Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ontogenesis of cells containing polypeptide hormones (ACTH, MSH, LPH, GH and Prolactin) was investigated in the fetal rat hypophysis by immunohistochemistry using the peroxidase-antiperoxidase complex. Corticotrophs, melanotrophs and lipotropic cells were revealed earlier in the pars distalis than in the pars intermedia. In the pars distalis, cells producing LPH were found in the morning of day 15 of gestation using anti-gamma- or anti-beta-LPH sera, and in afternoon using anti-alpha- or beta-endorphin sera. Cells containing beta-MSH were observed from the afternoon of day 15. The cells stainable with the anti-alpha-MSH, anti-beta-(17--39)ACTH and anti-beta-(1--24)ACTH sera appeared on day 16. In the pars intermedia, the cells producing alpha-MSH, beta-MSH, alpha- and beta-endorphin, gamma- and beta-LPH were observed in the morning of day 17, while cells containing ACTH were only revealed in the afternoon of the same day of gestation. Based on the treatment of serial paraffin sections with various antisera, it was clearly shown that MSH, ACTH, and LPH occur in the same cells located in the pars distalis as in the pars intermedia. The development of the corticotrophs, melanotrophs and lipotropic cells does not require the presence of the fetal hypothalamus or other central nervous structures. The pituitary glands of 21 day-old fetus encephalectomized on day 16 showed as many reactive cells as those of the littermate controls. The somatotrophs were first revealed in the pars distalis in the afternoon of day 19. The cells producing prolactin were not observed before day 21 of gestation. On some cases GH and prolactin were found together in one cell. The cytodifferentiation of GH and prolactin cells is apparently not under hypothalamic control.
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PMID:Ontogenesis of cells producing polypeptide hormones (ACTH, MSH, LPH, GH, prolactin) in the fetal hypophysis of the rat: influence of the hypothalamus. 37 82

A rapid (less than or equal to 60 seconds) immunological separation of antigen-antibody complexes from free antigen has been developed in radioimmunoassays (RIAs) of luteinizing hormone (LH), follicle stimulating hormone (FSH), prolactin (PRL) and beta-endorphin by using suspensions of dried Staphylococcus aureus rich in protein-A. In the systems tested parallel dose-response curves were obtained for protein-A and second antibody precipitations. The sensitivity of the protein-A method is equal to or higher than that of second antibody method. Tissue culture medium and serum hormone levels measured with RIAs using protein-A are similar to those detected with double antibody methods. The technique may be of general use in all RIAs utilizing antisera from species whose IgG are known to be bound by protein-A.
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PMID:Dried Staphylococcus aureus as a rapid immunological separating agent in radioimmunoassays. 42 90

The cholinergic agonists, pilocarpine, physostigmine and nicotine, inhibited the prolactin release induced by morphine in male rats in vivo. Pilocarpine also inhibited the release of prolactin induced by beta-endorphin or metoclopramide without affecting the basal and haloperidol-stimulated serum prolactin levels. The inhibitory effect of pilocarpine on the morphine-stimulated release of prolactin was antagonized by concurrent administration of atropine but not by atropine methylnitrate or by mecamylamine, while the inhibition by nicotine was antagonized by mecanylamine but not by atropine. The stimulation of prolactin release by morphine and its reversal by pilocarpine were observed after the administration of haloperidol or alpha-methyltyrosine. These results suggest that the central cholinergic system exertes an inhibitory influence on the prolactin release induced by morphine or beta-endorphin and the cholinergic inhibition is not mediated via catecholaminergic neurons.
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PMID:Inhibition by cholinergic agonists of the prolactin release induced by morphine. 50 52

To identify the site of action of opiate-induced prolactin elevation, in vitro rat hemipituitary incubations were performed in the presence of morphine, met-enkephalin, ala2-met5-enkephalinamide and dopamine (DA) and combinations of opiate with the catecholamine. No opiate stimulated prolactin release directly nor did any opiate block the inhibitory effect of DA. We conclude that this opiate endocrine action is not mediated at a pituitary level but may involve interference with hypothalamic DA release.
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PMID:Failure of opiates to reverse dopamine inhibition of prolactin secretion in vitro. 52 60

The objective in the present experiment was to study the effects of melengestrol acetate (0.5 mg for 14 days starting at day 15 of the estrous cycle) on the cytophysiologic character of the bovine adenohypophysis. Twelve Hereford and Angus heifers were used. A combination of thick-thin sectioning of resin-embedded material was used to aid in specific identification of individual hypophyseal cells. Alterations were not observed in the cytophysiologic activity of the presumptive prolactin-, somatotropin-, thyrotropin- or corticotropin-secreting cells. A marked increase in chromophobes was observed in animals given melengestrol acetate. Evidence indicated that these chromophobes originated from gonadotropin-secreting cells.
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PMID:Influence of a progestogen on the cytophysiologic character of the bovine adenohypophysis. 55 41

The effects of 5-fluorouracil (5-FU), 1,3 bis(2-chloroethyl)-1 nitrosurea (BCNU) and cyclophosphamide on plasma levels of corticosterone, prolactin and thyroid stimulating hormone (TSH) were investigated. All the three drugs produce a remarkable adrenocortical activation but the duration of this effect is different. Hypophysectomized rats do not show any increase of plasma corticosterone levels in response to the considered antineoplastic agents. This may be indicative of an action mediated by adrenocorticotropic hormone (ACTH). The same drugs caused a significant fall of plasma TSH. Also the duration of this effect was different for the three compounds. No relevant modifications of plasma prolactin were observed.
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PMID:Effects of some antineoplastic agents on plasma levels of corticosterone, prolactin and thyroid stimulating hormone. 60 26

Any biological function is at least bimolecular and its evolution therefore is at least dual, with variations in two lines of molecules. The hormone specificity results from a particular fit between the three-dimensional structure of the agent and that of the receptor but, because receptors are not known at the structural level, a discussion on the evolution of the polypeptide hormones is mainly limited to the possible progressive changes of the latter. As for other proteins (enzymes, oxygen carriers etc.) two degrees of complexity can be distinguished according to whether the hormone comprises one or several polypeptide chains. Protein assembly can bring new biological properties, each subunit playing a particular role. In this case, the 'internal' evolution (chain-chain interactions) overlaps the 'external' evolution (hormone-receptor contacts). The 'monomeric' hormones present the following problems: evolution of the prohormone and of the converting enzyme (for insulin), duplication and differentiation of two lines of hormones either by amino acid substitutions (neurohypophysial hormones and neurophysins) or by substitutions and size modifications (corticotropin and lipotropin), duplication and fusion leading to internal homology in the single polypeptide chain (somatotropin, prolactin, placental lactogen). The 'dimeric' hormones lead to several problems: successive duplications giving different subunits, selective associations between subunits, unequal rates of evolution of the subunits, the function of each subunit (lutropin, follitropin, thyrotropin, choriogonadotropin). An attempt is made to integrate the evolution of polypeptide hormones in the frame of the evolution of proteins.
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PMID:Molecular evolution of the polypeptide hormones. 78 77

Implantation of a mammotropic tumor (MtTF4), secreting growth hormone, prolactin, and corticotropin, in female rats of Fischer F344 strain causes hypertension, vasculitis, renal and cardiac hypertrophy, and extensive renal and cardiac lesions. When rats of the same strain were implanted with the MtTF4 tumor but sodium was withheld from the diet, systolic blood pressure rose more slowly but by six weeks reached the same values recorded in the animals implanted with the tumor and allowed to consume sodium ad libitum. In the rats, on sodium deficient diet, however, the vascular damage as well as the renal and cardiac lesions were minimal or absent. Implantation of the tumor caused adrenal cortical dysfunction, and elevated levels of deoxycorticosterone were seen in the peripheral plasma of the rats of all three groups. Nonetheless, plasma deoxycorticosterone was significantly lower in rats on a sodium deficient diet as compared with those having sodium added to the diet. Light microscopic and ultrastructural studies of the adrenal glands revealed that the lack of dietary sodium largely prevented the extensive damage of the zona fasciculata cells usually seen in the tumor-bearing rats, consuming sodium ad libitum. Both hypertensive MtT tumor-bearing animals and normotensive controls on a sodium deficient diet had a conspicuous increase of renal content of renin. It is evident that hypertension may be produced in rats bearing the MtTF4 tumor even in the virtual absence of dietary sodium. It does not appear that the hypersecretion of renal renin sustains the hypertension in these rats, since high levels of this substance were seen in the kidney of normotensive controls on the same sodium deficient diet. Elevated levels of plasma DOC may possibly explain the hypertension. In addition, it is likely that the animals may also have elevated levels of glucocorticoids.
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PMID:Deveolpment of hypertension in rats maintained on a sodium deficient diet and bearing a mammotropic tumor (MtTF4). 81 73

The effect of chlorpromazine (50 mg. im) on the plasma concentration of immunoreactive beta-melanocyte-stimulating hormone (beta-MSH) and prolactin was studied in 8 hospitalized subjects with non-endocrine skin disorders. Plasma beta-MSH concentrations remained unchanged over a period of 7 h in 6 subjects. In the remaining 2 subjects there was a slight increase. Plasma prolactin concentrations were greatly increased in all subjects 1 1/2-3 h after the injection and had almost returned to pre-injection levels by 7 h. This suggests that the control of beta-MSH secretion in man, unlike that of prolactin in man and MSH peptides in other mammals, is not predominantly inhibitory. The reason for this discrepancy may be that beta-MSH is not a natural MSH in man and occurs as part of the lipotropic hormone (LPH) or as a breakdown product.
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PMID:The effect of chlorpromazine on the secretion of immunoreactive beta-MSH and prolactin in man. 115 49

alpha-Adrenergic receptors are present on the plasma membrane of normal anterior pituitary cells and alpha-adrenergic agonists may play a role in the secretion of corticotropin (ACTH) and thyrotropin (TSH). However, alpha-adrenergic involvement in prolactin (PRL) secretion is uncertain. We have therefore examined this question in the PRL-secreting clonal rat pituitary tumor-derived GH4C1 cells. Norepinephrine (NE), an alpha-adrenergic agonist, had no effect on basal PRL secretion but abolished thyrotropin-releasing hormone (TRH)-induced PRL secretion in a dose-dependent manner (EC50 100 nM). NE also significantly suppressed the TRH-stimulated rise in [Ca2+]i. Phentolamine (PA), a non-selective alpha-adrenergic antagonist, reversed the inhibitory effect of NE on both the TRH-stimulated PRL secretion and [Ca2+]i rise. NE did not inhibit the rise in PRL secretion or [Ca2+]i induced by depolarizing 30 mM K+, 30% hyposmolarity or BAY K-8644, a specific L-type Ca2+ channel agonist. The inhibitory effect of NE on TRH-induced PRL and [Ca2+]i changes was also present when Ca2+ influx was prevented by removing medium Ca2+ or by blocking L-type Ca2+ channels with 2 microM nifedipine. The TRH-stimulated first-phase rise in [Ca2+]i in GH4C1 cells is believed to result primarily from release of sequestered Ca2+ from an intracellular pool through the activation of inositol 1,4,5-trisphosphate (IP3) and this [Ca2+]i spike stimulates PRL secretion. Our data thus suggest that GH4C1 cells have alpha-adrenergic receptors and that alpha-adrenergic agonists either suppress IP3 generation or block IP3 release of sequestered intracellular Ca2+.
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PMID:Alpha-adrenergic inhibition of thyrotropin-releasing hormone-induced prolactin secretion in GH4C1 cells is associated with a depressed rise in intracellular Ca2+. 128 Feb 33


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