Wyniki wyszukiwania

1

Melatonin in the thyroid gland: regulation by thyroid-stimulating hormone and role in thyroglobulin gene expression

100%

Garcia-Marin R., Fernandez-Santos J. M., Morillo-Bernal J., Gordillo-Martinez F., Vazquez-Roman V., Utrilla J. C., Guerrero J. M., Carrillo-Vico, Martin-Lacave I.

Journal of Physiology and Pharmacology

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2015

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tom 66

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nr 5

2

Thyrotropin-releasing hormone modulates vasopressin and oxytocin synthesis and release from the hypothalamo-neurohypophysial system of different age male rats

100%

Ciosek J., Izdebska K.

Journal of Physiology and Pharmacology

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2009

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tom 60

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nr 2

63-70

Thyrotropin-releasing hormone (TRH) is engaged in the modulation of the hypothalamo-neurohypophysial system activity. Effects of repeated intravenously injections of TRH in a dose of 100 ng/100 g b.w. on vasopressin (VP) and oxytocin (OT) biosynthesis and release from the hypothalamo-neurohypophysial system was investigated in rats in different age (1-, 3- or 7-months of the life). To estimate the biosynthesis rate of both neurohormones the colchicine procedure was used (the dose of 5 µg/5 µl icv 20 hours before the decapitation). It has been observed that vasopressin synthesis in the hypothalamus increased gradually with maturation of rats, while OT biosynthesis decreased in the same animals. Hypothalamic biosynthesis rate of VP and OT is most effective in youngest rats and declines during the adolescence of animals. Thyrotropin-releasing hormone directly affects VP-ergic and OT-ergic hypothalamic neurons activity and both neurohormones biosynthesis process. This effect, however, is opposed: TRH acts as a stimulator of vasopressin biosynthesis most of all in young male rats and as an inhibitor for oxytocin biosynthesis especially in mature animals.

3

Pharmacological characterization of lipidized analogs of prolactin-releasing peptide with a modified c-terminal aromatic ring

100%

Prazienkova V., Ticha A., Blechova M., Spolcova A., Zelezna B., Maletinska L.

Journal of Physiology and Pharmacology

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2016

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tom 67

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nr 1

4

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Thyrotropin-releasing hormone [TRH] modulates vasopressin and oxytocin release from the hypothalamo-neurohypophysial system in dehydrated rats

100%

Ciosek J., Guzek J. W., Orlowska-Majdak M.

Journal of Physiology and Pharmacology

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1993

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tom 44

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nr 3

5

The potential implication of neurokinin B in the modulation of prolactin secretion at the pituitary level in cyclic gilts

84%

Czelejewska W., Zmijewska A., Dziekonski M., Okrasa S.

Journal of Physiology and Pharmacology

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2020

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tom 71

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nr 2

6

Vasopressin release from the rat hypothalamo-neurohypophysial system: effects of gonadotrophin-releasing hormone [GnRH], its analogues and melatonin

84%

Boczek-Leszczyk E., Stempniak B., Juszczak M.

Journal of Physiology and Pharmacology

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2010

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tom 61

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nr 4

459-466

The influence of gonadotrophin-releasing hormone (GnRH) and its analogues (i.e., agonist and antagonist) on vasopressin (VP) release from the rat hypothalamo-neurohypophysial (H-N) system was studied both in vitro and in vivo. Additionally, it was determined whether the possible response of vasopressinergic neurones to these peptides could be modified by melatonin through a cAMP-dependent mechanism. In this study we demonstrate, for the first time, that the highly selective GnRH agonist (i.e., [Des-Gly10,D-His(Bzl)6,Pro-NHEt9]-LHRH; histrelin) stimulates the release of VP from the rat H-N system, while native GnRH and its antagonist remain inactive in modifying this process in vitro. Melatonin significantly inhibited basal and histrelin-induced release of VP in vitro, but displayed no significant influence on VP secretion when GnRH or its antagonist were present in a medium. Melatonin fully suppressed forskolin-stimulated VP release from the rat H-N system. On the other hand, addition of forskolin to a medium containing both histrelin and melatonin did not further alter the inhibitory influence of melatonin on the histrelin-dependent release of VP in vitro. After intracerebroventricular (i.c.v.) infusion of native GnRH or its agonist, blood plasma VP concentration was significantly higher than in control animals, which was accompanied by decreased content of the hormone in the neurohypophysis. Intravenous (i.v.) injection of melatonin did not change, in any subgroup, blood plasma VP concentration, when compared to the vehicle-injected rats. However, the neurohypophysial levels of the hormone were significantly higher after melatonin injection in control, GnRH- and histrelin-infused animals. Our present results suggest that activation of the GnRH receptor in the hypothalamus is involved in stimulation of VP secretion from the rat H-N system. We have also shown that melatonin, at a concentration close to its physiological level in the blood, significantly reduces the in vitro response of vasopressinergic neurones to a GnRH agonist - histrelin; this effect of melatonin could be mediated through intracellular processes that involve, among others, the cAMP-dependent mechanism.

7

Effects of intra-amygdaloid TRH injections on motor activity and dominant-submissive behavior in rats competing for water

84%

Pucilowski O., Trzaskowska E., Jankowska E., Kostowski W., Kupryszewski G.

Acta Physiologica Polonica

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1990

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tom 41

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nr 1-3

Puciłowski O., Trzaskowska E., Jankowska E., Kostowski W., Kupryszewski G.: Effects of intra-amygdaloid TRH injections on motor activity and dominant-submissive behavior in rats competing for water. Acta Physiol. Pol. 1990, 41(1-3); 71-77. The effect of thyrotropin releasing hormone (TRH) microinjections into the central amygdala (10 g in 0.5 1 into each side) on locomotor activity, water intake and dominance behavior in a water competition test was investigated in male Wistar rats. TRH increased the general motility without altering the number of rearings. Intra-amygdaloid TRH injection to submissive rats resulted in a loss ol subordinate position in these animals in the water competition test. A tendency to decrease dominance followed the injection оf the peptide to the dominant animals. The effect of TRH in the dominance test does not appear to involve influence on the thirst drive as microinjection of the peptide did not change significantly the water consumption in thirsty rats.

8

Neural aspects of prostaglandin involvement in gastric mucosal defense

84%

Peskar B. M.

Journal of Physiology and Pharmacology. Supplement

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2001

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tom 52

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nr 2

9

Thyrotropin-releasing hormone [TRH] inhibits vasopressin and oxytocin release from rat hypothalamo-neurohypophysial explants in vitro

84%

Ciosek J., Stempniak B.

Acta Neurobiologiae Experimentalis

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1996

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tom 56

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nr 1

10

Vasopressin and oxytoxin release as influenced by thyrotropin-releasing hormone in euhydrated and dehydrated rats

67%

Ciosek J.

Journal of Physiology and Pharmacology

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2002

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tom 53

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nr 3

Since the thyrotropin-releasing hormone (TRH) can modulate the processes of vasopressin (AVP) and oxytocin (OT) biosynthesis and release mainly at the hypothalamo-neurohypophysial level, the present experiments were undertaken to estimate whether TRH, administered intravenously in different doses, modifies these mechanisms under conditions of osmotic stimulation, brought about by dehydration. AVP and OT contents in the hypothalamus and neurohypophysis as well as plasma levels of AVP, OT, free thyroxine (FT4) and free triiodothyronine (FT3) were studied after intravenously TRH treatment in euhydrated and dehydrated for two days male rats. Under conditions of equilibrated water metabolism TRH diminished significantly the hypothalamic and neurohypophysial AVP and OT content but was without the effect on plasma oxytocin level; however, TRH in a dose of 100 ng/100 g b.w. raised plasma AVP level. TRH, injected i.v. to dehydrated animals, resulted in a diminution of AVP content in the hypothalamus but did not affect the hypothalamic OT stores. After osmotic stimulation, neurohypophysial AVP and OT release was significantly restricted in TRH-treated rats. Under the same conditions, injections of TRH were followed by a significant decrease of plasma OT level. I.v. injected TRH enhanced somewhat FT3 concentration in blood plasma of euhydrated animals but diminished FT4 plasma level during dehydration. Data from the present study suggest that TRH displays different character of action on vasopressin and oxytocin secretion in relation to the actual state of water metabolism.

11

Thyrotropin-releasing hormone affects the oxytocin, vasopressin and prolactin release in female rats during midlactation: relation to suckling

67%

Ciosek J., Guzek J. W.

Journal of Physiology and Pharmacology

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1998

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tom 49

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nr 1

12

Thyrotropin-releasing hormone [TRH] modifies oxytocin release from the hypothalamo-neurohypophysial system in salt-loaded rats

67%

Ciosek J., Stempniak B.

Journal of Physiology and Pharmacology

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1995

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tom 46

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nr 2

13

Neural aspects of prostaglandin involvement in gastric mucosal defense

67%

Peskar B. M.

Journal of Physiology and Pharmacology

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2001

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tom 52

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nr 4,1

In rats, central vagal stimulation by thyrotropin-releasing hormone protects against ethanol-induced gastric damage by muscarinic release of prostaglandins. In contrast, gastroprotection following capsaicin-induced stimulation of afferent neurons is prostaglandin-independent. Capsaicin-evoked protection is abolished by blockade of calcitonin gene-related peptide (CGRP) receptors and inhibition of nitric oxide (NO) synthase. Various peptides including gastrin 17, cholecystokinin octapeptide, thyrotropin-- releasing hormone, bombesin, corticotropin-releasing factor, epidermal growth factor, peptide YY, neurokinin A analogs and intragastric peptone exert gastroprotection that is abolished by afferent nerve denervation, blockade of CGRP receptors and inhibition of NO synthase. Indomethacin attenuates the protection of some peptides but has no effect with others. The hyperemic response to peptides is mediated by the afferent nerve/CGRP/NO system without contribution of prostaglandins. Furthermore, it was shown that NKA analogs exert afferent nerve-, CGRP- and NO-dependent gastroprotection in the face of substantial reduction of gastric mucosal blood flow indicating that gastroprotection is not necessarily mediated by mucosal hyperemia. In the rat stomach with functioning afferent nerves neither selective inhibition of cyclooxygenase (COX)-1 nor COX-2 is ulcerogenic and only simultaneous inhibition of both COX isoenzymes induces mucosal lesions. In the face of pending injury such as intragastric acid a COX-1 inhibitor evokes dose-dependent damage whereas COX-2 inhibitors are not injurious as long as the function of afferent nerves is not impaired. After afferent nerve denervation, however, COX-2 inhibitors or dexamethasone which suppresses the acid-induced up-regulation of COX-2 are highly ulcerogenic. In conclusion, release of prostaglandins following nerve stimulation can mediate protective effects under certain conditions but is not a prerequisite for neurally mediated mucosal defense. Prostaglandins are of particular importance for the maintenance of gastric mucosal integrity when neuronal defense mechanisms are impaired.

Ograniczanie wyników

Melatonin in the thyroid gland: regulation by thyroid-stimulating hormone and role in thyroglobulin gene expression

Thyrotropin-releasing hormone modulates vasopressin and oxytocin synthesis and release from the hypothalamo-neurohypophysial system of different age male rats

Pharmacological characterization of lipidized analogs of prolactin-releasing peptide with a modified c-terminal aromatic ring

Thyrotropin-releasing hormone [TRH] modulates vasopressin and oxytocin release from the hypothalamo-neurohypophysial system in dehydrated rats

The potential implication of neurokinin B in the modulation of prolactin secretion at the pituitary level in cyclic gilts

Vasopressin release from the rat hypothalamo-neurohypophysial system: effects of gonadotrophin-releasing hormone [GnRH], its analogues and melatonin

Effects of intra-amygdaloid TRH injections on motor activity and dominant-submissive behavior in rats competing for water

Neural aspects of prostaglandin involvement in gastric mucosal defense

Thyrotropin-releasing hormone [TRH] inhibits vasopressin and oxytocin release from rat hypothalamo-neurohypophysial explants in vitro

Vasopressin and oxytoxin release as influenced by thyrotropin-releasing hormone in euhydrated and dehydrated rats

Thyrotropin-releasing hormone affects the oxytocin, vasopressin and prolactin release in female rats during midlactation: relation to suckling

Thyrotropin-releasing hormone [TRH] modifies oxytocin release from the hypothalamo-neurohypophysial system in salt-loaded rats

Neural aspects of prostaglandin involvement in gastric mucosal defense