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)

Male and female, nonarteriosclerotic (virgin) and arteriosclerotic (breeder), Sprague-Dawley rats were subjected to the hypertension-producing regimen of uninephrectomy, 1% saline drinking water, and desoxycorticosterone (Percorten) pivalate. Just before autopsy, some of the animals were given a single injection of corticotropin. The acute challenge of corticotropin caused a definite increase in free fatty acids, systolic blood pressure, creatine phosphokinase, glucose, and corticosterone. The two weeks of desoxycorticosterone and 1% saline-induced hypertension caused myocarditis and hyalinization of the coronary arteries of the nonarteriosclerotic (virgin) rats and definite exacerbation of the preexisting arteriosclerosis in breeder rats, severe myocarditis, and polyarteritis nodosa. All of the treated animals manifested lipid depletion of the zona glomerulosa indicative of reduced biosynthesis and secretion of endogenous mineralocorticoids due to the exogenous desoxycorticosterone and saline treatment.
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PMID:Corticotropin stimulation of hypertensive rats with and without arteriosclerosis. 21 53

Two experiments were carried out in which a total of 602 pigs were slaughtered after being held in lairage for periods ranging from less than one hour to 21 hours. In the first experiment the pigs were handled under ideal conditions and slaughtered at the University of Bristol slaughterhouse; in the second the pigs were killed at a commercial plant. Blood samples collected at exsanguination were analysed for indices of stress. There were no consistent effects of time in lairage on the levels of lactate and creatine phosphokinase. Plasma cortisol and beta-endorphin levels were reduced by lairage for three hours or more in the first experiment and cortisol was reduced by lairage for two hours or more in the second; beta-endorphin was not measured in the second experiment. A period of rest in lairage allowed the pigs to recover from transport and the associated handling and the recovery appeared to be complete within two to three hours.
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PMID:Time in lairage needed by pigs to recover from the stress of transport. 144 Nov 75

The effect of differences in sympathoadrenomedullary and pituitary-adrenocortical responses of individual animals to 35% hemorrhage on severity of shock induction has been studied in unanesthetized unrestrained rats by measuring plasma concentrations of adrenaline (A), noradrenaline (NA), corticosterone (CS) and adrenocorticotropin (ACTH). The responses of A, CS and ACTH were related to the decrease of blood volume and mean arterial pressure (MAP), whereas plasma NA remained unchanged. Higher susceptibility to blood loss was characterized by more pronounced hemorrhage-induced increase in blood lactate concentration and plasma enzyme activities as well as lethal outcome of hemorrhagic shock. In animals with irreversible hemorrhagic shock, enhanced catecholamine secretion and reduced ACTH release was observed. Furthermore, a revealed direct correlation between A and blood lactate concentration and plasma enzyme activities (aspartate aminotransferase, isocitric dehydrogenase, creatine kinase, lipase and glutathione-S-transferase) may indicate its possible participation in the mechanism of shock induction. In contrast, an inverse relationship of plasma CS to the indicators of shock severity was demonstrated. In conclusion, non-optimal neuroendocrine regulation of cardiovascular adjustments to hemorrhage in shock-prone animals might cause an exaggerated compensatory activation of adrenomedullary catecholamine secretion, which in turn has been shown to exert deleterious vascular and metabolic effects. The mechanisms responsible for reduced ACTH secretion in shock-prone animals remain to be established.
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PMID:Hormonal responses to hemorrhage and their relationship to individual hemorrhagic shock susceptibility. 216 2

Changes in the blood and the behaviour of 14 growing pigs from 4 different litters were evaluated under different experimental conditions of blood sampling, grouping and adrenal stimulation. The results showed that the different techniques of blood sampling influenced lactic dehydrogenase (LDH) and creatine kinase (CK) activities. Cortisol, proteins and CK levels were negatively correlated with social hierarchy after regrouping. Cortisol was also correlated with total activity levels. Adrenal stimulation by adrenocorticotropic hormone (ACTH) administration caused a sharp increase in plasma cortisol levels. However, plasma glucose, plasma proteins and total leukocyte counts were not affected by the ACTH treatment.
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PMID:Effects of blood sampling procedures, grouping and adrenal stimulation on stress responses in the growing pig. 253 97

S-100 protein in clonal GA-1 and C6 rat glioma cell lines was released in serum-free medium supplemented with adrenocorticotropic hormone (ACTH). The induction of S-100 protein release by ACTH was dose-dependent, showing a half-maximal release at about 5 microM, and the S-100 protein concentration in the medium increased sharply within 3 min, but slightly during further incubation. The S-100 protein release was apparently accompanied by a decrease in the membrane-bound form of S-100 protein in the cell. The S-100 protein release was induced not by the ACTH1-24 fragment, which exhibits the known effects of ACTH, but by the ACTH18-39 fragment, which is designated as corticotropin-like intermediate-lobe peptide (CLIP). These results indicate that the C-terminal half of ACTH is responsible for the S-100 protein release. The enhancement of S-100 protein release by ACTH was also observed in normal rat glioblasts. The release induced by ACTH was apparently specific to S-100 protein, because little release of the cytoplasmic enzymes, creatine kinase, and enolase was observed under the same conditions. High concentrations (5 mM) of dibutyryl cyclic AMP or dibutyryl cyclic GMP were also found to induce S-100 protein release; however, catecholamines (epinephrine, norepinephrine, isoproterenol, and dopamine), acetylcholine, and glutamic acid did not enhance the release.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:S-100 protein in clonal astroglioma cells is released by adrenocorticotropic hormone and corticotropin-like intermediate-lobe peptide. 282 56

In a 19 yr old male with familial hyperkalemic periodic paralysis, paralysis was consistently induced by the administration of potassium chloride, corticotropin-gel, and a variety of glucocorticoids (dexamethasone, 6-methylprednisolone, triamcinolone) but not by mineralocorticoids (D-aldosterone, deoxycorticosterone) or by adrenocorticotropin (ACTH)-gel plus metyrapone. Induced attacks were virtually identical with spontaneous attacks, being associated, after a latent period of a few hours, with a rise in plasma K(+) and HCO(3) (-) and a simultaneous fall in plasma Na(+) and Cl(-) concentrations to an extent implying exchange of 1 K(+) with 2 Na(+) and 2 Cl(-) between extracellular and intracellular fluid. ACTH-induced paralysis was preceded by rising serum inorganic P, and associated with increased plasma glucose, blood lactate, and serum creatine phosphokinase concentrations. In normal subjects ACTH, cortisol, and triamcinolone administration failed to change plasma electrolytes or strength, while ingestion of KCl produced no weakness and smaller changes in plasma K and Na than in the patient.Since the patient and normal subjects showed the same changes in renal excretion of K after the administration of cortisol and KCl, it seems likely that paralysis in the patient resulted from abnormally slow uptake (and/or excessive loss) of K by the muscle cells, possibly caused by an abnormal "ion-exchange pump." Normal adrenocortical function and absence of a peak in plasma 11-hydroxycorticoid (11-OHCS) concentration preceding spontaneous paralysis, indicated that spontaneous paralysis did not result from changes in cortisol secretion. Similar hyperkalemic paralysis was precipitated by ACTH-gel in a brother and first cousin of the propositus. Administration of acetazolamide and fludrocortisone reduced the rise in plasma K concentration and prevented the weakness which otherwise invariably followed KCl administration to the patient. He and two close relatives have been completely protected from severe attacks of paralysis in the past 14 months by treatment with these two medications.
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PMID:Studies on hyperkalemic periodic paralysis. Evidence of changes in plasma Na and Cl and induction of paralysis by adrenal glucocorticoids. 432 66

The effects of a 1-h whole body massage on blood parameters were studied in nine healthy male volunteers. The venous blood samples were drawn just before treatment, immediately after, and after 2, 24, and 48 h. The parameters measured were blood leukocyte and erythrocyte counts, hemoglobin concentration, hematocrit, red cell indices, the activities of serum creatine kinase, lactate dehydrogenase and their isoenzymes, and the concentrations of serum sodium, potassium, total protein, haptoglobin, growth hormone, prolactin, cortisol, and plasma corticotropin. Decreases in serum haptoglobin concentrations suggested slight hemolysis. The rises in the activities of creatine kinase, lactate dehydrogenase, and its isoenzymes LDH4 and LDH5 and in the concentrations of serum potassium are indicative of increased permeability of the muscle cells. No statistically significant changes were seen for the other parameters. There were large individual variabilities in the hormone concentrations after massage, but some trends could be seen.
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PMID:Effects of whole body massage on serum protein, electrolyte and hormone concentrations, enzyme activities, and hematological parameters. 665 54

We studied a 23-year-old man with lipid storage myopathy. Five members of his family had hyperlipoproteinemia, and his consanguineous parents had elevated serum creatine kinase levels, although only the father showed clinical evidence of myopathy. The patient's intramuscular carnitine content was slightly reduced, but the reduction was not significant compared with the average value for reported cases with carnitine deficiency. Urinary excretion of carnitine showed good responses to starvation, long-chain fatty acid loading, and corticotropin administration. Therefore, his carnitine metabolism was normal. Administration of corticotropin or carnitine did not bring about any improvement of the symptoms. A connection between lipid storage myopathy and hyperlipoproteinemia was suggested.
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PMID:Lipid storage myopathy in familial hyperlipoproteinemia. 672 23

There is substantial evidence that cardiac opioid receptors are activated during arrhythmias induced by administration of opioid peptides or myocardial ischemia, supporting the hypothesis that endogenous opioid peptides (EOP) are involved in myocardial infarction. This prospective clinical trial is designed to determine whether the ischemia-induced arrhythmias and extent of the infarct are related to the release of the EOP beta-endorphin in patients with acute myocardial infarction. Two groups were included in the study, patients with acute myocardial infarction, and healthy volunteers who served as controls. The results indicate that, compared to the controls, there was augmentation of ischemic arrhythmias and ischemic damage as assessed by serum creatine kinase activity, accompanied by an elevated level of beta-endorphin, in patients with acute myocardial infarction. The above data strongly indicate that EOP are indeed involved in the pathophysiology of myocardial infarction, and suggest these peptides have an important role in ischemic heart disease.
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PMID:Plasma levels of endogenous opioid peptides in patients with acute myocardial infarction. 747 58

The pro-opiomelanocortin-derived peptides beta-endorphin (beta-EP) and alpha-melanocortin (alpha-MSH) were administered to normal and dystrophic C57BL6J mice. All groups of normal and dystrophic mice which had been treated with the two peptides gained significant body weight, as did the normal and dystrophic saline-treated male controls, but the normal and dystrophic female controls did not. The plasma activity of creatine phosphokinase (CPK) was lower in normal mice and dystrophic males which had been treated with the two peptides compared to the corresponding controls. There was no significant difference between the plasma LDH activity in any of the peptide-treated and the corresponding control groups. The activity of CPK was significantly higher in the extensor digitorum longus (EDL) muscles, but not the soleus muscles, of the peptide-treated dystrophic mice compared to the corresponding controls. Administration of alpha-MSH alone or beta-EP alone had no significant effect on the body weight or plasma CPK activity of dystrophic mice compared to the controls. However the activity of CPK was significantly higher in the EDL muscles of the alpha-MSH-treated mice than in the corresponding controls. It is possible that beta-EP and alpha-MSH act synergistically on the neuromuscular system to protect the muscles from damage.
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PMID:Effect of beta-endorphin and alpha-melanotropin on muscle wasting in mice. 759 3


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