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Search for other papers by H. O. Garland in
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ABSTRACT
Standard renal clearance techniques were used to investigate the acute effects of TRH on kidney function in anaesthetized rats. A significant reduction in salt and water outputs, glomerular filtration rate and renal plasma flow was produced within 10 min of infusion of 12 μg TRH over 30 min. The rapidity of the response may suggest a direct effect of TRH on the renal vascular system.
J. Endocr. (1987) 113,445–448
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Inhibin administered to adult male rats delayed the in-vivo pituitary responsiveness to thyrotrophin releasing hormone (TRH) as observed in terms of prolactin release in the serum. It also decreased the sensitivity of the pituitary gland to TRH, in terms of TSH release. However, inhibin alone did not alter the serum levels of prolactin and TSH, although it significantly suppressed serum FSH levels. In addition, the inhibin effect on FSH release was blocked by TRH.
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ABSTRACT
In order to determine whether pituitary prolactin release was directly related to the secretion of TRH into hypophysial portal blood, serial portal and jugular venous blood samples were collected from seven lactating and three non-lactating ewes. In another experiment, samples were collected from five ovariectomized ewes while being exposed to an audio-visual stress and then later administered with chlorpromazine. Secretion of TRH was pulsatile in all ewes and independent of prolactin secretion; TRH pulses coincided with significant increases in prolactin secretion in only 15% of cases and only 29% of prolactin pulses were associated with TRH pulses. Sixty-seven per cent of suckling bouts were associated with increases in prolactin secretion, but only 22% of these were associated with significant increases in TRH secretion. Chlorpromazine increased prolactin levels fourfold but did not affect portal concentrations of TRH. Audio-visual stress was not a reliable method of causing prolactin release in this model. Mean portal concentrations of TRH and jugular concentrations of prolactin were not significantly correlated. These results show that hypothalamic TRH and pituitary prolactin are secreted independently in the sheep, implying that increases in prolactin release caused by suckling or chlorpromazine are not the direct result of increased TRH secretion.
J. Endocr. (1988) 117, 115–122
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Plasma concentrations of prolactin in anoestrous ewes were respectively lowered or raised by the separate infusion of dopamine or thyrotrophin releasing hormone (TRH). Combined treatment with dopamine and TRH lowered the concentration of prolactin in plasma but the values increased markedly after the treatment was stopped and reached a level equivalent to that found in ewes treated with TRH alone. The results are interpreted as evidence that both dopamine and TRH play a regulatory role in determining the secretion of prolactin in the ewe.
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ABSTRACT
Pyroglutamylglutamylprolineamide (pGlu-Glu-ProNH2) is a tripeptide with structural and immunological similarities to thyrotrophin-releasing hormone (TRH; pGlu-His-ProNH2). Since TRH stimulates GH secretion in domestic fowl, the possibility that pGlu-Glu-ProNH2 may also provoke GH release was investigated. Unlike TRH, pGlu-Glu-ProNH2 alone had no effect on GH release from incubated chicken pituitary glands and did not down-regulate pituitary TRH receptors. However, pGlu-Glu-ProNH2 suppressed TRH-induced GH release from pituitary glands incubated in vitro and competitively displaced [3H]methyl3-histidine2-TRH from pituitary membranes. Systemic injections of pGlu-Glu-ProNH2 had no significant effect on basal GH concentrations in conscious birds, but promptly lowered circulating GH levels in sodiumpentobarbitone anaesthetized fowl. Submaximal GH responses of conscious and anaesthetized birds to systemic TRH challenge were, however, potentiated by prior or concomitant administration of pGlu-Glu-ProNH2. These results demonstrate, for the first time, that pGlu-Glu-ProNH2 has biological activity, with inhibitory and stimulatory actions within the avian hypothalamo-pituitary axis. These results indicate that pGlu-Glu-ProNH2 may act as a TRH receptor antagonist within this axis.
Journal of Endocrinology (1993) 138, 137–147
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ABSTRACT
Benzodiazepines are pharmacological agents widely used for their anxiolytic and anticonvulsant properties. However, as these drugs are known to antagonize the binding and action of thyrotrophin-releasing hormone (TRH) in pituitary tissue, the possibility that they may modulate GH secretion was investigated in domestic fowl, in which TRH is a GH-releasing factor. Chlordiazepoxide (an antagonist of central-type benzodiazepine receptors) had no significant effect on the basal release of GH from incubated chicken pituitary glands, but at concentrations > 10 μmol/l chlordiazepoxide suppressed somatotroph responsiveness and sensitivity to TRH stimulation. At this concentration, chlordiazepoxide competitively displaced the binding of [3H]3-methyl-histidine2-TRH ([3H]Me-TRH) to chicken pituitary membranes. The prior incubation of pituitary glands with chlordiazepoxide had no significant effect on the number of [3H]Me-TRH-binding sites, which were also unaffected by the administration of chlordiazepoxide in vivo. However, contrary to its effects in vitro, chlordiazepoxide reduced basal GH secretion in vivo, whilst potentiating the GH response to systemic TRH challenge. These results demonstrate benzodiazepine antagonism of TRH-binding sites in domestic fowl and a biphasic modulation of GH secretion, which may be mediated through opposing actions at pituitary and central sites.
Journal of Endocrinology (1993) 137, 35–42
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In 14 normal subjects constant TRH infusions for determination of plasma clearance rate (PCR) and half-life of disappearance (t ½) of TRH were carried out with simultaneous determination of half-life of disappearance of TRH in serum in vitro (t ½p). PCR, t ½ and t ½p were 1532 ± 423 ml/min, 6·6 ± 1·5 min and 16·8 ± 9·4 min respectively (mean ± s.d.) and displayed only minor fluctuations when determined repeatedly in the same subjects (coefficients of variation within individuals were 15·1, 10·6 and 7·5% respectively). Simultaneous determination of PCR, t ½ and t ½p enabled calculation of the half-life of disappearance of TRH in the extravascular tissue compartment (t ½t). Values of t ½t (6·3 ± 1·4 min) correlated to t ½p (r = 0·95). Activities of TRH-degrading enzymes in tissues and in serum were independent of sex, phase of female menstrual cycle, time of day and of the concentrations of TRH used. The methods employed for this investigation offer the possibility of examining the degradation of TRH and TRH analogues both in the serum and in the extravascular compartment during various conditions.
J. Endocr. (1988) 118, 511–516
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ABSTRACT
The changes in hypothalamic release of dopamine and thyrotrophin-releasing hormone (TRH) into the hypophysial portal vascular system during an oestrogen-stimulated surge of prolactin in ovariectomized rats were investigated.
A single injection of 5 μg oestradiol benzoate resulted in a reliable increase in the plasma levels of prolactin during the afternoon 3 days later. Anaesthesia did not block this afternoon surge of prolactin, although its magnitude was only half of that of unanaesthetized rats. Before and during this surge, hypophysial stalk blood was collected into methanol to analyse the hypothalamic release of dopamine and TRH. Immunoreactive TRH in these methanolic extracts eluted as a single peak with the same retention time as authentic TRH on reverse-phase high performance liquid chromatography. In comparison to the morning values, levels of dopamine decreased and those of TRH increased in hypophysial stalk blood by 50 and 240% respectively. These data indicate that hypothalamic dopamine and TRH may be involved in the afternoon surge of prolactin.
Daily treatment with parachlorophenylalanine, an inhibitor of serotonin synthesis, reduced the hypothalamic release of TRH by 50%, but did not prevent the afternoon surge of prolactin and TRH induced by oestradiol benzoate.
J. Endocr. (1985) 105, 107–112
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ABSTRACT
We have studied the secretion of TSH and prolactin from perifused rat anterior pituitary glands in vitro in response to single pulses of thyrotrophin releasing hormone (TRH) and KCl after prior exposure to TRH. Anterior pituitary fragments were incubated in normal medium or in medium containing 28 nmol TRH/1 for 20 h before perifusion. Thyrotrophin releasing hormone (28 nmol/l), administered as a 3-min pulse, stimulated TSH and prolactin release from control tissue to a peak value four or five times that of basal. After exposure of the pituitary tissue to TRH for 20 h, the subsequent response of TSH to a 3-min pulse of TRH was, however, markedly reduced; in contrast, the prolactin response was not significantly reduced. In a similar series of experiments KCl (60 nmol/l) was administered to both control and TRH-'treated' pituitary tissue as a 3-min pulse; no significant differences in TSH responses or prolactin responses were observed. These data indicate that TRH desensitizes the pituitary thyrotroph to a subsequent TRH stimulus but has very little effect on prolactin secretion.
J. Endocr. (1984) 101, 101–105
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Age-related changes in the response of GH to administration of thyrotrophin releasing hormone (TRH) have been investigated in the domestic fowl. In two strains of chicken the i.v. administration of TRH (10 μg/kg) to 4-week-old male and female birds markedly increased (> 200 ng/ml) the plasma GH concentration within 10 min of treatment and the concentration remained higher than the pretreatment level for at least a further 20 min. Saline (0·9%) administration had no effect on GH secretion in comparable groups of control birds. The same dose of TRH had no effect on plasma GH concentrations in adult (> 24-week-old) laying hens or cockerels. The administration of TRH at doses of 0·1–100 μg/kg (i.v.) or 0·39–50 μg/bird (s.c.) also had very little, if any, effect on GH secretion in laying hens. In laying hens slight increases (10–20 ng/ml, P < 0·05) in the plasma concentrations of GH were observed in one experiment 60 min after the s.c. injection of 100 μg TRH, and in another 60, 90 and 120 min after the serial s.c. injection of TRH (100 μg/bird) every 30 min over a 150 min period. The poor GH response of the adults to TRH stimulation was not due to high circulating concentrations of endogenous gonadal steroids, as surgical gonadectomy had no effect on the GH response to TRH. These results suggest maturational differences in the control of GH secretion in the fowl.
