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)

To determine the effects of the opioid peptides, beta-endorphin and dynorphin A, on airway smooth muscle function and its possible modulation by tissue peptidases, we studied canine bronchial segments under isometric conditions in vitro. Addition of beta-endorphin or dynorphin A did not alter the resting tension. However, beta-endorphin (10(-6) M) but not dynorphin A decreased the contractile responses to electrical field stimulation (EFS, 0.5-40 Hz). This effect was dose-dependent and reversed by naloxone. In contrast, acetylcholine-induced contractions were not affected by these opioids. The beta-endorphin-induced inhibition of the contractile responses to EFS was not augmented by peptidase inhibitors such as thiorphan, captopril, bestatin and leupeptin. These results suggest that beta-endorphin prejunctionally inhibits parasympathetic muscle contraction, and that endogenous peptidases do not play a modulatory role in this effect of beta-endorphin.
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PMID:Effects of beta-endorphin and dynorphin A on cholinergic neurotransmission in canine airway smooth muscle. 197 92

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

Previous studies have shown that 2 Hz but not 100 Hz electroacupuncture (EA) stimulation released beta-endorphin in PAG of the rat to induce analgesia. The present study was undertaken to see whether dynorphin plays a role in PAG in mediating analgesia induced by low and high frequency EA. Injection of affinity purified dynorphin antibody (1:350,000 in RIA titer) 1 microliter into PAG blocked 2 Hz EA analgesia almost completely, and 15 Hz EA analgesia partly, leaving 100 Hz EA analgesia intact. This blocking effect was totally disappeared when the antibody was diluted to 1/10 of its original concentration (1:35,000). Besides, injection of dynorphin into PAG through chronically implanted cannula showed no analgesic effect. The results suggest that the blockade of 2 Hz EA analgesia by high titer dynorphin antibody injected into PAG may have been the result of cross reactivity of the antibody to other opioid peptides (such as beta-endorphin, enkephalin, etc) released in the PAG area. The data also stress the importance of using antibodies of proper titer and concentration to exclude false positive or false negative conclusions in adopting the antibody microinjection techniques, as was repeatedly shown in the immunohistochemical studies.
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PMID:[Influence of microinjection of dynorphin antibody into periaqueductal gray (PAG) on analgesia induced by electroacupuncture of different frequencies in rats]. 198 Apr 31

Many laboratories have reported that systemically administered naloxone has little or no effect on lateral hypothalamic self-stimulation (LH ICSS). In the present study, lateral ventricular infusion of beta-endorphin antiserum and a high dose of naloxone (100 micrograms) produced small but significant increases in stimulation frequency threshold for LH ICSS. beta-Endorphin activity, mediated by a non-mu (e.g. delta or epsilon) receptor, may therefore be involved in the reinforcement of self-stimulation behavior. When rats are deprived of food for 24 h, LH ICSS thresholds decline. Under this condition, systemic naloxone elevates the LH ICSS threshold, often returning it to the pre-deprivation level. In the present study, lateral ventricular infusion of dynorphin A(1-13) antiserum similarly reversed the threshold-lowering effect of food deprivation. The effects of systemic naloxone and intraventricular dynorphin A antiserum on LH ICSS, which are specific to food-deprived animals, may be related to previous findings that these two treatments elevate LH stimulation threshold for eliciting feeding behavior. Results of the ICSS and stimulation-induced feeding studies suggest a model for the mediation of incentive stimuli by dynorphin A activity that is afferent to LH 'reward' neurons and positively gated by 'hunger'. An hypothesized role for 'hunger'-gated dynorphin A release in potentiating the hedonic response to alimentary stimuli and drugs of abuse is discussed.
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PMID:Effects of antibodies to dynorphin A and beta-endorphin on lateral hypothalamic self-stimulation in ad libitum fed and food-deprived rats. 198 87

Gastric function was studied in 69 peptic ulcer patients in the long-term period after gastric resection according to Billroth-I and Billroth-II. Enzyme-producing function of the stomach was appraised according to the blood pepsinogen content, acid-forming function was assessed with the aid of intragastric pH-metry, and mucus-forming one in accordance with the content of hexosamines and sialic acids in gastric juice. The patients showed different alterations in gastric function. A correlation analysis was used to establish the role played by the neurohormonal systems (leu-enkephalin, beta-endorphin, gastrin, somatotropin, triiodothyronine, thyroxine, cortisol) in the derangement of secretory function of the resected stomach. The data obtained enable one to come closer to understanding the ineffectiveness in some cases of drug and surgical therapy of peptic ulcer. On the other hand, specification of the regularities of the impairment of secretory function of the stomach will be helpful in elaborating methods of gastric function correction at the neurohormonal level.
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PMID:[Changes in gastric secretory function in peptic ulcer patients after gastric resection]. 204 10

Beta-endorphin (BE), met- and leu-enkephalin (ME and LE) contents have been determined in patients with circulating blood volume deficiency to 10, 15-20 and 25-30%. It has been established that with the mounting of circulating blood volume deficiency and a simultaneous decrease in central venous pressure, hematocrit and lactate level elevation there was an increase in BE, ME and LE blood plasma content. In up to 20% circulating blood volume deficiency LE blood plasma content decreases 2-3-fold, with an increase in more than 20% deficiency.
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PMID:[The content of beta-endorphin, met- and leu-enkephalin in the blood of patients with hemorrhages]. 207 21

Met- and leu-enkephalin contents in midbrain (including hypothalamus) and striatum of rats were determined by radioimmunoassay after bestatin (racemate) injection (200 g, i.c.v.). It was found that bestatin administration influenced the midbrain met-enkephalin content, values and directions of the changes observed being dependent upon the time after the injection. The data obtained confirm the participation of aminopeptidase in enkephalin inactivation and present evidence for the possibility of regional variations of enkephalin catabolism pathways in the brain.
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PMID:[The effect of the aminopeptidase inhibitor bestatin on the enkephalin level in the rat brain]. 208 25

Binding of human beta-endorphin (beta-EP) to rat renal basolateral membranes was characterized using [125I]Tyr27-beta-EP ([125I]beta-EP) as a primary ligand. Ten millimolar of ethylenediaminetetra acetic acid (EDTA) completely inhibited the degradation of [125I]beta-EP in the incubation mixture at 4 degrees C, thus making it possible to quantitatively examine the [125I]beta-EP binding. The specific binding of [125I]beta-EP to the basolateral membranes was reversible and saturable, and a nonlinear least-squares regression analysis of a saturation isotherm revealed two different classes of specific binding sites. One class had an apparent dissociation constant (Kd) of 0.68 nM and a lower number of binding sites (33 fmol/mg protein), whereas the other class had a lower affinity (apparent Kd of 210 nM) and a higher number of binding sites (7.3 pmol/mg protein). Inhibition of the [125I]beta-EP binding by naloxone (10 microM) was approximately only 20%, and that by D-Ala2-D-Leu5-enkephalin (10 microM) was null, suggesting the major role of a non-opioid binding component in specific [125I]beta-EP binding to basolateral membranes. Moreover, a 50% inhibition by 10 microM of dynorphin(1-13) suggests that a certain region of the primary structure of beta-EP, excluding at least the NH2-terminal enkephalin sequence, is of particular importance for the [125I]beta-EP binding. These lines of evidence suggest the existence of two different classes of specific binding sites for beta-EP on the renal basolateral membranes, and the high-and low-affinity bindings may be attributed to opioid and non-opioid receptors, respectively, as judged by known characteristics of opioid and non-opioid receptors in other peripheral tissues.
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PMID:Specific binding of beta-endorphin to the isolated renal basolateral membranes in vitro. 209 36

The effect of acute and repeated exposure to ethanol on endogenous opioid peptides level in rats was studied. Acute ethanol administration decreased beta-endorphin level in hypothalamus and anterior lobe of pituitary as well as alpha-neoendorphin in the spinal cord. In contrast, repeated ethanol treatment increased hypothalamic beta-endorphin content and did not affect the peptide level in the pituitary. No changes in alpha-neoendorphin and dynorphin level after repeated ethanol administration were observed. Exposure of rats to long-term noxious stimuli by means of induction of monoarthritis prevented the increase in hypothalamic beta-endorphin level by repeated ethanol treatment. As measured by tail-flick test only the first two administrations of ethanol resulted in analgesia. Further administration of increasing doses of ethanol did not affect the pain threshold. Altered response of endogenous opioid systems to repeated ethanol treatment as compared with effects of its acute administration may suggest involvement of these systems in development of tolerance to ethanol.
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PMID:The effects of ethanol treatment on endogenous opioid peptides level and analgesia in monoarthritic rats. 209 95

The aim of the present study is to review current knowledge of the endogenous opiates in order to identify both their basic features and their receptors' properties, including the biological effects of their stimulation, and finally their endocrine actions. Since the identification of methionine-enkephalin and leucin-enkephalin, many opioid peptides with higher molecular weight have been characterized, and their origin from specific precursor has been recognized: proopiomelanocortin, preproenkephalin A, preproenkephalin B. In particular we have analyzed the pharmacological properties and the biological effects of beta-endorphin and met -and leu-enkephalins, the most diffuse of opioids. The use of naloxone has permitted the study of endogenous opioid tone and its effects on the release of the pituitary hormones. The present study reports a summary of data in the literature and personal observation indicating that the peripheral sexual steroids are the most important modulators of naloxone effects on endogenous opioid tone. Finally, the paper reports preliminary observations indicating that during naloxone infusion, females with hypothalamic amenorrhoea show a hormonal profile which differs from normal subjects.
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PMID:[Role of endogenous opioids in the modulation of hypophyseal hormone secretion]. 215 87


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