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At least 37 records · Page 2Linked to original sources
PubMed1976

Hypothalamic inactivation of thyrotrophin-releasing hormone.

Following the demonstration of peptidases in the rat hypothalamus which inactivate thyrotrophin-releasing hormone (TRH), a sensitive and specific radioimmunoassay for the releasing hormone was used to investigate the presence of similar peptidases in the rabbit hypothalamus. TRH was found to be rapidly inactivated by supernatant and particulate hypothalamic fractions, with higher peptidase activity in the supernatant than in the particulate fraction. An optimum pH of 7.3 within physiological limits was obtained for the enzymes in both the fractions examined. The results obtained confirm that the rabbit hypothalamus contains enzymes capable of inactivating TRH, and since it has been found that such peptidases interfere with studies on TRH biosynthesis, it is possible that the peptidases may play a part in controlling the releasing hormone's production. The specificity of the antiserum used in the radioimmunoassay has also suggested that the peptidases may cleave the C-terminal-ProNH2,-NH2 or both from the TRH molecule to cause inactivation.

Animals↗
PubMed1976

Thyrotropin releasing hormone (TRH): restoration of oxotremorine tremor in mice. Comparison with quipazine, a serotoninergic and dopaminergic stimulant.

Both TRH and quipazine (2.5-25 mg/kg) were found to restore and to intensify the oxotremorine-induced tremor in mice when injected i.p. 60 min after oxotremorine 0.5 mg/kg s.c. This phenomenon does not seem to be due to an increase in body temperature or muscle tone. Also other dopaminergic drugs, e.g. amphetamine, methylphenidate, nomifensine and apomorphine had a significant but lesser effect than TRH or quipazine. Haloperidol and methysergide both antagonized the effect of quipazine but not that of TRH. Neither propranolol, phenoxybenzamine, alpha-methyl-p-tyrosine, nor p-chlorophenylalanine inhibited the activity of TRH or quipazine. The restoration of oxotremorine-induced tremor could be prevented by atropine but not by methylatropine. It is concluded that quipazine exerts its effect by direct stimulation of serotoninergic and dopaminergic receptors, whereas TRH receptors may represent separate entities and TRH may function as a neurotransmitter or neuromodulator.

Animals↗
PubMed1977

Comparison of adiphenine and TRH effects on TSH release by rat pituitary in vitro.

The mechanism of action of adiphenine on in vitro rat anterior pituitary TSH release was compared to that of the physiological stimulator TRH. The comparative study showed that adiphenine and TRH were able to increase TSH release in a dose-dependent manner, had similar time courses of action for equipotent stimulating concentrations and produced similar aspects of stimulated TSH cells. However, there were several differences between the effects of adiphenine and TRH. Adiphenine action was inhibited by 20 mM K+; was not calcium dependent; was inhibited by neither thyroid hormones nor somatostatin; was little affected by energy depression. It is concluded that adiphenine probably acts near the ultimate steps of the TSH release pathway and could be a useful pharmacological tool for studying the mechanism of TSH release.

Animals↗
PubMed1977

Triiodothyronine, T.S.H., and prolactin in obese women.

Basal levels of thyroid-stimulating hormone and prolactin and their response to thyrotrophin-releasing hormone are normal in obese women. Serum thyroxine and triiodothyronine are also normal and do not correlate with body-weight in healthy non-dieting women. After jejunoileal bypass, serum-triio-dothyronine levels fall, and this fall appears to depend more on the reduction in calorie intake after the operation than on the reduction in body-weight per se.

Adult↗
PubMed1976

Prolactin secretion by metoclopramide in man.

Six men and nine women were given intravenous injections of 2.5 mg of metoclopramide to assess its potential as a stimulus to prolactin release. Following the administration of metoclopramide, there was prompt increase in serum prolactin to a peak response of 38.2 +/- 3.9 ng/ml in men and 103 +/- 10.2 ng/ml in women. The prolactin response to metoclopramide in men was compared with the response to 400 mug of TRH in 10 men. The peak response after TRH was 22.4 +/- 2.2 ng/ml, which was significantly less than that observed after metoclopramide. Pretreatment with 500 mg of L-dopa suppressed the prolactin response to metoclopramide in 6 men to a mean response of 16.3 +/- 4.3 ng/ml. We have concluded that metoclopramide is a safe, reliable, and potent stimulus of prolactin secretion and exerts this effect by blocking dopamine receptors in the hypothalamus and decreasing prolactin inhibiting factor. It is free of side effects and is a useful alternative to chlorpromazine.

Adolescent↗
PubMed1976

[Prolactin in male reproduction].

Prolactin (PRL), a peptide hormon from the hypophysis, becomes more interesting, since it can be determined by radioimmunassays. The release of prolactin is controlled by two not yet identified factors, the prolactin-releasing-factor and the prolactin-inhibiting-factor. The latter predominantes. Many pharmacological substances can alter the release. The normal serum levels in the man are 6-13 ng/ml. Prolactin affects many organs, f.e. kidney, mamma, ovary, testis, hepar and skin. For clinical tests the raise in the serum levels after TSH or chlorpromacin and the drop after application of 2-brom-alpha-ergocryptin is used. Increased serum levels are found in patients with prolactin-producing tumors. In the male this is followed by disturbances of the sexual potency. Relations between prolactin and male infertility of gynecomastia are not yet known.

Animals↗
PubMed1979

[Role of 17-beta-estradiol in the synthesis and secretion of prolactin].

In 5 post-menopausal women TSH and prolactin secretions, induced by TRH, were studied before and after treatment with mg 20 of polyestradiol valerate. After this drug, plasma prolactin concentration increased, but no difference was observed in TSH secretion. The data suggest that 17-beta-estradiol doesn't increase the number of TRH receptors on pituitary cell surface, but stimulates prolactin synthesis.

Age Factors↗
PubMed1976

[New findings on human prolactin].

Since prolactin (HPRL) occurs as a separate pituitary hormone in man the paper will discuss results about the mechanisms involved regulation of HPRL secretion. A number of factors which lead to an increase in HPRL secretion are named. The clinical relevance of HPRL inhibiting substances as L-DOPA and 2-Br-alpha-ergocryptine is mentioned. The influence of HPRL in pregnancy and lactation period is described also the regulative effect of HPRL on hormone-dependent breast tumors.

Amenorrhea↗