothalamus did not differ from that of the control. These findings suggest that VIP acts on the hypothalamus, pituitary and thyroid gland to stimulate TRH, TSH and thyroid hormone release, respectively, and that its effect may be at least partially modified by the serotonergic system and opioid peptides.

Animals↗