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 effect of calcium and magnesium supplementation and the role of opioidergic system was examined in deoxycorticosterone acetate (DOCA)-salt hypertensive rats. The rats were divided into four groups receiving standard laboratory rat diet (control group; n = 9); a calcium-rich diet with 2% CaCl2 added (Ca-group; n = 12); a magnesium-rich diet with 0.5% MgO added (Mg-group; n = 11); and a calcium and magnesium-rich diet with 2% CaCl2 and 0.5% MgO added (Ca/Mg-group; n = 11); each diet contained 7% NaCl. After four weeks on these diets, the rats were decapitated and blood was obtained for the measurement of plasma electrolytes, intraerythrocyte sodium, potassium and magnesium content (RBC-Na, -K, in mEq/L cells and RBC-Mg, in mg/dL cells) and plasma beta-endorphin concentration (beta-END, in pg/mL). In the control group, systolic blood pressure and RBC-Na were obviously higher than in the other groups. Plasma beta-endorphin concentration was 45.1 +/- 13.4 in the control group, 70.7 +/- 17.4 in the Ca-group (P less than .05 v control group), 58.0 +/- 20.1 in the Mg-group and 83.8 +/- 24.8 in the Ca/Mg-group (P less than .01 v control group). The blood pressure correlated significantly with both RBC-Na (r = 0.416, P less than .01) and beta-END (r = 0.436, P less than .005). A negative correlation was also observed between RBC-Na and beta-END (r = 0.437, P less than .005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of Ca and Mg supplementation and the role of the opioidergic system on the development of DOCA-salt hypertension. 200 1

1. Aggregating fetal rat brain cells express a significant amount of proenkephalin A (PENK) mRNA, a selective radioimmunoassay shows that this mRNA is also translated into enkephalins. 2. Depolarization with potassium chloride (KCl) or veratridine increases the expression of PENK mRNA in a time-dependent fashion, with a maximal increase of sixfold. It is interesting, however, that depolarization of the same cultures with KCl has no effect on the expression of prodynorphin mRNA. 3. An increase in PENK mRNA levels has been also observed in cultures treated with 8-Br-cAMP, phorbol 12-myristate-13-acetate (TPA), or dexamethasone. 4. However, incubation of the cultures with the opioid agonist etorphine or the antagonist naltrexone did not alter PENK gene expression, suggesting that there is not feedback control of opioids on PENK biosynthesis in these cells. 5. The increase in PENK mRNA in depolarized and in TPA-dexamethasone-, or 8-Br-cAMP-treated cultures was not accompanied by a significant increase in the amount of free immunoreactive met-enkephalin. Fetal brain cell cultures are therefore a useful neuronal model system for studying the mechanism that regulated the expression of PENK mRNA.
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PMID:Regulation of proenkephalin A gene expression in aggregating fetal rat brain cells. 202 27

To determine the neurosecretory activity of hypothalamic beta-endorphin (beta EP)-containing neurons, rat fetal hypothalamic cells were mechanically dispersed and maintained in primary cultures for periods up to 24 days; their electrophysiological properties and regulation by depolarization, calcium and sodium channel-active agents were studied. Under culture conditions, the majority of the cells were immunopositive to neurofilament antibody, and a significant number (7-10%) were reactive to beta EP antibody. Cultured cells were often electrically excitable and possessed voltage-activated ionic conductances. In culture, there was a progressive increase in immunoreactive beta EP (IR-beta EP) in both cells and media, reaching maximum values at 12-16 days. The majority of IR-beta EP in both cells and media corresponded to [125I]beta EP on gel chromatography and was similar to the form previously found in the hypothalamus. These findings suggest viability of the beta EP neurons and continuing synthesis of IR-beta EP during the culture period. To evaluate the influence of membrane depolarization on IR-beta EP release, the cells were challenged with 56 mM potassium. This treatment induced a significant increase in medium IR-beta EP. The depolarization-induced IR-beta EP release was dependent upon calcium, since a calcium channel blocker, verapamil (0.1 microM), prevented the release; also a calcium ionophore, A23187 (1 microM), stimulated IR-beta EP release in the cultures. Activation of the sodium channel by veratridine (100 microM) also increased the medium content of IR-beta EP, and this effect was blocked by tetrodotoxin (1 microM). These results suggest that the beta EP neurons in primary culture respond to the well defined physiological challenges and that the culture system can be used in determining the regulation of hypothalamic beta EP activity.
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PMID:Characterization of the neurosecretory activity of hypothalamic beta-endorphin-containing neurons in primary culture. 213 25

In the present studies the direct effect of ethanol on the release of beta-endorphin by the rat hypothalamus was investigated. When various concentrations of ethanol (10-120 mM) were added into the incubation medium, it was noticed that though low concentrations of ethanol (10, 20 and 30 mM) induced a pronounced increase in the release of beta-endorphin-like peptides from the hypothalamus, high concentrations of ethanol (40, 60 and 120 mM) induced a less pronounced increase. Exposure of hypothalamus to depolarizing concentrations of potassium chloride (following washing of the ethanol), provoked a significant release of beta-endorphin-like peptides, regardless of the ethanol concentration the tissues were exposed prior to the stimulation with the potassium chloride. Chromatographic analysis of the incubation media with Sephadex-G-75 revealed that the hypothalamus released mainly beta-endorphin-sized peptides. Analysis of the beta-endorphin-sized peptides with reverse-phase high performance liquid chromatography indicated the presence of beta-endorphin-(1-31) as well as non-acetyl and acetyl beta-endorphin-(1-27). Thus ethanol exerts a biphasic effect on the release of beta-endorphin-like peptides by the rat hypothalamus, with low concentrations inducing a dose-dependent increase, reaching maximum at 20 mM ethanol, and with higher concentrations of ethanol inducing a less pronounced increase in the release of beta-endorphin-like peptides, leading to an inverted U-shaped dose response relationship of ethanol and release of beta-endorphin-like peptides from the rat hypothalamus.
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PMID:Characterization of the effects of acute ethanol administration on the release of beta-endorphin peptides by the rat hypothalamus. 214 93

Atrial natriuretic peptide (ANP) has been identified in the central nervous system and its participation in regulation of various regulatory brain functions has been postulated. To elucidate whether central ANP influences endocrine systems related to blood pressure regulation and renal excretory functions, effects of infusion of ANP at a rate of 120 ng.min-1 into the third cerebral ventricle on plasma level of epinephrine (E), norepinephrine (NE), renin, vasopressin and beta-endorphin as well as on excretion of urine, sodium, potassium (UKV) solutes and free water (CH2O) were investigated in conscious dogs. Significant decrease of plasma E from 77.6 +/- 7.0 to 62.1 +/- 4.8 pg.ml-1 and of NE from 345.5 +/- 20.7 to 286.4 +/- 15.0 pg.ml-1 was found at the end of 30 min lasting ANP infusion. Significant elevation of PRA and UKV and a decrease in CH2O were found 60 min after ANP infusion. No significant changes in other variables were found. In time control experiments plasma hormones concentration and renal excretory functions were not significantly influenced. The results suggest that central ANP may affect the sympatho-adrenal outflow.
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PMID:Central effects of atrial natriuretic peptide on plasma catecholamines, vasopressin, renin and beta-endorphin and on renal excretory functions in the dog. 214 67

To examine the effect of platelet-activating factor (PAF-acether) on pro-opiomelanocortin (POMC)-related peptides and on the hypothalamo-pituitary-adrenal axis, we administered PAF-acether and BN 52021, a selective PAF-acether antagonist, to freely moving rats. Minipumps loaded with either PAF-acether (30 micrograms/kg) or the vehicle alone were connected to the jugular vein for 7 days and positioned under the back skin of rats. A group of animals treated with PAF-acether also received 15 mg/kg of BN 52021 orally twice a day. In vivo treatment with PAF-acether alone or in association with BN 52021 did not affect the hypothalamic concentrations of corticotropin-releasing factor (CRF), alpha-melanocyte-stimulating hormone (alpha-MSH) and beta-endorphin. Using a perifusion system for rat hypothalamic slices, we did not observe any effect of PAF-acether on spontaneous or potassium-induced release of alpha-MSH in vitro. In addition, treatment of rats with PAF-acether alone or in association with BN 52021 did not modify the alpha-MSH or beta-endorphin concentration in the neurointermediate lobe of the pituitary. In contrast, in vivo administration of PAF-acether caused a significant reduction of ACTH concentration in the anterior lobe of the pituitary and a marked decrease in the corticosterone level in plasma and adrenal glands. The inhibitory effect of PAF-acether was reversed by concomitant administration of BN 52021. The ineffectiveness of PAF-acether to modulate in vitro ACTH release from perifused anterior pituitary fragments ruled out a direct effect of PAF-acether on corticotrophs. These findings support the view that PAF-acether exerts a specific inhibitory effect on the hypothalamo-pituitary-adrenal axis.
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PMID:Effect of platelet-activating factor on hypothalamic and hypophyseal pro-opiomelanocortin-related peptides and hypothalamo-pituitary-adrenal axis in the rat. 215 5

In a review of 74 autopsy cases of acquired immune deficiency syndrome (AIDS), the incidence of cytomegalovirus (CMV) infection was found in 50% (37 cases). Of these 37 cases the adrenal glands were affected by CMV in 84%. The authors analyzed the histologic features of 30 of these 37 cases of CMV adrenalitis by grading the CMV inclusions, inflammation and necrosis (CMV score), focal versus diffuse involvement, and the degree of fibrosis (fibrosis score). The clinical data were not significant except for sodium to potassium ratio (Na:K), which was less than 30 in 11 cases. Focal CMV adrenalitis had low CMV and fibrosis scores and Na:K ratio higher than 30, whereas diffuse adrenalitis had high CMV and fibrosis scores and Na:K ratio less than 30. Adrenocorticotropic hormone (ACTH) stimulation tests performed in three patients revealed normal or elevated baseline cortisol levels with a blunted response after stimulation. The authors conclude that the adrenal gland is the most frequently affected organ in AIDS with CMV infection. ACTH tests on a larger number of selected cases of AIDS are needed for further evaluation of functional status of adrenal glands. Selection criteria for the test should include evidence of CMV infection from any site and a low Na:K ratio.
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PMID:Cytomegaloviral adrenalitis and adrenal insufficiency in AIDS. 216 75

The neuropeptide alpha-melanocyte-stimulating hormone (alpha-MSH) is synthesized by discrete populations of hypothalamic neurons which project in different brain regions including the cerebral cortex, hippocampus and amygdala nuclei. The purpose of the present study was to identify the alpha-MSH-immunoreactive species contained in these different structures and to compare the ionic mechanisms underlaying alpha-MSH release at the proximal and distal levels, i.e. within the hypothalamus and amygdala nuclei, respectively. The molecular forms of alpha-MSH-related peptides stored in discrete areas of the brain were characterized by combining high-performance liquid chromatography (HPLC) separation and radioimmunoassay detection. In mediobasal and dorsolateral hypothalamic extracts, HPLC analysis confirmed the existence of a major immunoreactive peak which co-eluted with the synthetic des-N alpha-acetyl alpha-MSH standard. In contrast, 3 distinct forms of immunoreactive alpha-MSH, which exhibited the same retention times as synthetic des-, mono- and di-acetyl alpha-MSH, were resolved in amygdala nuclei, hippocampus, cortex and medulla oblongata extracts. The proportions of acetylated alpha-MSH (authentic alpha-MSH plus diacetyl alpha-MSH) contained in these extrahypothalamic structures were, respectively, 78, 80, 60 and 92% of the total alpha-MSH immunoreactivity. In order to compare the ionic mechanisms underlaying alpha-MSH release from hypothalamic and extrahypothalamic tissues, we have investigated in vitro the secretion of alpha-MSH by perifused slices of hypothalamus and amygdala nuclei. High potassium concentrations induced a marked increase of alpha-MSH release from both tissue preparations. However, a higher concentration of KCl was required to obtain maximal stimulation of amygdala nuclei (90 mM) than hypothalamic tissue (50 mM).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Characterization of alpha-melanocyte-stimulating hormone (alpha-MSH)-like peptides in discrete regions of the rat brain. In vitro release of alpha-MSH from perifused hypothalamus and amygdala. 216

The aim of this study was to investigate the pathogenesis of hypoaldosteronism in diabetes. Endogenous elevation of plasma renin activity and exogenous corticotropin were used to study steroidogenesis. Observations were made over 12 yr on the evolution and treatment of hyperkalemia in a diabetic subject. In 1977, potassium, baseline cortisol, aldosterone, and renin activity were normal; renin activity increased normally with posture; and cortisol responded normally to ACTH infusion. Nine yr later, persistent hyperkalemia was documented. Upright renin activity was elevated to 5.26 ng.L-1.s-1, with concomitant elevation of 18-hydroxycorticosterone (18-OHB) and a low-normal aldosterone level. One hour after administration of 0.25 mg i.m. cosyntropin, cortisol increased normally, aldosterone increased from 220 to 360 pM, and 18-OHB increased from 3700 to 4800 pM. During treatment with fludrocortisone, fludrocortisone with furosemide, and furosemide alone, improvement of hyperkalemia was noted. Endogenous hyperreninemia and basal elevations of 18-OHB, accompanied by limited aldosterone responsiveness to renin and ACTH, suggest the presence of a partial corticosterone methyl oxidase type II defect. Evolution of hyperkalemia between 1977 and 1986 suggests this defect was acquired.
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PMID:Acquired partial corticosterone methyl oxidase type II defect in diabetes mellitus. Case of hyperreninemic hypoaldosteronism. 216 93

To characterize the effect of ethanol on the hypothalamic beta-endorphin-containing neurons, rat fetal hypothalamic neurons were maintained in primary culture, and the secretion of beta-endorphin (beta-EP) was determined after ethanol challenges. Constant exposure to ethanol at doses of 6-50 mM produced a dose-dependent increase in basal secretion of beta-EP from these cultured cells. These doses of ethanol did not produce any significant effect on cell viability, DNA or protein content. The stimulated secretion of beta-EP following constant ethanol exposure is short-lasting. However, intermittent ethanol exposures maintained the ethanol stimulatory action on beta-EP secretion for a longer time. The magnitude of the beta-EP response to 50 mM ethanol is similar to that of the beta-EP response to 56 mM of potassium. Ethanol-stimulated beta-EP secretion required extracellular calcium and was blocked by a calcium channel blocker; a sodium channel blocker did not affect ethanol-stimulated secretion. These results suggest that the neuron culture system is a useful model for studying the cellular mechanisms involved in the ethanol-regulated hypothalamic opioid secretion.
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PMID:Effect of acute ethanol on beta-endorphin secretion from rat fetal hypothalamic neurons in primary cultures. 221 79


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