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 concentrations of beta-endorphin and cholecystokinin were measured in lymphocytes obtained from young or old rats and from humans at different ages. Both in rats and humans, beta-endorphin and cholecystokinin increase with age; also in vitro, after 48-h culturing, the concentrations of beta-endorphin and cholecystokinin in lymphocytes obtained from humans of different ages changed with the same pattern observed in ex vivo experiments. In the human, beta-endorphin in lymphocytes shows a circadian rhythm that shifts approximately 6 h when compared to plasma ACTH and cortisol rhythm. The HPLC analysis of the molecular forms of beta-endorphin in lymphocytes revealed the presence of N-acetyl-beta-endorphin, with a ratio of beta-endorphin to N-acetyl-beta-endorphin ranging from 1 to 2. The concentrations of beta-endorphin and cholecystokinin were also measured in lymphocytes obtained from rats and human subjects undergoing different pharmacological treatments. In rat, the serotonin receptor antagonist metergoline decreased basal concentrations of the opioid peptide and blocked the increase of beta-endorphin concentrations induced by the serotonin precursor 5-hydroxytryptophan and the tricyclic antidepressant chlorimipramine. Also in the human, the antidepressant drug chlorimipramine increased lymphocyte beta-endorphin concentrations. In contrast to what was observed for beta-endorphin, cholecystokinin concentrations were not affected by the modulation of the serotoninergic system. Chronic treatment of rats with the dopamine receptor antagonist haloperidol induced an increase of beta-endorphin concentrations in lymphocytes that was reversed by the concomitant treatment with the dopamine receptor agonist bromocriptine, which when given alone decreased the basal concentrations of the peptide. In the human, haloperidol increased concentrations of beta-endorphin after both 24 h and chronic treatment, while cholecystokinin was never affected. Finally, beta-endorphin, but not cholecystokinin, increases both in rat and human lymphocytes after treatment with the GABA agonist sodium valproate.
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PMID:Effect of psychoactive drugs on lymphocyte neuropeptides. 214 59

Atrial natriuretic peptide (ANP) has been identified in the central nervous system and its participation in regulation of various regulatory brain functions has been postulated. To elucidate whether central ANP influences endocrine systems related to blood pressure regulation and renal excretory functions, effects of infusion of ANP at a rate of 120 ng.min-1 into the third cerebral ventricle on plasma level of epinephrine (E), norepinephrine (NE), renin, vasopressin and beta-endorphin as well as on excretion of urine, sodium, potassium (UKV) solutes and free water (CH2O) were investigated in conscious dogs. Significant decrease of plasma E from 77.6 +/- 7.0 to 62.1 +/- 4.8 pg.ml-1 and of NE from 345.5 +/- 20.7 to 286.4 +/- 15.0 pg.ml-1 was found at the end of 30 min lasting ANP infusion. Significant elevation of PRA and UKV and a decrease in CH2O were found 60 min after ANP infusion. No significant changes in other variables were found. In time control experiments plasma hormones concentration and renal excretory functions were not significantly influenced. The results suggest that central ANP may affect the sympatho-adrenal outflow.
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PMID:Central effects of atrial natriuretic peptide on plasma catecholamines, vasopressin, renin and beta-endorphin and on renal excretory functions in the dog. 214 67

In a review of 74 autopsy cases of acquired immune deficiency syndrome (AIDS), the incidence of cytomegalovirus (CMV) infection was found in 50% (37 cases). Of these 37 cases the adrenal glands were affected by CMV in 84%. The authors analyzed the histologic features of 30 of these 37 cases of CMV adrenalitis by grading the CMV inclusions, inflammation and necrosis (CMV score), focal versus diffuse involvement, and the degree of fibrosis (fibrosis score). The clinical data were not significant except for sodium to potassium ratio (Na:K), which was less than 30 in 11 cases. Focal CMV adrenalitis had low CMV and fibrosis scores and Na:K ratio higher than 30, whereas diffuse adrenalitis had high CMV and fibrosis scores and Na:K ratio less than 30. Adrenocorticotropic hormone (ACTH) stimulation tests performed in three patients revealed normal or elevated baseline cortisol levels with a blunted response after stimulation. The authors conclude that the adrenal gland is the most frequently affected organ in AIDS with CMV infection. ACTH tests on a larger number of selected cases of AIDS are needed for further evaluation of functional status of adrenal glands. Selection criteria for the test should include evidence of CMV infection from any site and a low Na:K ratio.
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PMID:Cytomegaloviral adrenalitis and adrenal insufficiency in AIDS. 216 75

In a modified Krebs buffer at 37 degrees C, the selective mu agonist [3H] D-Ala2,MePhe4,Gly-ol5]enkephalin [( 3H]DAMGO) and the nonselective mu/delta agonist human [125I]beta-endorphin [( 125I]beta-endH) bound to rat striatal membranes with a Kd of about 7 and 5 nM and a Bmax of about 95 and 260 fmol/mg of protein, respectively, consistent with labeling of mu receptors by the former ligand and labeling of both mu and delta receptors by the latter. The binding of 2 nM [125I]beta-endH was displaced by unlabeled DAMGO (IC50 30 nM), [D-Ala2-D-Leu5]enkephalin (IC50 60 nM) as well as by the selective delta agonists [D-Ser2(O-tert-butyl),Leu5]enkephalyl-Thr6 (DSTBULET, IC50 500 nM) and Tyr-Ala-Phe-Asp-Val-Val-Gly-NH2 (IC50 700 nM) in a monophasic manner within 2 to 3 log concentration units, suggesting an allosteric interaction between mu and delta sites labeled by [125I]beta-endH under these conditions. Accordingly, 500 nM DSTBULET caused almost 40% inhibition of the apparent Bmax without changing the apparent Kd of [3H] DAMGO. The kappa agonist U 50,488 was ineffective as competing ligand even at a concentration of 10 microM. Upon affinity cross-linking of [125I]beta-endH (2 nM) to rat striatal mu- and delta-opioid receptors, sodium dodecyl sulfate-polyacrylamide gel electrophoresis of the solubilized tissue under reducing conditions followed by autoradiography of the dried gels revealed a major broad band of covalently labeled protein with an apparent molecular weight of 80 kDa.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cross-linking of human [125I]beta-endorphin to opioid receptors in rat striatal membranes: biochemical evidence for the existence of a mu/delta opioid receptor complex. 215 52

Digitonin-solubilized opioid receptors from rat brain were purified with an affinity resin, AH-Sepharose coupled with [D-Ala2, D-Leu5]enkephalin (DADLE). Radioreceptor binding assay showed that the purified materials had specific opioid-binding activity of 310 pmol/mg protein on DADLE binding. Analyses by polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate (SDS-PAGE) revealed that the materials were rich in two polypeptides; the major component had a molecular weight of 62000-64000. To establish the materials responsible for binding opiates, the purified materials were cross-linked with 125I-labeled beta-endorphin using bis[2-(succinimidooxycarbonyloxy)-ethyl]sulfone as a cross-linker. The molecular weight of 62000-64000, the major band of the purified materials on SDS-PAGE, agreed closely with that determined by the cross-linking experiment. The results suggest that the purified materials contained opioid-binding materials (opioid receptors).
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PMID:Identification of opioid-binding materials of rat brain. 215 52

Some of the functional effects of beta-endorphin on immune cells are resistant to inhibition by naloxone. To further characterize the beta-[125I]endorphin-binding site mediating these effects and its response to cations and GTP, the human monocyte-like cell line U937 was used. Incubation of intact cells and beta-[125I]endorphin for 60 min at 4 C demonstrated a saturable, high affinity binding site [Kd = 1.2 +/- 0.5 X 10(-8) M (mean +/- SE; n = 4] competed by equimolar beta-endorphin and N-acetyl (Ac)-beta-endorphin but not by naloxone, morphine, or selective opiate receptor agonists. Competition studies showed that beta-endorphin-(6-31) and beta-endorphin-(28-31) were approximately 5- and 100-fold less potent, respectively, whereas beta-endorphin-(1-16) or -(1-27) was ineffective. Covalent cross-linking of beta-[125I]endorphin to intact cells and resolution by gel electrophoresis showed dominant bands at 59K and 44K and a minor band at 66K. The bands at 44K and 66K were completely displaced by increasing equivalent concentrations of beta-endorphin and N-Ac-beta-endorphin. Increasing concentrations of mono (Na+, K+)- and divalent (Ca2+, Mg2+, Mn2+) cations reduced the binding of beta-[125I]endorphin to U937 membrane; beta-[125I]endorphin binding to rat brain membrane showed similar cation sensitivity. GTP gamma-sulfate (GTP gamma S; 10(-4) M) alone reduced binding to U937 membrane by 25%. In the presence of Na+ (100 or 150 mM) or Mg2+ (10 mM), GTP gamma S reduced binding by an additional 50%. Moreover, GTP gamma S (10(-8)-10(-4) M) in the presence of Na+ (100 mM) reduced binding in a dose-dependent manner, whereas GMP was ineffective. In conclusion, beta-endorphin binds to sites on human U937 cells similar to those observed on normal murine splenocytes. Although naloxone insensitive, these sites exhibit properties, such as size, salt sensitivity, and coupling to a GTP-binding protein, that are similar to those observed for agonist binding to brain opiate receptors.
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PMID:Beta-endorphin binding to naloxone-insensitive sites on a human mononuclear cell line (U937): effects of cations and guanosine triphosphate. 216 44

Tyrosinase synthesis and its regulation in human melanocytes was studied by measuring the incorporation of [35S] methionine into incubated skin biopsies. Tyrosinase was detected in all skin samples with the highest levels in skin type IV and the lowest levels in skin type I. Following psoralen ultraviolet A (PUVA) therapy for several weeks, significant increases in the amounts of tyrosinase were found in skin types III and IV. The presence of alpha-melanocyte-stimulating hormone (alpha-MSH) (100 mumol/l) or the long-acting analogue [Nle4, DPhe7] alpha-MSH (1-10 mumol/l) in the incubation medium failed to alter tyrosinase levels in the skin biopsies taken from patients both before and after receiving PUVA therapy. Bromo-adenosine 3,5-cyclic monophosphate sodium salt (8-bromo-cAMP) (10 mmol/l), on the other hand, increased the amounts of tyrosinase both before and after PUVA, but these effects were only seen in biopsies of type III and IV skin. These results indicate that MSH fails to stimulate tyrosinase synthesis in human melanocytes. Nevertheless, tyrosinase synthesis and its regulation by cyclic AMP-dependent mechanisms could be important control points in the pigmentary response.
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PMID:Tyrosinase synthesis in different skin types and the effects of alpha-melanocyte-stimulating hormone and cyclic AMP. 217 91

In addition to its effect of inhibiting adrenocorticotropic hormone (ACTH) secretion, cortisol (hydrocortisone) inhibits the renin-angiotensin system in both fetal and adult sheep. We have found that progesterone attenuates the inhibition of ACTH by cortisol. These studies test whether progesterone interacts with cortisol in control of the renin-angiotensin-aldosterone system. Conscious adult ewes were infused with vehicle, cortisol (4 micrograms.kg-1.min-1), progesterone (0.5 microgram.kg-1.min-1), or cortisol with progesterone for 60 min. Beginning 120 min after the start of the infusion, renin secretion was stimulated by infusing sodium nitroprusside (10 micrograms.kg-1.min-1 iv). Cortisol infusion decreased plasma K+ concentration and reduced the plasma renin activity (PRA) and aldosterone responses to nitroprusside. Progesterone alone had no effect on PRA, aldosterone, or K+. Progesterone reduced the inhibition of PRA, but not aldosterone or K+, by cortisol. The data also indicate that the suppression of renin, as well as the suppression of ACTH, involves receptors or intracellular mechanisms with which progesterone interacts, whereas the inhibition of aldosterone involves a mechanism that progesterone does not affect.
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PMID:Progesterone-cortisol interaction in control of renin activity but not aldosterone. 220 Dec 19

120 SD rats were randomly divided into three groups: the sham operation group, the AP (acute pancreatitis) group, the naloxon treated group. AP was induced by intraductal injection of 5% sodium taurocholate solution. Naloxon was given intramuscularly at the dosage of 0.1 g/100 gw immediately after the injection and 90 minutes later. The survival rate and the mean survival time of the rats during 3 days after the induction of AP were determined. The pancreata were sampled for semiquantitative histopathologic evaluation. By using the fractional indicator distribution technique with 86 RB, QP/CO and pancreatic tissue perfusion performed 1 and 6 hours after the induction of AP, the amount of beta-endorphin in the hypothalamus and pituitary was measured 1 and 4 hours after the induction of AP. It was found in the naloxon treated group, the pancreatic blood flow and tissue perfusion was greatly increased, the mortality rate was decreased, and the rats survival time was significantly prolonged. The results suggest that: (1) The hemodynamic changes play an important role in the pathogenesis of AP. (2) Beta-Endorphin may play a role in the pathophysiological process of AP. (3) naloxon has good therapeutic effects on AP.
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PMID:[An experimental study on the role of beta-endorphin in the pathogenesis of acute pancreatitis and the effects and mechanisms of naloxone]. 226 55

Plasma levels of the N-terminal peptide of proopiomelanocortin (NPP) were measured in rainbow trout, Salmo gairdneri, following treatment of handling stress with or without administration of dexamethasone, adaptation to white and black background, and maintenance on a constant light/dark cycle. Effects of exogenously administered NPP on plasma constituents were also examined to provide insight into the biological significance of NPP. Thirty minutes of handling stress in shallow water had no effect on plasma levels of NPP during and after the stress period, whereas significant increases in plasma cortisol and glucose were observed. Intraperitoneal administration of dexamethasone blocked the stress-induced elevation of plasma levels of cortisol and caused a depression of plasma NPP. No difference was observed in plasma levels of NPP between trout adapted to a white background and those adapted to a black background. No diurnal changes in NPP were observed under an artificial light/dark cycle (14L/10D light cycle, 0500-1900 hr light) in May and September. Thus, plasma levels of NPP were considerably constant under various physiological conditions, and no synchronism was observed between plasma NPP and cortisol, although NPP modifies the corticotropin-induced release of cortisol from the interrenal. Plasma constituents such as cortisol, total protein, albumin, plasma amino nitrogen, glucose, free fatty acid, ketone body, sodium, potassium, calcium, and magnesium were not altered by intraperitoneal injections of NPP (1 or 10 micrograms) once daily for 6 days (total of six injections) or once every other day for 28 days (14 injections). High concentrations of NPP were found in the plasma 24 hr after cessation of the serial injections of NPP (10 micrograms), suggesting slow metabolic clearance of the peptide.
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PMID:Plasma profiles of the N-terminal peptide of proopiomelanocortin in the rainbow trout with reference to stress. 229 28


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