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)

These three neuropeptides were measured at daily baseline values by radioimmunoassay. Stimulated parotid saliva was collected from 31 subjects using a modified Carlson-Crittenden device affixed over Stenson's duct. Methionine enkephalin-like immunoreactivity ranged from 6.6 to 11.7 fmol/ml, with a mean of 9.3 fmol/ml. Substance P-like immunoreactivity ranged from 6.1 to 12.6 fmol/ml, with a mean of 9.3 fmol/ml. beta-Endorphin-like immunoreactivity ranged from 1.2 to 3.6 fmol/ml, with a mean of 2.6 fmol/ml. This is believed to be the first documentation of methionine enkephalin- and substance P-like activities in human parotid saliva and the first demonstration of beta-endorphin-like activity in any type of human saliva. Substance P-like activity was significantly higher in morning than evening samples; beta-endorphin-like activity also tended to be higher in the morning samples. Substance P and beta-endorphin-like immunoreactivities covaried in a significant positive manner, suggesting either common control mechanisms or similar responses to physiological variables.
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PMID:Methionine enkephalin-like, substance P-like, and beta-endorphin-like immunoreactivity in human parotid saliva. 138 60

The influences of opioids on pial arteriolar diameter and cortical periarachnoid cerebrospinal fluid prostanoid concentration were investigated in piglets with closed cranial windows. Methionine enkephalin (10(-12)-10(-6) M) increased pial arteriolar diameter (139 +/- 4, 149 +/- 3, 178 +/- 3 microns, for control, 10(-12), and 10(-6) M, respectively). Leucine enkephalin produced similar pial arteriolar dilation. In contrast, dynorphin elicited dilation during normotension and constriction during hypotension. beta-Endorphin (10(-12)-10(-6) M) decreased pial arteriolar diameter (137 +/- 6, 128 +/- 6, 92 +/- 7 microns, for control, 10(-12) and 10(-6) M, respectively). All four opioids increased cerebrospinal fluid 6-keto-prostaglandin (PG)F1 alpha, PGE2, PGF2 alpha and thromboxane B2. Indomethacin (5 mg/kg i.v.) blocked methionine and leucine enkephalin and dynorphin-induced pial arteriolar dilation, but potentiated beta-endorphin-induced constriction and the constriction caused by dynorphin in hypotensive piglets. These data indicate that prostanoids modulate opioid effects on the cerebral vasculature.
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PMID:Prostanoids modulate opioid cerebrovascular responses in newborn pigs. 197 12

Methionine enkephalin, leucine enkephalin, [D-Ala2, D-Leu5] enkephalin, alpha-neoendorphin, beta-endorphin, dynorphin (1-13) and ethylketocyclazocine inhibited the contractions of rabbit ear artery ring segments elicited by transmural nerve stimulation at 8 Hz. Ethylketocyclazocine, dynorphin (1-13) and leucine enkephalin produced partial inhibition, their apparent intrinsic activities (alpha) being 0.57, 0.75 and 0.66, respectively. Morphine and normorphine, which are agonists at mu-receptors, did not inhibit the response of the artery. Naloxone antagonized the actions of opioids and ethylketocyclazocine, and was more effective against methionine enkephalin, leucine enkephalin and [D-Ala2, D-Leu5] enkephalin than against alpha-neoendorphin, ethylketocyclazocine and dynorphin (1-13). The pA2 values of naloxone against so-called delta-agonists were approx. 8.5, and against so-called kappa-agonists were approx. 7.7. The supposed kappa-antagonist, Mr2266, was more effective than naloxone in antagonizing the actions of alpha-neoendorphin, and the kappa-agonists dynorphin (1-13) and ethylketocyclazocine. The pA2 values of Mr2266 against kappa-agonists were 8.5-9.0, and against delta-agonists were 7.8 or less. The opioid peptides and opioids tested did not cause dilatation of the artery previously contracted with histamine. These results suggest that the opioid peptides and ethylketocyclazocine acted on opioid receptors at adrenergic nerve terminals in the ear artery. The opioid receptors appear to be of the delta- and kappa-types, not the mu-type.
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PMID:Opioid receptor types on adrenergic nerve terminals of rabbit ear artery. 299 21

The effects of beta-endorphin (lipotropin 61-91) and related naturally-occurring peptides upon acetylcholinesterase activity in rat hind-limb muscles was investigated. beta-endorphin weakly inhibited the activity in a plasma membrane-enriched fraction. The inhibition by beta-endorphin of the membrane-associated acetylcholinesterase was less marked when the fractions were prepared from muscles which had been denervated 4-6 days previously. The membrane-associated acetylcholinesterase was solubilised from normal muscle preparations and separated by sucrose density gradient centrifugation into three major peaks (16S, 10S and 4S). beta-Endorphin inhibited the activity in the 16S peak but not that in the 10S and 4S peaks, whilst tensilon, a competitive inhibitor of acetylcholinesterase, inhibited the activity of all three peaks. beta-Endorphin inhibited the activity in the 16S peak but not that in the 10S and 4S peaks, whilst tensilon, a competitive inhibitor of acetylcholinesterase, inhibited the activity of all three peaks. beta-Endorphin inhibited the 16S activity in a concentration-dependent manner and its action was partly prevented if naloxone was added simultaneously. Purified natural porcine and bovine beta-endorphin were equipotent in terms of effective concentration range but the maximum inhibition was greater with the bovine peptide. beta-Lipotropin was approximately 4 times less potent than beta-endorphin, whilst C-fragment (lipotropin 61-87) was 100 times less potent. Prolonged treatment with collagenase did not reduce the catalytic activity of 16S acetylcholinesterase, but it was no longer susceptible to the inhibitory action of beta-endorphin. Kinetic studies indicated a complex type of inhibition by beta-endorphin (hyperbolic Lineweaver-Burke plot). Methionine enkephalin inhibited acetylcholinesterase in a weakly non-competitive manner and its action was not abolished if the enzyme was predigested with collagenase. beta-Endorphin produces a novel form of inhibition of acetylcholinesterase, acting only on the 16S (A12 or 'motor endplate-specific') form of the enzyme. The findings are discussed in the light of evidence that beta-endorphin-related immunoreactivity is expressed in motor nerve axons in the immature rat.
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PMID:Selective inhibition of 'motor endplate-specific' acetylcholinesterase by beta-endorphin and related peptides. 628 23

The inhibition of the calmodulin-mediated stimulation of bovine brain cyclic nucleotide phosphodiesterase activity (3':5'-cyclic adenosine monophosphate 5'-nucleotidohydrolase, EC 3.1.4.17) by the 31-residue opiate peptide beta-endorphin has been investigated. Using conditions in which porcine brain calmodulin (6 nM) is limiting (i.e., to give a 3-fold, Ca2+-dependent stimulation of enzymic activity toward cyclic guanosine monophosphate), the domain of beta-endorphin responsible for the inhibition was mapped by using a series of deletion peptides. beta-Endorphin exhibited an ED50 of several micromolar under the conditions employed, and several amino-terminal deletion peptides were essentially as inhibitory as the parent peptide. Methionine enkephalin and various carboxy-terminal deletion peptides had no demonstrable effect at concentrations of 100-200 microM. Peptides 1-25 and 1-27 (C' fragment) inhibited the calmodulin-dependent activity of phosphodiesterase, but higher concentrations were required than of beta-endorphin. Studies using combined amino- and carboxy-terminal deletion peptides demonstrate that peptide 14-25 was the shortest peptide examined that was capable of inhibiting calmodulin stimulation of phosphodiesterase activity under the conditions used. There was no evidence to indicate that the amino-terminal region comprising residues 1-13 of beta-endorphin contributes to the measured inhibition of calmodulin-stimulated enzymic activity. The circular dichroic spectra of calmodulin, beta-endorphin, and mixtures of the two were obtained, and the ellipticity of the peptide-protein mixtures at 221 nm exceeded that expected by assuming simple additivity. This finding is consistent with a direct interaction of beta-endorphin with calmodulin which seems to lead to enhanced helicity of one or both components.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Identification of beta-endorphin residues 14-25 as a region involved in the inhibition of calmodulin-stimulated phosphodiesterase activity. 631 22

beta-Endorphin, leucine enkephalin and methionine enkephalin, were measured in 41 samples of human lumbar cerebrospinal fluid (CSF) of patients with different neurological diseases. beta-Endorphin-like immunoreactivity (beta-ELI) was present in concentrations between 10 and 150 fmol/ml CSF, and in 30 of the 41 samples studied the levels ranged from 10 to 40 fmol/ml. Methionine enkephalin-like immunoreactivity (MELI) measured 1-85 pmol/ml CSF, with 24 of the 41 samples having values between 3 and 4 pmol/ml. CSF concentrations of leucine enkephalin-like immunoreactivity (LELI) ranged from 0.1 to 12.5 pmol/ml, and in 31 of the 41 CSF samples studied LELI was present in concentrations of 0.1-0.25 pmol/ml. No significant relationship exists between the concentrations of beta-endorphin in CSF and sex and age of patients, CSF protein, CSF IgG and CSF leukocytes. No interrelationship could be found between beta-ELI, MELI and LELI concentrations.
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PMID:Beta-endorphin-, leucine enkephalin- and methionine enkephalin-like immunoreactivity in human cerebrospinal fluid. Simultaneous determination and relation to neurological disorders. 632 13

Neuropeptidergic systems have been studied in human tissues and fluids, which include the pituitary and lumbar cerebrospinal fluid, respectively. This paper reviews the qualitative and quantitative mass spectrometric analytical data obtained from three areas of study. Methionine enkephalin (ME) and beta-endorphin (BE) were quantified in the human pituitary by liquid secondary ion mass spectrometry (LSI MS)-tandem mass spectrometry. Corresponding stable isotope-incorporated synthetic peptide internal standards were used. Proenkephalin A and proopiomelanocortin produce ME and BE, respectively. The analysis of neuropeptides in macroadenomas demonstrated a decrease in both of those neuropeptidergic systems relative to controls. An analysis of prolactin-secreting microadenomas showed an increase in the proenkephalin A system. Mass spectrometry was also used to detect opioid peptide-containing proteins in the pituitary. Enzymes that process the precursors of proenkephalin A and tachykinin (substance P) neuropeptides were studied in human lumbar cerebrospinal fluid. Electrospray ionization mass spectrometry was used to characterize the molecular mass of each peptide product.
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PMID:Mass spectrometric analysis of neuropeptidergic systems in the human pituitary and cerebrospinal fluid. 1049 85