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)

Beta-endorphin, cholecystokinin and vasoactive intestinal peptide were measured in peripheral blood mononuclear cells of healthy controls, and schizophrenic patients at the first diagnosis before any treatment and after 2 or 15 d of treatment with haloperidol. Beta-endorphin concentrations were similar in controls and untreated patients, and increased with treatment. Cholecystokinin concentrations were higher in patients than in controls, and decreased during treatment. Vasoactive intestinal peptide was lower in patients and did not change with treatment. These observations are consistent with measurements of the same peptides in autopsy samples or cerebrospinal fluid. Peripheral blood mononuclear cells might be an useful tool for the study of some neuropeptides in brain.
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PMID:Beta-endorphin, vasoactive intestinal peptide and cholecystokinin in peripheral blood mononuclear cells from healthy subjects and from drug-free and haloperidol-treated schizophrenic patients. 156 92

The effect of four neuropeptides and acetylcholine on the release of leukotrienes LTC4, LTD4 and LTE4 from platelet activating factor-stimulated rat lung and ionophore A23187-stimulated guinea pig lung, as detected by the combined use of HPLC and radioimmunoassay, was studied. Both vasoactive intestinal peptide and calcitonin gene-related peptide were found to inhibit the release of leukotrienes in both preparations. This effect was most marked in platelet activating factor-stimulated rat lung, where inhibition of LTC4 release was more pronounced than either inhibition of LTD4 or LTE4 production. The effect of vasoactive intestinal peptide on LTC4 biosynthesis was dose-related in rat lung. Neither substance P nor beta-endorphin were found to inhibit leukotriene release in rat lung. Vasoactive intestinal peptide inhibition of leukotriene release is independent from its actions on the muscarinic receptor, since acetylcholine was found to have no effect in the same preparation.
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PMID:The effect of vasoactive intestinal peptide and calcitonin gene-related peptide on peptidoleukotriene release from platelet activating factor stimulated rat lungs and ionophore stimulated guinea pig lungs. 243 97

Recent evidence has suggested that stress may suppress the immune system and increase the frequency and severity of viral and neoplastic disease. The mechanisms for stress-induced modulation of immune function are unclear, but several neuropeptides are thought to be involved. Because macrophages play an important role in the host defense against infection and neoplasia, several stress-related neuropeptides were screened in efforts to determine whether these substances affect macrophage-mediated tumoricidal activity. Adrenocorticotropin and noradrenaline each completely blocked the capacity of mouse recombinant interferon-gamma (INF-gamma) to activate murine peritoneal macrophages to a tumoricidal state as measured by the lysis of 125I-UdR-labeled melanoma target cells. Vasoactive intestinal peptide significantly potentiated the suppressive effects of noradrenaline. In contrast, neurotensin markedly enhanced the cytolytic capability of peritoneal macrophages activated with INF-gamma. Several other neuropeptides, including substance P, alpha-endorphin, beta-endorphin, Leu-enkephalin, and Met-enkephalin, had no effect on macrophage activation. These findings demonstrate that selected stress-related neuropeptides and neurohormones significantly modulate the capacity of macrophages to attain a tumoricidal state and suggest that alteration of macrophage function by neuropeptides may be a prominent feature of stress-induced enhancement of neoplastic disease.
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PMID:Modulation of macrophage-mediated tumoricidal activity by neuropeptides and neurohormones. 258 37

In an attempt to characterize GH and PRL secretion in acromegaly, the effects of various stimuli on GH and PRL release by cultured pituitary adenoma cells derived from acromegalic patients were studied. In addition, the PRL responses of somatotroph adenoma cells were compared to those of prolactinoma cells. GH-releasing hormone-(1-44) (GHRH) consistently stimulated GH secretion in all 14 somatotroph adenomas studied in a dose-dependent manner. The sensitivity as well as the magnitude of the GH responses to GHRH were highly variable in individual tissues. Somatotroph adenomas that did not respond to dopamine were more sensitive and had greater GH responses to GHRH. In 8 of 9 somatotroph adenomas that concomitantly secreted PRL, the addition of GHRH likewise increased PRL release. Omission of extracellular Ca2+ blocked the stimulatory effect of GHRH on GH and PRL secretion. When cells were coincubated with 0.1 nM somatostatin, GH and PRL secretion induced by 10 nM GHRH were completely blocked in most adenomas. Similarly, coincubation of dopamine resulted in inhibition of GHRH-induced hormone secretion in some adenomas. Addition of TRH to the incubation medium, on the other hand, significantly stimulated GH secretion in 8 of 14 adenomas, while TRH stimulated PRL release in all of the adenomas. Vasoactive intestinal peptide (VIP) and corticotropin-releasing hormone (CRH) produced an increase in GH and PRL secretion in other adenomas. In prolactinoma cells, somatostatin and dopamine unequivocally suppressed PRL secretion; however, other stimuli including GHRH, VIP, and CRF were ineffective. TRH induced a significant increase in PRL secretion in only one prolactinoma. These results suggest that responsiveness to GHRH and somatostatin is preserved in somatotroph adenomas; the responsiveness to GHRH is inversely correlated to that to dopamine; and PRL cells associated with somatotroph adenomas possess characteristics similar to those of GH cells. Further, the GH stimulatory actions of TRH and VIP are different.
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PMID:Effects of hypophysiotropic factors on growth hormone and prolactin secretion from somatotroph adenomas in culture. 285 94

HCO3- secretion by surface epithelium in duodenum devoid of Brunner's glands was titrated in situ in anesthetized rats. Intravenous injection of small amounts (20 ng/kg) of the endogenous opioid peptide beta-endorphin significantly increased secretion. Naloxone prevented this effect, suggesting that stimulation is mediated by mu-opiate receptors. Morphine 50 microgram/kg had a similar stimulatory action. Vasoactive intestinal peptide (VIP) 0.5-100 microgram/kg dose-dependently increased secretion and this response was independent of simultaneous cholinergic stimulation. The HCO3- secretion maintained pH in the mucus gel adherent to the luminal surface at neutrality for long periods of time (greater than or equal to 60 min); even when the pH in the terminal bulk solution was as low as 2.0. Mucosal HCO3- secretion is thus very probably important in mucosal protection and VIP and endogenous opioid peptides may have a role in its control.
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PMID:Gastroduodenal bicarbonate secretion in mucosal protection. Possible role of vasoactive intestinal peptide and opiates. 293 24

It has been previously demonstrated that thyrotropin-releasing hormone (TRH) stimulates in vitro the release of alpha-melanocyte-stimulating hormone (alpha-MSH) in frog. In the present study, the effects of various neuropeptides on spontaneous and/or TRH-induced alpha-MSH secretion were investigated, using a well-defined perifusion system technique. Vasoactive intestinal peptide, (VIP) a neurohormone which stimulates TRH target cells in mammals, was totally devoid of effect on frog melanotrophs although VIP-like material could be detected in neurointermediate lobe extracts. Somatostatin-like immunoreactive material was found in high concentrations in the frog neurointermediate lobe complex, but synthetic somatostatin (from 10(-10) to 10(-6) M) did not modify the spontaneous release of alpha-MSH. At doses of 10(-8) and 10(-6) M, synthetic somatostatin did not modify TRH-induced alpha-MSH secretion. Morphine (10(-5) M) and opioid peptides (10(-10) to 10(-6) M) had no effect on spontaneous alpha-MSH secretion. In addition, methionine enkephalin (10(-5) M) did not modify the stimulatory effect of TRH on alpha-MSH secretion. From these results we conclude that, among the neuropeptides which modulate prolactin secretion in mammals, only TRH is involved in alpha-MSH secretion in the frog.
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PMID:In vitro study of frog (Rana ridibunda Pallas) neurointermediate lobe secretion by use of a simplified perifusion system. III. Effect of neuropeptides on alpha-MSH secretion. 614 Feb 3

Peptide, 5-hydroxytryptamine (5-HT)-, tyrosine hydroxylase (TOH)-, and glial fibrillary acidic protein (GFAP)-like immunoreactivity was studied in the optic tectum of Rana pipiens. Peroxidase-antiperoxidase and indirect immunofluorescence single- and double-labeling methods were used to compare differential laminar distribution of each of these substances. Substance P (SP), leucine-enkephalin (LENK), cholecystokinin octapeptide (CCK8), bombesin (BOM), avian pancreatic polypeptide (APP), and possibly neurotensin display unique individual patterns of laminar distribution of processes and cell bodies throughout the tectum. A correlative analysis of the topographical distribution of SP, LENK, BOM, and APP on the basis of double-labeled sections shows a precise laminar segregation of these substances. Vasoactive intestinal peptide-, beta-endorphin-, and ranatensinlike immunoreactivity is consistently absent from our material. 5HT- and TOH-like immunoreactivity discloses a reticular array of fibers without clear evidence of laminar organization. This peptide-like laminar organization is particularly elaborate throughout the superficial neuropil of the optic tectum, the major retinorecipient zone. The pattern of lamination demonstrated in the present study differs in several important features from that previously described on the basis of several histological methods. The cells of origin of processes (axons and/or dendrites) in the superficial tectal neuropil may be either intrinsic or extrinsic to the tectum. Special reference is made to conflicting evidence regarding the possibility of a retinal contribution to peptide-like tectal lamination.
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PMID:Laminar organization of peptide-like immunoreactivity in the anuran optic tectum. 619 80

In order to identify prolactin regulating factors, the effect of various neuropeptides on prolactin secretion by the adenohypophysis has been tested. 1 degree Histidyl-proline-diketopiperazine (DKP), a major degradation product of TRH in hypothalamus and pituitary, inhibited prolactin secretion from incubated hemipituitaries (Fig. 1) with an apparent affinity of 0.5 nM. Histidyl-prolineamide and histidyl-proline, other degradation products of TRH, had no effect. TSH secretion was not affected under the same conditions. 2 degrees Vasoactive intestinal peptide (VIP) stimulated prolactin secretion in vitro in a dose dependent manner. The secretion of other adenohypophyseal hormones was not affected. This effect is not mediated by a dopaminergic mechanism, since it was not blocked by neuroleptics (Table I). 3 degrees Morphinomimetic peptides had no effect on prolactin secretion in vitro, but blocked the dopamine inhibition of prolactin secretion. The effect of metenkephalin and beta-endorphin was dose dependent and was blocked by naloxone (Fig. 2 and 3). Thse results indicate that specific receptors to various neuropeptides seem to be present on prolactin cells.
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PMID:[Effect of neuropeptides on prolactin secretion by the adenohypophysis (author's transl)]. 741 81

In human Y-79 retinoblastoma cells, corticotropin-releasing hormone (CRH) stimulates adenylyl cyclase activity and increases cyclic AMP accumulation. Different CRH analogues mimic the CRH stimulation of adenylyl cyclase and show similar sensitivity to the CRH receptor antagonist alpha-helical CRH9-41. Vasoactive intestinal peptide (VIP) also increases the enzyme activity but less potently than CRH, and its effect is counteracted by the VIP receptor antagonist [D-p-Cl-Phe6,Leu17]VIP. The VIP antagonist does not affect the response to CRH. The CRH-stimulated adenylyl cyclase activity is amplified by Mg2+, is inhibited by submicromolar concentrations of Ca2+, and requires GTP. Moreover, the CRH stimulation is reduced by pretreatment of cells with cholera toxin and by incubation of membranes with the RM/1 antibody, which recognizes the C-terminus of the alpha subunit of Gs. In immunoblots, the RM/1 antibody identifies a doublet of 45 and 52 kDa. Two proteins of similar molecular weights are ADP-ribosylated by cholera toxin. These data demonstrate that in human Y-79 retinoblastoma cells, specific CRH receptors stimulate cyclic AMP formation by interacting with Gs and by affecting a Ca(2+)-inhibitable form of adenylyl cyclase.
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PMID:Coupling of corticotropin-releasing hormone receptors to adenylyl cyclase in human Y-79 retinoblastoma cells. 779 37

Vasoactive intestinal peptide (VIP) concentration-dependently enhanced corticosterone and cyclic-AMP release by dispersed rat inner adrenocortical cells. A VIP-receptor antagonist and the ACTH-receptor antagonist corticotropin-inhibiting peptide annulled both adrenocortical-cell responses to VIP, while the protein kinase (PKA) inhibitor H-89 blocked only corticosterone response. Collectively, these findings suggest that VIP stimulates glucocorticoid secretion of rat adrenals, through the aspecific activation of ACTH receptors coupled with the adenylate cyclase/PKA-dependent signaling pathway.
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PMID:Vasoactive intestinal peptide stimulates rat adrenal glucocorticoid secretion, through an ACTH receptor-dependent activation of the adenylate cyclase signaling pathway. 966 80


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