Thyrotropin-Releasing Hormone

Prasad, Chandan

doi:10.1007/978-1-4684-7018-5_8

Cited by 25 publications

(19 citation statements)

References 192 publications

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“…TRH is a major hypothalamic simulating hormone for the secretion of pituitary TSH in mammals (Prasad 1985). In the teleosts, the presence of immunoreactive TRH has been found in common carp (Hamano et al 1990), sea bass (Batten et al 1990), and chinook salmon (Matz & Takahashi 1994).…”

Section: Discussionmentioning

confidence: 99%

Cloning of the cDNA for thyroid stimulating hormone beta subunit and changes in activity of the pituitary-thyroid axis during silvering of the Japanese eel, Anguilla japonica

Han

Liao²,

Tzeng³

et al. 2004

Journal of Molecular Endocrinology

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The purposes of this study were: (1) to clone the cDNA encoding pituitary thyroid-stimulating hormone beta subunit (TSH ) of the Japanese eel, Anguilla japonica, together with its genomic DNA sequence, for phylogenetic analysis, and to study the regulation of the TSH gene expression in cultured pituitaries; and (2) to investigate the transcript levels of pituitary TSH mRNA and the serum thyroxine profiles at different stages of ovarian development before and during silvering in the wild female eels. The maturity of female eels was divided into four stages, juvenile, sub-adult, pre-silver, and silver, based on skin color and oocyte diameter. The genomic DNA of the TSH subunit contains two introns and three exons, and the TSH protein possesses a putative signal peptide of 20 amino acids and a mature peptide of 127 amino acids. The amino acid sequence identities of TSH mature peptide of Japanese eel compared with those of teleosts and other vertebrates are: European eel (98·4%), salmonids (60·6 -61·3%), carps (52·0 -56·7%), sturgeon (48·4%), and tetrapods (42·9 -45·2%). In in vitro studies of the regulation of TSH mRNA it was found that thyrotropin-releasing hormone increased while thyroxine decreased its expression. RT-PCR and real-time quantitative PCR analysis showed that the transcript levels of TSH subunit increased during eel silvering. The serum thyroxine levels also increased in parallel with TSH mRNA expression during silvering, supporting the hypothesis that the hypothalamus-pituitary-thyroid axis is correlated to silvering in the wild female Japanese eels.

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Section: Discussionmentioning

confidence: 99%

Cloning of the cDNA for thyroid stimulating hormone beta subunit and changes in activity of the pituitary-thyroid axis during silvering of the Japanese eel, Anguilla japonica

Han

Liao²,

Tzeng³

et al. 2004

Journal of Molecular Endocrinology

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“…The cardiovascular changes caused by TRH were relatively shortlasting, whereas CG3703, at the highest dose, produced prolonged increases in blood pressure, heart rate, and total peripheral resistance but only a brief elevation of cardiac index. The increase in cardiac index by CG3703 in anesthetized rats might be due to antagonism by TRH analogues of the effects of anesthesia (19,20), since in the conscious rat exposed to the hemorrhage the TRH analogue, CG3703, caused a marked, prolonged increase in vascular resistance with no beneficial effect on the cardiac index. This is further supported by the fact that the base-line Ievels for cardiac index were significantly reducEd by anesthesia as reported also by others earlier (22).…”

Section: Discussionmentioning

confidence: 99%

“…The increase in total peripheral resistance induced by TRH was short-lasting: the maximum rise became apparent a few minutes after · the drug injection, arid the effect subsided in about [10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25] min. Cardiac index, on the other hand, increased immediately after the drug administration and remained high during the whole observation period (60 min).…”

Section: Effects On Cardiac Index and Total Peripheral Resistance Indmentioning

confidence: 99%

“…W e now report the effects of systemically injected TRH on cardiac output and total peripheral resistance following hemorrhagic shock in both anesthetized and conscious rats. Because TRH is rapidly inactivated after systemic administration (20), the effect of a degradation stable TRH analogue, CG3703 (10), on thesevariables was also examined. Furthermore, the effect of CG3703 on regional blood flow distribution and on blood gases and Iactate after bleeding was investigated in the conscious rat.…”

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confidence: 99%

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Thyrotropin releasing hormone in hypovolemia: a hemodynamic evaluation in the rat

Sirén¹,

Powell²,

Feuerstein³

1986

American Journal of Physiology-Heart and Circulatory Physiology

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H1093-H1101, 1986.-ln the present study the effects of thyrotropin releasing hormone (TRH) and its stable analogue, CG3703, on cardiac output (thermodilution, Cardiomax) and regional blood flow (BF; directional pulsed Doppler technique) were investigated in hypovolemic hypotension in the rat. In urethan-anesthetized rats TRH (0.5 or 2 mg/ kg ia) or CG3703 (0.05 or 0.5 mg/kg ia) reversed the bleeding (27% of the blood volume)-induced decreases in mean arterial pressure (MAP) and cardiac index (Cl) and increased the heart rate (HR) and total peripheral resistance index (TPRI) in a dose-related manner. In the conscious rat exposed to a 45% hemorrhage, CG3703 (0.5 mg/kg ia) significantly raised MAP, HR, and TPRI with maximum changes of +67 ± 6 (SE) mmHg, + 123 ± 30 beats/min, and + 101 ± 2%, respectively. CG3703 (0.5 mg/kg ia) also further enhanced the hemorrhage-induced reduction of hindquarter, mesenteric, and renal BF. The changes in BF in saline-treated vs. CG3703-treated rats 2 h after the bleeding were -32 ± 6 vs. -55 ± 6% (P < 0.001) in hindquarter, -9 ± 8 vs. -61 ± 11% (P < 0.001) in mesenteric, and -2 ± 9 vs. -33 ± 9% (P < 0.01) in the renal artery; the changes in vascular resistance +30 ± 7 vs. +309 ± 167% (P < 0.001) in hindquarter, -4 ± 8 vs. +349 ± 244% in the mesenteric, and -10 ± 9 vs. +80 ± 10% (P <: 0.01) in the renal artery.The survival rate after the 45% hemorrhage was significantly reduced by both TRH and CG3703. The results suggest that TRH reverses the hypovolemic hypotension mainly by increasing vascular resistance and causing impairment of BF to vital organs, thereby exacerbating the shock and leading to an increased mortality. cardiac output; total peripheral resistance; regional blood flow THYROTROPIN RELEASING HORMONE (TRH) is a tripeptide found in cell borlies and nerve fibers of mammalian brain and spinal cord (for review see Ref. 20). In addition to its endocrine effects, TRH induces strong cardiorespiratory stimulation that is of central origin (2,5,8,16). Recent sturlies have shown that TRH is able to antagonize the hypotension in various experimental shock models (for review see Ref.3). Systemic injection of TRH following endotoxic or hemorrhagic shock in the rat significantly improved the cardiovascular function (13, 15). TRH also reversed hypotension induced by leukotriene (LT)D4, platelet activating factor, soybean lipoxygenase, or antigen-induced anaphyla:x;is in the conscious guinea pig (7,17,18).The beneficial effect of TRH in experimental shock appears to be due to an action on the central nervous system, since doses of TRH that have no effect after sytemic injection reverse shock (14) and improve survival ( 1) after intracerebroventricular administration. Furthermore, the pressor effect of TRH on LTD 4 -induced hypotension is totally abolished in the pithed rat in which the complete central nervous system is destroyed (9). In intact rats, TRH induces marked rises of plasma Ievels of norepinephrine and epinephrine (4,8), and, at least in endotoxic shock in the rat, the revers...

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“…Moreover, over 70% of the total central nervous system TRH is located outside the hypothalamus, although the highest local concentrations of TRH in the brain are found in the hypothalamus and pituitary gland. Outside the nervous system, relatively high levels ofTRH are found in the gastrointestinal system (for review 1,2).…”

Section: Trh and Its Receptors In The Central Nervous Systemmentioning

confidence: 99%