UNIPROT:P01189 - FACTA Search

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Query: UNIPROT:P01189 (beta-endorphin)
21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study was aimed at evaluating the capacity of anterior pituitary cells from neonatal rats to bind arginine vasopressin (AVP) and show AVP-receptor-mediated signal transmission. We found that in cultures of pituitary cells of 10-day-old pups, in contrast to cultures of cells of adults, AVP was unable to trigger sustained adrenocorticotropin (ACTH) secretion and, in addition, was also less potent in synergizing with the effect of corticotropin-releasing factor (CRF) on both ACTH output and cyclic AMP formation. Binding studies revealed the existence of a much lower number of AVP receptor sites in membranes of neonatal pituitary gland than in those of adult tissue (32.3 +/- 9.0 and 137.6 +/- 6.2 fmol/mg protein, respectively), although the binding of agonists and the apparent molecular weight (Mr about 120,000) of the receptors were similar. Activation by phorbol ester PMA of protein kinase C, a messenger involved in AVP action, resulted in a dose-related enhancement of ACTH secretion that was 2-3 times smaller for immature corticotrophs than for mature ones. Importantly, PMA treatment allowed AVP to significantly stimulate ACTH secretion from neonatal cells, while it failed to similarly affect AVP-evoked hormone output from adult tissue. Our results indicate that pituitary corticotrophs of rat pups fail to properly transduce AVP-receptor-mediated signalling and, thereby, suggest an explanation for the postnatal 'stress nonresponsive period'.
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PMID:The vasopressin receptor system in the neonatal pituitary gland: evidence for reduced binding capacity and signal transmission. 216 16

Cold stress stimulates the release of both ACTH and TSH from the pituitary. More striking changes in ACTH content have been seen in the intermediate lobe after cold stress. Therefore, this study was designed to test responses of individual anterior lobe corticotropes to cold exposure. Male rats were exposed to either 30 min of cold (+3-5 C), 30 min of a novel, temperate environment (+24 C) or were unstressed (+24 C). Pituitaries were fixed and embedded in preparation for immunolabeling for ACTH or TSH-beta at the light (semithin sections) and electron microscopic levels. The semithin sections were used to measure areas of corticotropes and thyrotropes with Bioquant image analysis equipment. Separate groups of pituitaries were dissociated and the cells were cultured for 2 or 15 h. Then the cells were stimulated for 5-10 min with biotinylated analogs of corticotropin-releasing hormone (bio-CRH) or arginine vasopressin (bio-AVP) to detect the target cells cytochemically. A third group of dissociated cells were fixed for immunolabeling for ACTH, 16K fragment of pro-opiomelanocortin, beta-endorphin, or TSH-beta. Cold exposure resulted in a 1-4-fold increase in the levels of serum ACTH over that of unstressed rats. This was correlated with a 40% increase in the percentage of cells that contained 16K fragment and a 30-40% increase in percentages of cells storing ACTH or beta-endorphin. Cold stress also increased the percentage of cells that bound bio-CRH or bio-AVP by 45%. Analyses of semithin sections showed that areas of corticotropes increased by 21% following cold stress. The number of rows of immunolabeled (ACTH) secretion granules also increased in corticotropes from cold-stressed rats. Exposure to a novel environment for 30 min resulted in no significant increase in serum ACTH over that of unstressed rats. There was, however, a 20% increase in percentages of cells that stored 16K fragment, beta-endorphin, or target cells that bound bio-CRH. However, the corticotropes were not significantly larger. Many of the cells exhibited reduced numbers of immunolabeled secretory granules. Other corticotropes resembled those from cold-stressed rats. When TSH cells were studied, their percentages increased from 8 +/- 3% to 15.8 +/- 4% and their areas increased by 22% following exposure to cold. After exposure to a novel environment, percentages of cells that stored TSH-beta increased to 11 +/- 2%, however, no changes in areas of TSH cells were measured. These studies demonstrated that the anterior lobe corticotrope is clearly activated by exposure to both cold and novel environment.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cytochemical studies of responses of corticotropes and thyrotropes to cold and novel environment stress. 216 13

This study was undertaken to define the roles of corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) in the regulation of adrenocorticotropin (ACTH) release and biosynthesis in cultured ovine anterior pituitary cells and to define the intracellular mechanisms responsible for their action. At 4 h, CRF and AVP increased both ACTH release and total ACTH content, with AVP clearly the more potent agonist (maximal ACTH release: AVP, 22.8-fold; CRF, 7.6-fold; maximal increment in total ACTH content: AVP, 1.9-fold; CRF, 1.1-fold; EC50 for ACTH release: AVP, 2.3 +/- 0.5 nM; CRF, 9.2 +/- 5.0 nM). The increase in total ACTH content was interpreted to reflect an augmentation of ACTH biosynthesis since it was abolished by 10 microM cycloheximide. Exposure of the anterior pituitary cells to increasing concentrations of forskolin or 8-bromo-cAMP elicited increases in ACTH release and total ACTH content that were similar to those caused by CRF. A 30-min incubation with phorbol 12-myristate 13-acetate (PMA) caused a dose-related translocation of protein kinase C from the cytosol to the cell membrane; after 4 h, the increases in ACTH release and total ACTH content in response to increasing concentrations of PMA were similar to those caused by AVP. Chronic (24 h) exposure to 150 nM PMA caused an almost total depletion of both cytosolic and membrane-bound protein kinase C activities. When protein kinase C-depleted cells were subsequently exposed to AVP, the increases in ACTH release and total ACTH content were markedly attenuated, but the responses to CRF were preserved. Finally, the combination of CRF and AVP, CRF and PMA, or AVP and 8-bromo-cAMP increased ACTH release and total ACTH content in a synergistic manner. We conclude that: 1) in ovine anterior pituitary cells, AVP is the predominant regulator of ACTH secretion and biosynthesis; 2) the action of AVP is predominantly mediated by activation of protein kinase C, whereas the action of CRF is likely to be mediated by activation of the cAMP-dependent protein kinase (protein kinase A); and 3) the ability of CRF and AVP to increase total ACTH content and secretion in a synergistic manner provides a demonstration in normal pituitary cells that protein kinases C and A may interact in a unidirectional manner to regulate ACTH biosynthesis in addition to ACTH release. This interaction may take place within, or between, individual corticotropes.
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PMID:The biosynthesis and secretion of adrenocorticotropin by the ovine anterior pituitary is predominantly regulated by arginine vasopressin (AVP). Evidence that protein kinase C mediates the action of AVP. 216 7

In adult healthy beagle dogs, plasma concentrations of ACTH, cortisol, alpha-MSH, GH, prolactin and arginine vasopressin (AVP) were measured after i.v. administration of [D-Ala2,N-Me-Phe4,Met-(O)5-ol]-enkephalin (DAMME) at doses of 0.1, 0.5, 1, 5 and 10 micrograms/kg body weight. Significant dose-dependent increases occurred for ACTH, cortisol and GH at dose rates of 0.5, 1, 5 and 10 micrograms/kg body weight. Increments in plasma concentrations of prolactin were significant only at 5 and 10 micrograms DAMME/kg, and there was no significant effect on plasma concentrations of alpha-MSH and AVP. Prior i.v. administration of the opiate antagonist naloxone (0.1 mg/kg) attenuated the DAMME (10 micrograms/kg)-stimulated release of ACTH and cortisol. The results demonstrate that the [Met]-enkephalin analogue DAMME stimulates the release of ACTH, cortisol, GH and prolactin in dogs, and that this stimulation is, at least in part, mediated by mu-opioid receptors. The observations for ACTH and cortisol are different from those in man, where DAMME lowers their basal concentrations.
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PMID:Effects of a [Met]-enkephalin analogue ( [D-Ala2,N-Me-Phe4,Met-(O)5-ol]-enkephalin) on canine pituitary function. 217 54

Plasma arginine vasopressin (AVP), plasma renin activity (PRA), and water intake (H2OIN) are increased by thoracic inferior vena caval constriction (TIVCC). To assess the role of the cardiac and sinoaortic baroreceptors in these responses, 9 sham-, 10 cardiac-(CD), 6 sinoaortic-(SAD), and 4 combined cardiac and sinoaortic-(CD + SAD) denervated conscious dogs were studied. All animals were studied while normally hydrated 1) with no access to water (H2O-) and 2) while drinking was permitted (H2O+). TIVCC caused similar reductions (P less than 0.001) of mean arterial (-32 +/- 4 mmHg), left atrial pressure (-6.5 +/- 1.1 cmH2O), and right atrial pressure (-4.2 +/- 0.8 cmH2O) in all groups. After TIVCC in sham dogs with H2O-, AVP increased from 3.6 +/- 0.7 to 72.8 +/- 12.6 pg/ml (P less than 0.001). AVP was similar with SAD (57.1 +/- 6.9) but was reduced with CD (30.9 +/- 3.0) and CD + SAD (17.7 +/- 4.0). In all groups, PRA increased from 4.5 +/- 0.7 to 23.8 +/- 3.0 ng.ml-1 x 3 h-1 and plasma angiotensin II (ANG II) increased from 14.0 +/- 2.8 to 59.5 +/- 13.0 pg/ml (P less than 0.001). Plasma adrenocorticotropic hormone (ACTH) increased similarly in all groups (55 +/- 5 to 128 +/- 25 pg/ml). Plasma norepinephrine (NE) levels increased similarly in all groups (298 +/- 61 to 654 +/- 88 pg/ml).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of baroreceptor denervation on endocrine and drinking responses to caval constriction in dogs. 220 83

The aims of the present experiments were: 1) to test whether substances which modulate beta-endorphin-immunoreactive (beta E-ir) release from the pituitary gland might act similarly in hypothalamic tissue; and 2) to further characterize the beta E-ir forms which are released from hypothalamus. To address these questions, hypothalamic tissue was incubated in vitro for 10 min periods in either normal media (basal conditions) or in media containing 55 mM KCl or one of several other test substances (stimulation conditions) and release was estimated by measuring the beta E-ir concentrations in the media. Depolarizing concentrations of K+ increased beta E-ir release 2-3 fold over basal levels and this effect appeared to be Ca2(+)-dependent. Dose-dependent increases in beta E-ir release were elicited by nanonolar to micromolar concentrations of either corticotropin-releasing hormone (CRH), arginine vasopressin (AVP), or 5-hydroxytryptamine (5-HT). Conversely, dopamine (1 microM) inhibited both the basal and K(+)-stimulated release of beta E-ir from hypothalamus. Gel filtration chromatography revealed that beta E1-31 and beta E1-27/beta E1-26 were the primary beta E-ir peptides released under either basal or CRH-stimulated conditions; the relative amounts of the beta E-ir peptides found in the media were nearly identical to those found in the hypothalamus itself. This result indicates that the release of different beta E-ir peptides into the media appears to be proportional to the relative amounts stored in tissue.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:In vitro release of hypothalamic beta-endorphin (beta E) by arginine vasopressin, corticotropin-releasing hormone and 5-hydroxytryptamine: evidence for release of opioid active and inactive beta E forms. 225 Jul 65

The effects of salt loading and adrenalectomy on arginine vasopressin (AVP) mRNA levels in the paraventricular nucleus (PVN) and the supraoptic nucleus (SON) of the hypothalamus were studied by semiquantitative in situ hybridization histochemistry, using a synthetic oligonucleotide probe and a computer-assisted image analysis system. Salt loading (2% NaCl) for 7 days produced marked increases in AVP mRNA levels in the magnocellular neurons of the PVN, SON, and accessory nuclei. Adrenalectomy caused an increase in AVP mRNA expression in the magnocellular part of the PVN and the expansion of hybridization signals into its medial parvocellular region, where the cell bodies of corticotropin-releasing hormone (CRH) neurons are located. No apparent alteration of AVP mRNA levels was observed in the SON following adrenalectomy. These results indicate that hyperosmotic stimulation and the loss of circulating glucocorticoids had differential effects on AVP gene expression in the PVN and SON, and that the magnocellular PVN and SON neurons responded in different manners to the loss of feedback signals.
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PMID:Effects of hyperosmotic stimulation and adrenalectomy on vasopressin mRNA levels in the paraventricular and supraoptic nuclei of the hypothalamus: in situ hybridization histochemical analysis using a synthetic oligonucleotide probe. 226 Apr 95

The infusion of either 30 micrograms/microliters (approx. 100 micrograms/kg/h) of sodium salicylate or 10 ng/microliters (10(-5) M) arginine vasopressin within the ventral septal area of the Brattleboro rat brain reduced a centrally induced prostaglandin E1 (PGE1) hyperthermia when compared with infusions of artificial cerebrospinal fluid. Conversely, the infusion of a related peptide, oxytocin (10 ng/microliters (10(-5) M), or 33 ng/kg/h) failed to alter the rise in core temperature following the PGE1 injection. These results suggest that the vasopressin receptors reported to be present in the Brattleboro rat may respond normally to exogenously administered vasopressin, thus allowing for the antipyretic action. Moreover, the antipyretic effects of sodium salicylate suggest that aspirin-like drugs may induce the release of alpha-melanocyte-stimulating hormone which, in turn, attenuates the PGE1-evoked fever. Given recent evidence, however, which suggests that the Brattleboro rat may contain vasopressin both peripherally and within the brain, the antipyretic action of sodium salicylate may be alternatively explained through the endogenous release of vasopressin.
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PMID:The effectiveness of arginine vasopressin and sodium salicylate as antipyretics in the Brattleboro rat. 235 61

Viable pituitary target cells were identified with biotin-labeled corticotropin-releasing factor (1-Bio-CRF) or arginine vasopressin (Bio-AVP) and avidin-fluorescein (cell sorter grade). Stain was reduced from 8-10% of pituitary cells to less than 3% if nonbiotinylated ligands were added to compete with their respective biotinylated ligand for specific binding sites. However, AVP did not decrease the stain for 1-Bio-CRF nor did CRF decrease the Bio-AVP stain. Media adrenocorticotropin (ACTH) levels increased 4-18 times when 1-Bio-CRF or Bio-AVP were added during the staining process. One hour after staining, the cells secreted ACTH at levels identical to prestain basal levels. When challenged with CRF or AVP after this hour, the cells responded again with increases not different from those seen during staining. Tests of stained cell populations also showed that the cells were fully responsive 24 h after staining. The reverse hemolytic plaque assay for ACTH, which was used to study secretion from individual stained cells, showed that approximately 80% of plaques contained a stained cell and that plaque numbers and areas were like those of unstained populations. These data show that corticotropes are not chronically desensitized during exposure to low doses of biotinylated ligands (50-500 pM).
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PMID:Secretion from corticotropes after avidin-fluorescein stains for biotinylated ligands (CRF or AVP). 243 66

In this study in conscious rats, we tested the hypothesis that substance P, a central pressor peptide and a potential transmitter substance of pain pathways, could be involved in the cardiovascular defense reaction that is typically associated with unpleasant sensory stimuli. The hemodynamic responses to centrally administered substance P were pharmacologically characterized. The increases in blood pressure and heart rate after intracerebroventricular injections of substance P were accompanied by mesenteric and renal vasoconstriction and hind limb vasodilation (pulsed-Doppler flow probes). The pressor and vasoconstrictor responses were attenuated by peripheral alpha 1-adrenoceptor blockade with prazosin but were not influenced by blockade of vascular vasopressin receptors with d(CH2)5Tyr(Me) arginine vasopressin (AVP). Cardiac beta 1-adrenoceptor blockade with metoprolol abolished the tachycardic and reduced the pressor responses. Substance P-induced hind limb vasodilation was not sensitive to intravenous atropine but was largely prevented by peripheral beta 2-adrenoceptor blockade with ICI 118,551. Thus, the substance P-induced pressor effects are mediated by alpha 1-adrenergic sympathetic vasoconstriction and beta 1-adrenergic cardiac stimulation, whereas the hind limb vasodilation is mainly due to beta 2-adrenergic stimulation. Substance P dose-dependently (0.01-10 micrograms i.c.v.) released oxytocin but not vasopressin or adrenocorticotropic hormone (ACTH) from the pituitary gland. High doses reduced basal ACTH levels. Together with the hemodynamic responses, a behavioral arousal reaction was observed, which included increased locomotion, grooming, scratching, and skin biting. Our results demonstrate that a neuropeptide can induce classic cardiovascular defense reaction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Substance P induces a cardiovascular defense reaction in the rat: pharmacological characterization. 245 61

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