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 catalytic dehalogenation of iodinated derivatives of corticotropin in the presence of tritium was investigated. In 0.1 M acetic acid, complete and rapid removal of iodine was achieved in the presence of freshly prepared palladium or palladium oxide as catalyst, but the specific radioactivity of the product was only 10-20% of the theoretically attainable value. Synthetic human corticotropin containing a 3,5-diiodo tyrosine in position 23 in place of tyrosine was successfully dehalogenated in solvent mixture 0.1 M acetic acid: hexamethylphosphoramide: dimethylformamide (1 : 10 : 90, v/v) in the presence of palladium oxide and calcium carbonate. The product was obtained in 30% yield after purification by carboxymethyl cellulose chromatography. The tritiated hormone had a specific radioactivity of 46 Ci/mmol (80% of the theoretical value) and was as potent as synthetic human corticotropin in stimulating steroidogenesis and lipolysis.
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PMID:Preparation and characterization of specifically tritiated adrenocorticotropin. 18 37

Corticotropin is one of the few accepted treatments for acute exacerbations of multiple sclerosis and retrobulbar neuritis. Psychosis is a serious side effect usually necessitating discontinuation of the drug therapy. Because mood disorders preponderated in most patients previously described with this psychosis, 27 patients were empirically treated with lithium carbonate concurrently with corticotropin. In none of the patients treated with lithium did a psychotic reaction occur, although in a comparable group of 44 patients previously treated identically with corticotropin but without lithium, six (14%) became psychotic.
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PMID:Lithium prophylaxis of corticotropin-induced psychosis. 21 18

Previous work indicated that brain contains 3 types of lipolytic-melanotropic peptide: (1) in adenohypophysis: ACTH, alpha-MSH, beta-MSH, peptide I, peptide L', beta-lipotropin and gamma-lipotropin; (2) in neurohypophysis: peptide 7D6, also termed neurophysin I, peptide II or Wuu-Saffran peptide; (3) in extrahypophyseal regions: peptide IIF. Bovine and human neurophysin I prepared by R. Walter has now been found devoid of lipolytic and melanotropic activities. Porcine and bovine peptide 7D6, closely similar or identical to bovine neurophysin I in electrophoretic mobility and amino acid composition, were therefore reexamined to determine whether their lipolytic-melanotropic property resided in a contaminating factor. When peptide 7D6 was analyzed in 100 transfer counter current distribution (1 butanol/0.1M NH4 HCO3), the neurophysin was recovered in tubes 1-9 (7D6-alpha) representing 95% of 7D6. 7D6-alpha was inactive in lipolytic and melanotropic assays. The biologic activities of 7D6 were recovered instead in tubes 50-70 (labeled 7D6-beta), representing 5% of 7D6. 7D6-beta proved to be a peptide with MW 1000-3000, closely similar to peptide IIF in amino acid composition, MW, and Rf values in 4 systems of paper chromatography.
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PMID:Observations on the lipolytic and melanotropic properties of neurophysin proteins. 105 49

The effects of 2 weeks of lithium carbonate administration at therapeutic plasma levels were examined in 11 normal volunteers. Serotoninergic function before and after lithium administration was assessed using low-dose intravenous clomipramine hydrochloride challenge, while urinary and plasma metabolites of norepinephrine (NE) were used to assess noradrenergic systems. Long-term lithium administration in normal subjects did not significantly or consistently enhance serotonin-mediated neuroendocrine responses but did increase measures related to neuronal release of NE. No statistically significant effects of lithium on prolactin, corticotropin, or cortisol responses to serotoninergic challenge could be detected. The probability of a type II error was assessed, and a doubling of prolactin level was unlikely to have been missed, although more modest increases (less than 75%) could have been overlooked. After 2 weeks of lithium administration, there were significant increases in 24-hour urinary excretion of NE, normetanephrine, and fractional NE release, compatible with increased neuronal release of NE and a lithium-induced subsensitivity in alpha 2-adrenergic receptor function. These changes were not statistically significant after 1 week of administration, suggesting that increased NE release is characteristic of long- rather than short-term lithium administration. Since previous reports have demonstrated enhanced prolactin responses after short- but not long-term lithium use, the present study points to temporal specificity in lithium's effects on both serotoninergic and noradrenergic function. Lithium's effects on NE release were consistent but small (a 16% increase), while its effects on serotoninergic responses were larger (a 50% increase in prolactin responses) but quite inconsistent, suggesting that neither of these systems is the primary site of action of lithium.
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PMID:The mechanisms of action of lithium. I. Effects on serotoninergic and noradrenergic systems in normal subjects. 842 26

Bicarbonate secretion by duodenal mucosa free of Brunner's glands was titrated in situ in anesthetized rats. Intracerebroventricular infusion of thyrotropin-releasing hormone (0.01-1 microgram/h), bombesin, gastrin-releasing peptide, or corticotropin-releasing factor increased the bicarbonate secretion and the transmucosal electrical potential difference. The increase in secretion in response to thyrotropin-releasing hormone and bombesin was prevented by cervical vagotomy. Intravenous administration of the alpha-adrenoceptor antagonist phentolamine increased the magnitude and duration of the response, suggesting that these two peptides in addition to eliciting vagal stimulation of the duodenal secretion, by sympathetic activation, inhibit the secretion. Intravenous thyrotropin-releasing hormone (3.6 mg/kg) did not affect the secretion, further indicating that effects were elicited within the central nervous system. Intracerebroventricular infusion of cholecystokinin-octapeptide or beta-endorphin had no effect on duodenal bicarbonate secretion or on the potential difference. The latter peptide was a potent stimulant of the secretion when injected intravenously and probably acts at a peripheral site. The central nervous control of duodenal mucosal bicarbonate secretion is thus influenced by some specific peptides that are known to occur in brain tissue, and duodenal protection against acid might be modulated by agents affecting this control.
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PMID:Stimulation of duodenal mucosal bicarbonate secretion in the rat by brain peptides. 222 6

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

Immunoreactive and bioactive luteinizing hormone (LH) has been shown to be widely distributed in the rodent central nervous system (CNS), particularly in the hypothalamus. Subcellular localization of this LH in fractions rich in synaptosomes and in vitro release by potassium-induced depolarization suggests that this peptide may act in trans-synaptic neuromodulatory roles. Furthermore, a variety of experiments have proved that this brain-based LH is not of pituitary origin. In the in vitro studies reported here characterization of brain-based LH release, in response to gonadotropin-releasing hormone (GnRH), beta-endorphin, and biogenic amines, was examined. Adult male rats were sacrificed by decapitation, hypothalami removed, quartered, and incubated in Krebs Ringer's Bicarbonate (KRB). High potassium concentration and GnRH induced release of LH from these hypothalamic explants in short-term culture and serotonin significantly inhibited release of LH from these explants. In contrast, however, beta-endorphin, norepinephrine, dopamine, and acetylcholine, agents known to modulate pituitary LH release, had no effect on the release of LH from hypothalamic tissues in vitro. Furthermore, beta-endorphin did not alter potassium-induced release of LH from the hypothalamus. Whereas there are some similarities between LH release from the pituitary and from the CNS, the differences reported here suggest that hypothalamic LH does not simply serve as a supplemental source for LH in the general circulation but more likely subserves an entirely different role(s) than its pituitary counterpart, presumably acting in a neuromodulatory fashion within the brain.
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PMID:In vitro LH release from the hypothalamus-pars tuberalis; effects of gonadotropin-releasing hormone (GnRH), beta-endorphin and biogenic amines. 296 55

Secretion of HCO3- by duodenum just distal to the Brunner's glands area and devoid of pancreatic HCO3- was titrated in situ in anesthetized rats. Secretion increased significantly after intravenous injection of small amounts (10-20 ng/kg) of the opioid peptides beta-endorphin, methionine-enkephalin, and leucine-enkephalin. Maximum (approximately twofold) stimulation by beta-endorphin and leucine-enkephalin occurred at 20 ng/kg. Morphine (50 micrograms/kg) caused a similar stimulation and the mu-selective opiate antagonist naloxone prevented the stimulation by beta-endorphin and morphine. The synthetic analogue [D-Ala2,D-Leu5]-enkephalin (500 ng/kg), which is an agonist primarily at delta-opiate receptors, had no effect, further suggesting that the stimulation of duodenal HCO3- secretion is mediated by mu-receptors. Naloxone alone did not affect basal HCO3- secretion but reduced the duration of the rise in secretion in response to a 5-min exposure to luminal acid (pH 2.00). Endogenous opioid peptides may thus have a role in the humoral or neural control, or both, of duodenal surface epithelial HCO3- secretion and mucosal protection.
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PMID:beta-Endorphin and enkephalins stimulate duodenal mucosal alkaline secretion in the rat in vivo. 300 Aug 61

The effect of met-enkephalin on pure exocrine pancreatic secretion was studied in five subjects with external transduodenal drainage of the main pancreatic duct carried out after biliary tract surgery. Intravenous infusion of a low dose of met-enkephalin (0.15 micrograms/kg/h) during submaximal pancreatic stimulation with secretin (25 ng/kg/h) and cerulein (10 ng/kg/h) significantly increased pancreatic outputs. Bicarbonate secretion increased 50% above control values, a more marked effect than the increase in enzyme secretion (maximal rise averaged 22%). The effect of the peptide was rapid, persisted for the duration of met-enkephalin infusion and then tended gradually to diminish.
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PMID:Stimulation of exocrine pancreatic secretion by met-enkephalin. 380 24

Bicarbonate secretion by 12 mm segments of duodenum just distal to the Brunner's glands area and devoid of pancreatic bicarbonate was titrated in situ in anaesthetised rats. The secretion increased significantly after intravenous injection of small amounts (20 ng/kg) of the endogenous opioid peptides beta-endorphin and methionine enkephalin and maximal (approximately twofold) stimulation occurred after 200-500 ng/kg. Morphine (50 micrograms/kg) caused a similar stimulation and the mu-opiate antagonist naloxone prevented stimulation by morphine. The synthetic analogue [D-Ala2, D-Leu5]-enkephalin (500 ng/kg) which is an agonist at delta-opiate receptors, did not affect the secretion, further suggesting that stimulation is mediated by mu-receptors. VIP (5-100 micrograms/kg) increased the secretion dose-dependently to levels considerably higher than those observed with opiates, and pretreatment with atropine or indomethacin did not affect the response to VIP. The results suggest a role of endogenous opioid peptides and VIP in the humoral and/or nervous control of duodenal surface epithelial bicarbonate secretion and mucosal protection.
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PMID:Effects of some opiates and vasoactive intestinal peptide (VIP) on duodenal surface epithelial bicarbonate secretion in the rat. 386 Sep 26


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