Thyrotropin-releasing hormone does not inhibit lysine vasopressin-induced growth hormone secretion in normal men

Summary In order to establish whether thyrotropin-releasing hormone (TRH) inhibits lysine-vasopressin (LVP)-induced growth hormone (GH) release, six normal men were tested with LVP alone or in combination with TRH. LVP strikingly increased serum GH levels; this response was not altered by TRH. These results indicated that in man TRH is not involved in the control of GH secretion in response to LVP.     

Thyrotropin-releasing hormone does not inhibit lysine vasopressin-induced growth hormone secretion in normal men

In order to establish whether thyrotropin-releasing hormone (TRH) inhibits lysine-vasopressin (LVP)-induced growth hormone (GH) release, six normal men were tested with LVP alone or in combination with TRH. LVP strikingly increased serum GH levels; this response was not altered by TRH. These results indicate that in man TRH is not involved in the control of GH secretion in response to LVP.     

Hyperthermia after intrahypothalamic injections of thyrotropin releasing hormone (TRH) in the pigeon

Thermoregulatory responses to intrahypothalamic injections of thyrotropin releasing hormone (TRH) were recorded from unanesthetized pigeons exposed to 6 degrees C, 20 degrees C and 32 degrees C. Our results suggest that TRH is a non-specific excitatory neuromodulator or neurotransmitter for heat production in the pigeon.     

Effects of thyrotrophic-releasing hormone (TRH) on thermoregulation in the rat

At ambient temperatures (Ta) of both 8 and 22 degrees C, intraventricular administration of TRH (10-80 microgram) produced a dose-dependent hypothermia in rats. The hypothermia was due to both decreased metabolic heat production and cutaneous vasodilatation. In contrast, at 30 degrees C Ta, TRH increased metabolic heat production (due to behavioral excitation) and led to hyperthermia.     

The influence of somatostatin on drug-induced prolactin release in the monkey

Summary The infusion of linear somatostatin did not block prolactin release induced by either perphenazine, TRH or serotonin. Somatostatin infusion, however, potentiated prolactin release induced by perphenazine and TRH but not that induced by serotonin.Supported in part by NIH General Research Support Grant No. RR5384 to Wayne State University School of Medicine and by NIH Research Grant No. HDO7722.The authors wish to express their appreciation to Mrs.Cynthia Van De Walle for her outstanding technical assistance in the performance of the prolactin RIA and the statistical analyses. We also appreciate receiving linear somatostatin from Dr.R. Makineni, Bachem Inc., Marina Del Ray, California, USA and from Dr.N. H. Grant, Wyeth Laboratories, Philadelphia, Pa. USA. We would like to thank Abbott Laboratories, North Chicago, Ill. USA for the gift of TRH and the Schering Corp., Bloomfield, N.J. USA for the gift of perphenazine.     

Thermogenic effects of thyrotrophin-releasing hormone and its analogues in the rat

Acute or chronic injection of RX 77,368 (a TRH analogue; 1 mg/kg s.c.) stimulated oxygen consumption (VO2) and brown adipose tissue activity in the rat, and decreased weight gain. Other TRH analogues (CG 3509, RGH 2202) and TRH itself also stimulated VO2. These thermogenic actions are probably mediated centrally by stimulation of sympathetic outflow to brown fat.     

Thermogenic effects of thyrotrophin-releasing hormone and its analogues in the rat

Summary Acute or chronic injection of RX 77368 (a TRH analogue; 1 mg/kg s.c.) stimulated oxygen consumption (VO₂) and brown adipose tissue activity in the rat, and decreased weight gain Other TRH analogues (CG 3509, RGH 2202) and TRH itself also stimulated VO₂. These thermogenic actions are probably mediated centrally by stimulation of sympathetic outflow to brown fat.     

Effects of thyrotrophic-releasing hormone (TRH) on thermoregulation in the rat

Summary At ambient temperatures (T_a) of both 8 and 22°C, intraventricular administration of TRH (10–80 g) produced a dose-dependent hypothermia in rats. The hypothermia was due to both decreased metabolic heat production and cutaneous vasodilatation. In contrast, at 30°C T_a, TRH increased metabolic heat production (due to behavioral excitation) and led to hyperthermia.This work was supported by the grants from the National Science Council of Republic of China and the Pjing-Ling Neurological Foundation (VGH, Taipei, Taiwan).     

Antagonism by thyrotropin-releasing hormone (TRH) of pentobarbital-induced hypothermia in rats with brain lesions

Summary Anesthesia with a large dose of pentobarbital (55 mg/kg, i.p.) caused a sustained decrease in brain temperature (Tb), which was monitored with a probe placed in the midbrain reticular formation. The administration of TRH to the lateral ventricle antagonized this hypothermia. None of the acute surgeries examined in this paper (adrenal-demedullectomy, septal knife cuts, electrolytic lesions of the hypothalamus and midbrain knife cuts) had any essential effect on this antagonism by TRH. These results suggest that centrally-administered TRH exerts its effect on thermoregulation, at least in part, through brain structure(s) caudal to the midbrain.     

Antagonism by thyrotropin-releasing hormone (TRH) of pentobarbital-induced hypothermia in rats with brain lesions

Anesthesia with a large dose of pentobarbital (55 mg/kg, i.p.) caused a sustained decrease in brain temperature (Tb), which was monitored with a probe placed in the midbrain reticular formation. The administration of TRH to the lateral ventricle antagonized this hypothermia. None of the acute surgeries examined in this paper (adrenal-demedullectomy, septal knife cuts, electrolytic lesions of the hypothalamus and midbrain knife cuts) had any essential effect on this antagonism by TRH. These results suggest that centrally-administered TRH exerts its effect on thermoregulation, at least in part, through brain structure(s) caudal to the midbrain.     

Intravenous thyrotropin releasing hormone (TRH) enhances the excitatory actions of acetylcholine (ACh) on rat cortical neurons

Summary I. v. administered TRH (1.25-10 mg/kg) enhanced the excitatory actions of iontophoretically applied ACh on spontaneously active cerebral cortical neurons of pentobarbital-anaesthetized rats. These observations are consistent with the hypothesis of a cholinergic-link in the anti-anaesthetic actions of exogenously administered TRH.     

Presence of thyrotropin-releasing hormone in porcine and bovine retina

Summary The thyrotropin-releasing hormone (TRH) has been found in porcine and in bovine retina, and it is indistinguishable from synthetic TRH in its immunological and biological properties. The role of retinal TRH is unknown, it probably acts as a neurotransmitter.     

Pituitary growth hormone and hypothalamic somatostatin in young female rats versus old constant estrous female rats

Pituitary content and concentration of growth hormone was significantly reduced, and hypothalamic somatostatin content significantly increased, in old constant estrous as compared to young female rats. Increased levels of somatostatin may contribute to the decrease in pituitary growth hormone levels in these animals.     

Development and evaluation of a method of high pressure liquid chromatography for the determination of the level of degradation of thyroliberin (TRH) in blood]

The degradation of the TRH by plasma was studied using a sensitive method for the separation of TRH and products formed by high-pressure liquid chromatographic analysis (HPLC). The detected products are TRH-3H or synthetic TRH. The HPLC analysis is performed on a microparticulate (10 mu) silica gel chromatographic column with CH3CN/0,01 M NH4OAc, at pH 6 (30/70) (V/V). This technique provides a good separation of TRH and the other products of degradation. In our experimental conditions, the human plasma degrades 62.5 +/- 5% of of TRH in 60 mn; very similar results are obtained with thin layer chromatography.     

Effects of thyroidectomy and thyroxine replacement on the responsiveness of the anterior pituitaries from male rats to thyrotropin-releasing hormone in vitro

Summary Thyroidectomy decreased prolactin concentrations in the anterior pituitary (AP) and serum of the male rat. The amount of basal and thyrotropin-releasing hormone (TRH)-stimulated release of prolactin by AP in vitro was lower in thyroidectomized (Tx) rats than in sham Tx rats. These results suggest that the inhibitory effects of thyroidectomy on pituitary and serum prolactin in male rats are mediated in part by the reduction of the production and spontaneous release of prolactin and the responsiveness of prolactin to TRH.     

A new improved synthesis of thyrotropin releasing hormone

Summary This synthesis of thyrotropin releasing hormone (TRH) is particularly suitable for large scale production of highly purified TRH, thanks to its high yields of the coupling and deprotection reactions together with the very simple final purification step. The authors are indebted to Mr.I. Lalle for his excellent technical assistance.     

Pituitary growth hormone and hypothalamic somatostatin in young female rats versus old constant estrous female rats

Summary Pituitary content and concentration of growth hormone was significantly reduced, and hypothalamic somatostatin content significantly increased, in old constant estrous as compared to young female rats. Increased levels of somatostatin may contribute to the decrease in pituitary growth hormone levels in these animals.This work was supported by NIH Research grants AG-00416 (J.M.) from the National Institute on Aging, AM-04784 (J.M.) from the NIAMDD, and NIA postdoctoral fellowships AG-05208 (L.J.F.) and AG-05147 (W.E.S.).     

A new type of antiserum to thyrotropin-releasing hormone; detection of new TRH-immunoreactive cell groups in rat hypothalamus

Summary We produced a new type of antiserum to thyrotropin-releasing hormone (TRH) in rabbits. The immunogen is TRH-BSA, the production of which is based on the formation of an amide bond using carbodiimide (EDC). The specificity of the antiserum was assessed by enzyme immunoassay (EIA) and immunohistochemistry. When using the anti-TRH serum for immunohistochemistry in rat hypothalamus, new magnocellular groups were detected in the ventrolateral parts of the posterior hypothalamus and the dorsal parts of the third ventricle. Colchicine treatment was found not to be necessary to visualize perikarya containing TRH.     

Tremorogenic effect of thyrotropin releasing hormone in rats

Zusammenfassung Thyrotropin-Releasing Hormon (TRH) erzeugt unmittelbar nach i.v. Injektion an Pentobarbital-narkotisierten Ratten einen feinschlägigen Tremor und Haarsträuben. Diese Symptome werden durch eine direkte zentralnervöse Wirkung von TRH und nicht durch Stimulation der Schilddrüse ausgelöst. Die Wirkung ist dosisabhängig und spezifisch für das Tripeptid pGlu-His-Pro.

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Acknowledgments. The authors gratefully acknowledge the advice of Dr.P. A. Desaulles and Dr.W. Rittel and the skilled technical assistance of Mr.B. Latscha and Mr.J. C. Dalmer.     

Peptide-stimulated release of prolactin from the fowl anterior pituitary gland

Summary Anterior pituitary glands from broiler fowl were preincubated for 24 h in either medium 199 only or medium containing estradiol 17, following which they were incubated in medium containing thyrotrophin releasing hormone (TRH), vasoactive intestinal polypeptide (VIP) or substance P (SP), alone or with the dopamine agonist, apomorphine. Estradiol priming stimulated release of prolactin and enhanced apomorphine-inhibition of prolactin release. TRH stimulated prolactin release, an effect reversed by apomorphine, and priming with estradiol potentiated both effects. VIP stimulated prolactin to a lesser degree and again this was inhibited by apomorphine and potentiated by estradiol. SP had little effect on the nonsteroid-primed pituitary, but stimulated release of prolactin after estradiol treatment, though less effectively than TRH or VIP.