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)

Binding of [3H]methionine-enkephalin to intact N1E-115 neuroblastoma cells (competing ligand: naloxone) revealed a homogenous population of receptors with a density (Bmax) of 79.0 +/- 6.5 fmol/mg protein (mean SEM, N = 3) and an apparent Kd of 5.33 +/- 1.63 mM. The order of displacement of [3H]met-enkephalin was met-/leu-enkephalin greater than naloxone greater than morphine, suggesting that it is of the delta receptor class. Specific binding was heat-labile, stereospecific and sensitive to Na+. Adding met-enkephalin to intact neuroblastoma caused reductions of both basal and prostaglandin E1-stimulated levels of cyclic AMP (41.4 +/- 4.0% (N = 6) and 45.1 +/- 2.4% (N = 3) of control levels, respectively). Maximum inhibition (naloxone-reversible) was observed as low as 10(-7) M met-enkephalin. Preliminary results suggest that cells grown in cholesterol-supplemented medium show reduced binding of [3H]met-enkephalin.
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PMID:Opiate peptide receptors on intact NIE-115 neuroblastoma: radioligand binding properties, intracellular response, and effects of increasing membrane cholesterol. 609 92

The spontaneously hypertensive rat (SHR) and the stroke-prone substrain (sp-SHR) have been reported to have several abnormalities in levels of peptides both in tissue and in plasma (beta-endorphin, prolactin, thyroid stimulating hormone and vasopressin) when compared to the Wistar Kyoto (WKY) normotensive control rat. As the secretion of these peptides is under dopaminergic control and the abnormalities consistently suggest under-activity of the dopaminergic control system in the brain, injections of dopamine (0.4 mg/kg) were given i.c.v. to 10 SHR, 10 renal artery stenosis hypertensive rats (LRAS) and 10 genetically hypertensive rats of the New Zealand strain (GHR). Mean blood pressure fell from 205 +/- 6 (SEM) mmHg to 128 +/- 8 mmHg in the SHR (p less than 0.001), from 184 +/- 7 mmHg to 176 +/- 7 mmHg in the LRAS (p greater 0.05) and from 157 +/- 5 mmHg to 138 +/- 6 mmHg in he GHR (p less than 0.02). These effects were unlikely to be due to leakage of dopamine out into the periphery as i.v. dopamine (0.4 mg/kg) increased blood pressure in these animals.
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PMID:Neuropeptide abnormalities suggest a dopaminergic basis for high blood pressure in the spontaneously hypertensive rat. 609 77

Using the methods of immunocytochemistry and radioimmunoassay, five peptides (vasoactive intestinal polypeptide (VIP), substance P, somatostatin, met-enkephalin, and bombesin) have been found in the gall bladder and the biliary tracts of guinea pig and each of them possesses a characteristic distribution pattern. Networks of nerves containing each peptide were found in the smooth muscle, around blood vessels and, occasionally, in the lamina propria. The distribution of the peptide immunoreactive nerves in the gall bladder and biliary tract is similar to those found in the gut. Vasoactive intestinal polypeptide (11 +/- 1.5 pmol/g in the sphincters, mean +/- SEM) and substance P (21.5 +/- 1.8 pmol/g in the common bile duct) were found to be the most abundant peptides and a few VIP and substance P immunoreactive neurones were localised in the ganglionated plexus. Bombesin immunoreactive nerves were mainly seen in the sphincter of Oddi, where the mean concentration of extractable bombesin was 14.6 +/- 2 pmol/g. Somatostatin immunoreactive mucosal endocrine cells were identified in the epithelium of the common bile duct and the sphincter. The extractable somatostatin in these regions were 76 +/- 19 pmol/g and 162 +/- 30 pmol/g respectively.
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PMID:Peptide immunoreactive nerves and cells of the guinea pig gall bladder and biliary pathways. 619 57

Since plasma ACTH, beta-lipotropin [beta-LPH-(1-91)], gamma-lipotropin (gamma-LPH: [beta-LPD-(1-58)]), and beta-endorphin (beta-EP: [beta-LPH-(61-91)]) are all derived from a common precursor molecule, their quantification in the same plasma under basal and stimulatory conditions should help to elucidate factors involved in their secretion and regulation. A sequential immune affinity chromatographic procedure was used to separate immunoreactive beta-LPH, gamma-LPH, and beta-EP on individual patient samples. Basal morning plasma concentrations [femtomoles per ml (to convert values to picograms per ml, femtomoles per ml values are multiplied by 10 for beta-LPH, by 5.8 for beta-LPH, by 4.5 for ACTH, and by 3.4 for beta-EP; n = 19; mean +/- SEM)] were: beta-LPH, 6.1 +/- 0.8; gamma-LPH, 4.4 +/- 0.5; and ACTH, 11.1 +/- 1.3. beta-EP was undetectable (< 1.5 fmol ml-1) in 7 of the 19 basal samples. The mean +/- SEM for the 12 remaining samples was 2.3 +/- 0.2. Insulin-induced hypoglycemia and Pitressin administration were associated with nearly equivalent increments of immunoreactive ACTH and beta-LPH concentrations. The resolving power of the technique was tested by separately applying the immunoreactive beta-LPH, gamma-LPH, and beta-EP fractions obtained from plasma pools to Sephadex G-50 gel filtration for molecular weight estimation. Greater than 88% of all immunoreactive material eluted with a Kav similar to the appropriate standard peptide markers. This immune affinity chromatographic system, therefore, permits simultaneous quantification of these peptides on small plasma volumes more rapidly and with greater resolution than when molecular sieve chromatography is used as an adjunct to RIA.
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PMID:Simultaneous determination of human plasma immunoreactive beta-lipotropin, gamma-lipotropin, and beta-endorphin using immuno-affinity chromatography. 625 27

Morphine and naloxone were administered to five dogs to assess their effects on endogenous opioid release. Morphine (3 mg/20 kg) produced a significant (P less than 0.05) increase in plasma beta-endorphin immunoreactivity(beta EI) compared to saline control. The peak stimulation [19.2 +/- 4.97 baseline to 48.1 +/- 6.82 (SEM) pg/ml] occurred at +10 min and rapidly returned to preinjection levels at +60. At a dose 10 times equipotent to circulating basal beta EI, morphine (4-6 micrograms) failed to affect beta EI release. Naloxone, surprisingly, also caused a significant (P less than 0.025) release of beta EI. After naloxone, beta EI rose from a preinjection baseline of 36.4 +/- 5.82 pg/ml to a peak of 172 +/- 44.1 pg/ml at 45 min post injection. Naloxone pretreatment also obscured the effect of subsequently injected morphine (3 mg/20 kg). In three naloxone-treated dogs, gel chromatography of pooled basal and peak plasma revealed a preponderance of beta-lipotropin compared to beta-endorphin. To determine the site of stimulation of beta EI by opiates and opioids, a series of rat anterior pituitary incubations were performed. Neither morphine (10(-6) M) nor D-Ala2-methionine enkephalinamide (10(-6) M) nor naloxone (10(-6) M) had an effect significantly different from control medium on the release of beta EI from the pituitaries. In a second set of experiments we compared the effect on beta EI release of hypothalamic median eminence extract alone or with morphine. Hypothalamic median eminence extract at two concentrations produced significant release of beta EI, which was unaffected by the addition of morphine. These results suggest that stimulation of release of endogenous opioid peptides by opiates occurs at a suprapituitary level.
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PMID:Morphine and naloxone: effects on beta-endorphin immunoreactivity in canine plasma and secretions from rat pituitaries. 626 81

We have further characterized angiotensin receptors on bovine adrenal fasciculata cells whose presence was previously demonstrated by the intrinsic agonistic activity of angiotensin II (AII), dex-Asp1-AII, angiotensin I (AI), and des-ASp1-AI on steroidogenesis. The specific binding of AII and des-Asp1-AII labeled with 125I to dispersed bovine fasciculata cells was studied. For both peptides, a single class of binding sites accounted for the data with a mean (+/- SEM) Ka value of 0.23 +/- 0.123 X 10(8) liters/mol for AII and 0.68 X 10(8) liters/mol for des-Asp1-AII. The concentration at which unlabeled AII and des-Asp1-AII displaced 50% of the tracers (Kd) was similar to that at which they induced half-maximal stimulation of steroidogenesis (Kact). For AI and des-Asp1-AI, Kd greater than Kact. Analogs of AII or des-Asp1-AII with antagonistic properties upon steroidogenesis competed also with binding of the tracers. Corticotropin (ACTH) did not inhibit binding. Although ACTH stimulated the formation of cyclic AMP, none of the angiotensins with intrinsic activity did so. Calcium, but not potassium, appeared to potentiate the steroidogenic activity of AII. These data suggest that there is a single class of receptors for angiotensins and analogs in zona fasciculata. These receptors show characteristics that differentiate them from ACTH receptors in zona fasciculata or angiotensin receptors in zona glomerulosa cells.
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PMID:Characterization of angiotensin receptors on bovine adrenal fasciculata cells. 626 51

Beta-endorphin-like immunoreactivity was determined in the plasma of twenty patients suffering from hypoxia of various etiologies and in twenty healthy adult volunteers who served as controls. Mean beta-endorphin-like immunoreactivity in the hypoxic patients was 53.2 +/- 5.5 (SEM) pg/ml, as compared to the volunteer subjects in whom the mean level was 6.2 +/- 1.9 pg/ml (P less than 0.01). Significant negative correlations were present between both arterial pH (r = -0.85; P less than 0.01) and arterial PO2 (r = -0.80; P less than 0.01) and beta-endorphin-like immunoreactivity. These findings seem to lend support to the hypothesis that hypoxia and acidosis represent stressful conditions which may stimulate the release of beta-endorphin in humans.
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PMID:Respiratory distress and beta-endorphin-like immunoreactivity in humans. 627 Oct 27

The presence of beta-endorphin-like immunoreactivity (beta-EpLI) in human duodenum and its release were studied. beta-EpLI was detected in the duodenum (mucosa, 26.7 +/- 6.3 pmol/g wet weight, mean +/- SEM; remaining tissue 23.1 +/- 5.3 pmol/g wet weight) and the stomach (7.1 pmol/g wet weight). The two activities gave similar curves for inhibition of beta-Ep radioimmunoassay of synthetic beta-Ep. On gel-filtration chromatography of a duodenal extract, two components of beta-EpLI were separated. When human duodenal mucosa was perfused with a solution of pH2 or 1mM or 5mM taurocholate, the release of beta-EpLI from mucosa into the perfusate increased 2-4 fold. These results indicate that beta-EpLI present in human duodenal is released by the direct action of low pH or taurocholate on the duodenal mucosa and suggest that it may have a physiological role.
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PMID:Effects of solution of low pH and taurocholate on release of beta-endorphin-like immunoreactivity from human duodenal mucosa in vitro. 628 54

1. We examined the effect of ischaemic pain and sustained isometric muscle contraction on plasma immunoreactive gamma-lipotropin (gamma LPH), beta-endorphin/beta-lipotropin (beta END/beta LPH) and corticotropin (ACTH), which are all synthesized from a common precursor (pro-opiocortin), and plasma cortisol in 10 normal subjects. 2. Experimental pain was produced by inflation to 250 mmHg of a sphygmomanometer cuff, placed above the elbow of the 'dominant' arm, after which the subject squeezed a hand dynamometer, loaded to 12 kg, 20 times at 2 s intervals. Blood was drawn before, after 5 and 10 min of pain, and 30 min after release of the cuff. In a control session, the subjects were asked to squeeze the handgrip alone for 5 min at 30% of their maximum strength, a procedure which elevates the blood pressure without causing pain. 3. One subject had unexplained high (30--71 pmol/l) baseline peptide concentrations. Baseline values for the nine other subjects were: ACTH, 7.3 +/- 1.9 pmol/l (mean +/- SEM); gamma LPH, 18.6 +/- 1.0 pmol/l; beta END/beta LPH, 10.0 +/- 1.1 pmol/l; cortisol, 599 +/- 55 nmol/l. Neither procedure significantly increased the plasma concentration of ACTH or any other peptide, whereas plasma cortisol was significantly increased at both 5 min and 10 min. Plasma ACTH was positively correlated with plasma gamma LPH (r = 0.701; P less than 0.001), beta END/beta LPH (r = 0.970; P less than 0.001) and plasma cortisol (r = 0.758; P less than 0.05). 4. The present study demonstrates that, in normal man, plasma endorphins do not change with experimental ischaemic pain. The rise in plasma cortisol without concomitant rise in ACTH is not explained, but suggests the action of some other agent at the level of the adrenal cortex.
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PMID:The response of plasma immunoreactive adrenocorticotropin, beta-endorphin/beta-lipotropin, gamma-lipotropin and cortisol to experimentally induced pain in normal subjects. 628 7

The association between central (cerebrospinal fluid [CSF]) and peripheral (plasma) levels of beta-endorphin-like immunoactivity (beta-ELI) in nonpregnant women (n = 8) and pregnant women (a) at 16 to 20 weeks of gestation (n = 6), (b) at term (n = 21), and (c) in labor (n = 15) was investigated. Umbilical arterial (n = 11) and venous (n = 11) samples were also obtained. In agreement with previous investigations, it was found that plasma levels of beta-ELI increased during labor (mean +/- SEM: nonpregnant women, 63.5 +/- 18.2; pregnant women at term, 64.0 +/- 12.2; women in labor, 110.8 +/- 30.3 pg/ml), and that levels of umbilical arterial plasma of beta-ELI exceeded those in umbilical venous plasma (132.5 +/- 34.0 versus 68.2 +/- 22.2). However, CSF levels of beta ELI did not change over the course of pregnancy or during labor (nonpregnant women, 36.5 +/- 15.8; pregnant women at 16 to 20 weeks of gestation, 60.1 +/- 10.3; pregnant women at term, 57.5 +/- 8.4; women in labor 48.5 +/- 8.3 pg/ml). This evidence that plasma and CSF levels of beta-ELI are dissociated during labor calls into question inferences regarding behavioral changes during parturition based on plasma beta-ELI measurements.
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PMID:Dissociation of plasma and cerebrospinal fluid beta-endorphin-like immunoactivity levels during pregnancy and parturition. 629 32


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