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 interaction of beta-endorphin with opiate receptors was studied by using the radioiodinated, metabolically stable D-Ala2 derivative of human beta-endorphin. This analog binds specifically to rat brain membrane preparations with an apparent Kd of about 2.5 x 10-9 M. The ability of various enkephalin analogs, as well as opiate agonists and antagonists, to inhibit the binding of beta-endorphin clearly demonstrates that this peptide can bind to opiate receptors. However, the effects of various cations on the binding of 125I-[D-Ala2]beta-endorphin are markedly different from those found for enkephalin binding. Sodium ion at physiological concentrations decreases substantially the binding of enkephalins but only slightly decreases endorphin binding, whereas manganese enhances enkephalin binding but has no effect on endorphin binding. Moreover, potassium (100 mM) decreases the binding of beta-endorphin but does not affect enkephalin binding. These results suggest that beta-endorphin and enkephalin bind differently to the same receptor or bind to different receptors with overlapping specificity.
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PMID:Interaction of iodinated human [D-Ala2]beta-endorphin with opitate receptors. 21 69

Sodium and water intake and excretion of wild rabbits was studied during intracerebroventricular (icv) infusion of corticotropin-releasing factor (CRF). Icv infusion of 200 and 600 pmol/h for 22 h induced changes in the ingestive and general behavior of animals. Increased consumption of 0.5 M NaCl solution was observed during the day of infusion, accompanied by increased sodium excretion, and food intake was decreased. The rabbits maintained the high sodium turnover, together with a high water turnover, for 2-3 days after the icv infusion stopped. Icv infusion of CRF induced strange behaviour in wild rabbits, they appeared to react with fright to normal daily events around them. The strange behaviour started about two hours after the beginning of icv infusion and disappeared immediately after the infusion stopped. On the basis of present and earlier observations, that systemic administration of adrenocorticotropin (ACTH) and adrenal steroid hormones induce increased sodium turnover, it is proposed that changes in the sodium and water metabolism might constitute part of the general stress reaction of the body.
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PMID:Corticotropin-releasing factor enhances sodium and water intake/excretion in rabbits. 202 32

Pituitary cells were shown to release corticotropin (ACTH) in response to interleukin-2 (IL-2) and to express a protein that is related to the alpha-chain of the IL-2 receptor (IL-2R). The alpha-chain-like molecule was bound by a rat monoclonal antibody to the murine IL-2 receptor as well as to IL-2. Sodium dodecylsulfate-polyacrylamide gel electrophoretic analysis of the affinity-purified material from pituitary cells demonstrated a protein which was similar to that which was isolated from activated splenocytes. Thus, IL-2 and its receptor may be one of several hormone-receptor pairs utilized by both the immune and neuroendocrine systems for intersystem communication.
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PMID:Interleukin-2 induction of ACTH secretion: presence of an interleukin-2 receptor alpha-chain-like molecule on pituitary cells. 253 95

Sodium uptake by rat adrenal glomerulosa cells was stimulated by intracellular acidosis evoked by Na+-propionate. This process was inhibited by 5-(N,N-hexamethylene) amiloride (HMA), a known inhibitor of the Na+-H+ exchange. These experiments demonstrate the existence of the Na+-H+ exchange in glomerulosa cells. Although amiloride inhibited the angiotensin II- and adrenocorticotropic hormone (ACTH)-induced aldosterone response, HMA, a more specific inhibitor of Na+-H+ exchange, failed to do that. 45Ca2+ influx and efflux were dependent on intra- and extracellular Na+ concentrations. Amiloride analogues, known to inhibit Na+-Ca2+ exchange, reduced basal 45Ca influx. Although we could not reveal the activation of Na+-Ca2+ exchange by angiotensin II, inhibitors of Na+-Ca2+ exchange also inhibited the angiotensin- and ACTH-induced aldosterone response of glomerulosa cells. Our results suggest that Na+-Ca2+ exchange supports the maintenance of basal Ca2+ level in the cytoplasma of glomerulosa cells, and amiloride derivatives inhibit aldosterone production by reducing Ca2+ level below resting values.
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PMID:Na+-H+ and Na+-Ca2+ exchange in glomerulosa cells: possible role in control of aldosterone production. 283 93

This study reviews the effects of intracerebroventricular (i.c.v.) infusion of corticotrophin releasing factor (CRF) and adrenocorticotrophic hormone (ACTH) (1-24) on blood pressure in conscious sheep. The effects of sauvagine, a peptide with 50% homology with CRF and ACTH (4-10) and other analogues of ACTH were studied. Intracerebroventricular infusion of CRF for 24 h at 10 and 100 micrograms/h increased blood pressure and heart rate. Sodium (Na) excretion also increased. Sauvagine at 10 micrograms/h also increased blood pressure. Both peptides raised body temperature and produced 'arousal' behaviour. ACTH (1-24) at 0.8 microgram/h for 48 h raised blood pressure and body temperature but had no significant effect on Na excretion or behavior. ACTH (4-10) and other related analogs (alpha-MSH, alpha gamma 1-MSH) at up to 10 micrograms/h for 48 h had no effects. These studies show that neuropeptides involved in the physiological response to 'stress' may have central effects on blood pressure.
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PMID:The effect of intracerebroventricular infusions of CRF, sauvagine, ACTH (1-24) and ACTH (4-10) on blood pressure in sheep. 610 Jul 57

The interaction of human beta-endorphin with binding sites in rabbit spinal cord has been characterized. The stereospecific high-affinity binding sites are concentrated in the dorsal half of the spinal cord. Scatchard analysis of the binding data shows heterogeneity of the binding sites that can be resolved into two populations with apparent dissociation constants of 3.0 (+/-2.0) X 10(-10) and 3.3 (+/- 0.5) X 10(-9) M. Sodium ions decrease the binding of human beta-endorphin to spinal cord to the same extent as found in rat brain. The ability of several opiates and opioid peptides to inhibit the binding of human beta-endorphin is also presented.
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PMID:beta-Endorphin: characteristics of binding sites in rabbit spinal cord. 625 63

Six naturally occurring homologs of beta-endorphin were tested for their potency in inhibiting the binding of [3H]naloxone and [3H]-beta h-endorphin either in the presence or in the absence of Na+. Sodium ion reduces inhibitory potency of these homologs against [3H]-beta h-endorphin and [3H]naloxone to about the same extent. The ratio of the IC50 obtained with Na+ to that obtained without Na+ is not highly correlated with analgesic potency. Very high (greater than 300) sodium ratios are observed with some homologs. A significant rank correlation was found between the ratio of the relative potency in displacing [3H]beta h-endorphin to the relative potency in analgesia and potency in inhibiting the binding of the pure antagonist naloxone.
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PMID:Beta-endorphin: opiate receptor binding activities of six naturally occurring beta-endorphin homologs studied by using tritiated human hormone and naloxone as primary ligands--effects of sodium ion. 628 71

The established human glioblastoma cell line SF126 was found to bind tritiated human beta-endorphin (beta h-EP) in a saturable fashion. From displacement studies, the ED50 was estimated to be about 2.5 nM. The Kd was estimated as 1.9 X 10(-9) M and Scatchard analysis showed a biphasic pattern with a predominant low-affinity component. Binding reached a maximum at about 90 min at 22 degrees C and was instantaneously reversible. Tritiated [D-Ala2,D-Leu5]enkephalin and tritiated dihydromorphine did not bind to the cells. Sodium at a concentration of 150 mM decreased the specific binding by 80%. The interaction with the cellular binding site appeared to be mediated by the COOH-terminal segment of beta h-EP, as beta h-EP-(6-31) retained a high potency for displacing tritiated beta h-EP, and beta h-EP-(1-27) has no activity. Camel beta-EP was only about 1% as active as the human hormone.
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PMID:beta-Endorphin: characterization of binding sites specific for the human hormone in human glioblastoma SF126 cells. 632 53

Sodium is an essential nutrient for life, and its level in the body is tightly regulated. When sodium deficient, some mammals alter their behavior towards salt by avidly consuming it, even at concentrations animals typically choose to avoid. This change in acceptance is accompanied by a reduction in the response of the gustatory chorda tympani nerve to sodium solutions. More specifically, the response rate of the sodium-specialist units to NaCl stimulation is reduced following sodium deficiency or adrenalectomy. The initial transduction of the chemical signal is mediated, in part, by Na+ influx through epithelial Na+ channels in the apical membrane of taste cells that synapse with the specialist neurons. Circulating hormones like angiotensin II and adrenocorticotropin hormone, which are released in response to sodium deficiency and adrenalectomy, could regulate the activity of Na+ channels through G-protein linked second-messenger systems. These putative pathways are of interest because they have been described in mammalian taste receptor cells. The present review will summarize evidence linking some hormones of fluid homeostasis with the apparent attenuation of input from sodium-specialist neurons.
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PMID:Potential mechanisms for functional changes in taste receptor cells following sodium deficiency in mammals. 986 15

Experiments in Cushing patients and healthy control subjects receiving adrenocorticotropic hormone (ACTH) indicate that transient renal sodium retention may contribute to the generation of hypertension. Here we have investigated the effect of chronic ACTH infusion on renal sodium handling in adult male C57BL/6J mice using selective antagonists to dissect mineralocorticoid and glucocorticoid receptor-mediated pathways. Mice were infused via osmotic minipump with ACTH (2.5 microg/d) or saline for 2 weeks before being anesthetized for renal function experiments. ACTH caused an increase in blood pressure and a reduction in fractional sodium excretion associated with enhanced activity of the epithelial sodium channel. Given separately, spironolactone and RU38486 blunted the pressor response to ACTH and the increased epithelial sodium channel activity; combined mineralocorticoid and glucocorticoid receptor blockade was required to resolve the response to ACTH excess. Dietary sodium depletion also prevented ACTH-induced hypertension. The effect of increased sodium reabsorption in the distal nephron is offset by downregulation of Na-K-Cl cotransport in the loop of Henle. Sodium excretion is normalized chronically, but blood pressure remains high; acute blockade of V1 receptors and alpha1 adrenoceptors in combination restored blood pressure to control values. In summary, ACTH excess promotes renal sodium reabsorption, contributing to the increased blood pressure; both glucocorticoid and mineralocorticoid receptor pathways are involved. These data are relevant to conditions associated with overactivity of the hypothalamic-pituitary-adrenal axis, such as obesity and chronic stress.
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PMID:Mineralocorticoid and glucocorticoid receptors stimulate epithelial sodium channel activity in a mouse model of Cushing syndrome. 1963 86


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