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)

A 32-year-old male (Mr. A.), monitored during an 8-d heat acclimation (HA) investigation, unexpectedly exhibited heat intolerance and heat exhaustion. Thirteen other males completed HA without indications of either heat intolerance or heat exhaustion. Because Mr. A. responded normally to HA on days 1-4, the intervention of an unknown host factor on days 5-8 was suggested. Mr. A.'s heat exhaustion episode (day 8) was apparently forewarned by loss of body weight and increased delta HR, delta Tsk (days 5-8) and delta Tre (days 7-8) during daily 90-min trials. His symptoms indicated classical salt depletion heat exhaustion, but the calculated salt deficit (less than 0.1 g NaCl.kg-1 body weight) was mild. Post-heat exhaustion serum enzyme levels were either normal (ALT, AST) or acutely elevated (CPK). Blood beta-endorphin and cortisol levels were six times and two times greater than control values, respectively. This case report is unique because clinical/physiological measurements and blood analyses were performed before, during, and after heat intolerance and heat exhaustion.
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PMID:Heat intolerance, heat exhaustion monitored: a case report. 335 82

Cannulas were implanted into forebrain loci of goldfish (Carassius auratus; 45-90 g) to determine the effects and site of action of intracranial norepinephrine (NE) injections on behavioral thermoregulation. Following 30 min in a thermal gradient, implanted fish were injected with norepinephrine-bitartrate salt (2.5-500 ng NE) in 0.2 microliter 0.7% NaCl. Injections of 5, 10, 25, and 50 ng NE into the anterior aspect of the nucleus preopticus periventricularis (NPP, Ref. 25) led to consistent dose-dependent decreases in selected temperature (Tsel). No effect on Tsel was observed following injections of 2.5 ng NE or control injections of 100 ng tartaric acid. The effects of injections into other loci, including intraventricular injections, were dependent on the dose and proximity to the anterior NPP; at sites adjacent to the anterior NPP, larger doses were required, and the effects became inconsistent. At sites further removed, no effect on Tsel was observed. Included in this category were more caudal sites within the NPP and the nucleus preopticus. We postulate that in fish the anterior NPP is an important locus for thermoregulatory integration and that increased release of NE in this area leads to the selection of cooler water.
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PMID:Thermoregulatory effects of intracranial norepinephrine injections in goldfish. 342 60

Corticotropin-releasing factor (CRF) stimulates the synthesis and release of adrenocorticotropin in the anterior pituitary and may help maintain fluid and electrolyte balance. 'Salt-loaded' rats had an increase in CRF mRNA in hypothalamic magnocellular neurons of the paraventricular and supraoptic nuclei and a decrease in message in the parvocellular paraventricular neurons. After salt-loaded rats were adrenalectomized, CRF mRNA increased in the parvocellular cells. In contrast to salt loading, water deprivation lead to a decrease in CRF mRNA in magnocellular and parvocellular neurons. These results show that CRF synthesis within separate populations of hypothalamic neurons is regulated differently under various conditions.
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PMID:Corticotropin-releasing factor mRNA in the hypothalamus is affected differently by drinking saline and by dehydration. 349 Apr 4

A method is described for the separation and analysis of multiple molecular forms of immunoreactive beta-endorphin and its alpha-N-acetylated congeners by a combination of reversed-phase and size-exclusion high-performance liquid chromatography coupled with two specific radioimmunoassays. Both chromatographic procedures are fast (less than 50 min per analysis) providing good resolution and high recovery (greater than 90%). The solvents used in both systems are ultraviolet transparent (less than 214 nm), non-corrosive, low salt (less than 0.05 M) and after evaporation fully compatible with subsequent radioimmunoassay. We have evaluated these techniques using both synthetic and purified peptide standards and have applied these procedures to characterize immunoreactive beta-endorphin and alpha-N-acetylendorphin in rat and sheep pituitary extracts, and the low levels found in sheep hypothalamus and rat ovary. These chromatographic procedures are not only applicable to the study of pro-opiomelanocortin-derived peptides, but also could be employed to examine the processing pathways of other biologically active polypeptides, in both central and peripheral tissue extracts.
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PMID:The combined use of size-exclusion and reversed-phase high-performance liquid chromatography for characterization of beta-endorphin processing pathways. 361 Dec 58

The consumption of saline and water in a two-bottle test of salt-preference was measured after the administration of sulpiride, a dopamine receptor antagonist and of naloxone, an antagonist at opiate receptors. The two drugs were injected alone, or in combination. Three concentrations of saline (0.125, 0.6 and 1.7% NaCl solutions) were used and the tests were carried out using both male and female, water-deprived rats. When the rats were allowed the choice between a highly-preferred 0.125% NaCl solution and water, sulpiride (30 mg kg-1, i.p.) produced an increase in the intake of the two fluids. When naloxone (1 mg kg-1, s.c.) was given alone, it had no effect in this test of salt preference, but when given in combination, completely eliminated the hyperdipsic effect of sulpiride, providing behavioural evidence of a significant interaction between sulpiride and naloxone. When choices of either 0.6 or 1.7% NaCl solutions and water were given, the baseline levels of the consumption of the fluids were increased. Under these circumstances, sulpiride did not significantly increase the consumption of fluids; instead, naloxone significantly reduced the level of fluid consumption. In a further experiment, apomorphine, at dose levels which stimulate dopamine autoreceptors, had no effect on either fluid intake or saline preference in water-deprived male rats. Biochemical data showing that dopamine inhibits the release of beta-endorphin in the hypothalamus through the dopamine D-2 receptor, suggests a possible mechanism for a blockade of sulpiride-induced hyperdipsia by naloxone.
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PMID:Naloxone antagonizes the hyperdipsic effect of sulpiride in a salt-preference test in male and female rats. 374 20

Patients with the "non-salt-losing" form of the adrenogenital syndrome were studied before and after suppression of adrenal cortical activity with carbohydrate-active steroids. The response of aldosterone secretion to sodium deprivation was measured; in some patients response to adrenocorticotropic hormone (ACTH) was measured as well. The aldosterone secretion was normal and responded normally to sodium deprivation in all patients studied during suppression with carbohydrate-active steroids. This finding suggests that 21-hydroxylation of progesterone is normal in this syndrome. The sole abnormality in the production of aldosterone in these patients was found to be excessive secretion of aldosterone while they were not receiving suppressive doses of carbohydrate-active steroids. This finding strongly supports the view that the biogenetic pathways through which aldosterone is produced from progesterone are intact in this syndrome. No patient showed hypertension or hypokalemic alkalosis despite very high aldosterone secretion rates. This observation suggests that the hyper-aldosteronism is secondary to a tendency to sodium loss in the patient whose ACTH production is not suppressed. These studies provide additional evidence in support of the hypothesis that the salt-losing and "non-salt-losing" forms of adrenogenital syndrome are genetically and biochemically distinct.
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PMID:Aldosterone hypersecretion in "non-salt-losing" congenital adrenal hyperplasia. 429 11

The molecular forms of acetylcholinesterase in extracts of gastrocnemius muscle from four vertebrate species and in electric eel (Electrophorus) electric organ were separated and identified by low-salt precipitation and velocity sedimentation. The activity of the heavy insoluble (A12) form of human muscle acetylcholinesterase was inhibited by synthetic human beta-endorphin (500 mM). The homologous form in rat muscle extracts was poorly inhibited by human beta-endorphin at the same concentration, but was more effectively inhibited by camel beta-endorphin. The activities of heavy forms of pseudocholinesterase, present in small amounts in both species, were not reduced by beta-endorphin. Selective inhibition of homologous heavy forms of acetylcholinesterase activity by camel and human beta-endorphin was also seen in skeletal muscle extracts from frog and pigeon, but with decreased effectiveness. No inhibition was detectable in the heavy acetylcholinesterase form from extracts of electric organ tissue of the electric eel. The inhibition of heavy acetylcholinesterase activity in human muscle by human beta-endorphin was dependent on the presence of its NH2-terminal pentapeptide sequence. Maximal inhibitory potency depended on the presence of the entire amino acid sequence, since potency was considerably reduced in synthetic peptide analogues lacking either middle or COOH-terminal segments of beta-endorphin. The relative potency of beta-endorphin from various species as inhibitors of rat heavy acetylcholinesterase activity was also investigated. beta-Endorphin sequences most closely resembling that of the rat peptide (camel, equine) were most potent, whereas those with sequence differences of more than one amino-acid were less potent (turkey, human) or had no inhibitory activity (ostrich). The selective inhibition of heavy acetylcholinesterase by beta-endorphin thus exhibits species specificity, even among mammals, in which homologues of this molecular form of the enzyme are otherwise indistinguishable.
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PMID:Structural requirements and species specificity of the inhibition by beta-endorphin of heavy acetylcholinesterase from vertebrate skeletal muscle. 608 17

Thyropin binding to high affinity receptors on human and porcine membranes was studied at pH 7.4, 37 degrees C, in 10 mM Tris-HCl, 150 mM NaCl, 0.1% albumin. By preincubating the membranes in high salt concentration before binding studies, the number of high affinity receptors could be increased 4- to 8-fold. The salt-induced exposure of high affinity TSH receptors was pH- and temperature-dependent and was maximal at pH 5.0, 37 degrees C in the presence of 1 M (NH4)2SO4. Other salts tested, including NaCl, HN4Cl, and Na2SO4, were also able to increase high affinity THS binding. The receptors exposed by salt were indistinguishable from those present on the membranes before such treatment. They had an affinity constant of 0.5 to 1 X 10(10 M-1, and a high TSH specificity with no inhibition of 125I-TSH binding in the presence of a thousandfold excess of gamma-globulin, thyroglobulin, corticotropin, cholera toxin, and gangliosides. Thyrotropin binding to low affinity TSH binding sites (affinity constant 1 to 3 X 10(7) M-1) measured at pH 6.0, 4 degrees C in 10 mM Tris/acetate, 0.1% albumin was unaltered by pre-exposure of membranes to high salt concentrations. These receptors had low TSH specificity and binding was inhibited by gamma-globulin, thyroglobulin, cholera toxin, and gangliosides. The salt-induced selective exposure of high affinity receptors with unaltered number of low affinity sites is further support for the existence of two separate TSH binding sites on thyroid membranes.
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PMID:Salt-induced exposure of high affinity thyrotropin receptors on human and porcine thyroid membranes. 625 Oct 45

We describe a premature female infant exposed in utero to danazol during the first trimester of pregnancy. She was first observed in the newborn period with marked degree virilization and clinical findings suggestive of salt-losing congenital adrenal hyperplasia. This was supported by the high plasma levels of 17 alpha-hydroxyprogesterone and adrenocorticotropic hormone and low plasma cortisol level. Levels of testosterone, androstenedione, 11-deoxycortisol, and renin were also elevated. An excessive increase in the levels of 17 alpha-hydroxyprogesterone and 11-deoxycortisol to corticotropin administration associated with impaired increase in plasma cortisol level strongly suggests a partial block in the 21-hydroxylation of 17 alpha-hydroxyprogesterone. However, the high levels of 11-deoxycortisol also suggest a block of the steroid 11 beta-monooxygenase. A year later she was found to have normal basal levels of the adrenal steroids and normal response to corticotropin administration, pointing out the transitory nature of these abnormalities. It may be hypothesized that danazol produced a transitory block of the steroid 21- and 11 beta-monooxygenases in this child.
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PMID:Transient adrenogenital syndrome due to exposure to danazol in utero. 627 Oct 10

A histological and ultrastructural study has demonstrated that cutaneous pigmentation in primary biliary cirrhosis (PBC) is due to the presence of increased amounts of melanin, widely dispersed throughout both epidermis and dermis. No deposits of stainable iron were observed. Compared with skin from matched sites from control patients with alcoholic cirrhosis and no pigmentation, the melanocyte: keratinocyte ratio was not significantly higher in PBC. However, in PBC, melanosomes persisted to unusually high levels in the epidermis and were packaged in larger membrane-bound clusters than was the case in the controls. Whether excess melanin results from increased melanogenesis or defective melanin degradation remains unclear, although there is some evidence favouring the latter mechanism. No hormonal (beta-MSH and ACTH) or chemical (bile salt irritation) stimuli to increase melanogenesis were demonstrated.
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PMID:Melanin pigmentation of the skin in primary biliary cirrhosis. 627 1


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