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)

Salt glands of ducks were induced to secrete sodium through the ingestion of salt water. In salt-adapted animals the administration of melanocyte-stimulating hormone (MSH) produced a rise in the sodium excreted by the salt gland, an effect which was not mimicked by adrenocorticotropin. Studies in vitro using incubations of gland slices and radioactive sodium ion showed that MSH increased sodium efflux, indicating that it acted directly upon the gland. We have previously observed that MSH has no effect on the pigmentary system of the duck. It is proposed that in the evolutionary process this hormone has acquired new target tissues in these birds.
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PMID:Alpha-melanocyte-stimulating hormone stimulates sodium excretion in the salt gland of the duck. 133 Aug 7

Antisera to the naloxone-insensitive receptor for beta-endorphin expressed on the U937 cell line were generated by using the complementary peptide strategy. A nanopeptide complementary to a C-terminal fragment of human beta-endorphin was synthesized as predicted by reading the beta-endorphin antisense mRNA 3' to 5'. By using enzyme-linked immunosorbent assay, rabbit antisera specific for the peptide complementary to beta-endorphin (C'-peptide) were characterized. With the exception of C'-peptide, preabsorption of the antisera with human-beta-endorphin1-31 or 10 unrelated peptides of 5 to 21 amino acids failed to reduce the enzyme-linked immunosorbent assay titer. Sucrose gradient separation was also used to show that the antisera failed to recognize beta-[125I]endorphin. Immunoglobulin to C'-peptide (10-800 micrograms/tube) inhibited the binding of beta-[125I]endorphin (1-2 nM) to intact U937 cells in a dose-dependent manner, whereas control immunoglobulin was ineffective. Moreover, immunoglobulin to C'-peptide failed to reduce [3H]naloxone binding to rat brain membrane. After binding and cross-linking of beta-[125I]endorphin to U937 cell membrane in the presence of beta-endorphin (2.5 x 10(-5) M), control immunoglobulin or anti-C'-peptide immunoglobulin, sodium dodecyl sulfate polyacrylamide gel electrophoresis showed that anti-C'-peptide immunoglobulin inhibited binding to 44 and 59 kDa bands. Nonspecific antibody was completely ineffective, whereas beta-endorphin completely inhibited binding to the 44 kDa and partially to the 59 kDa band. Western blot analysis of U937 cell membrane showed bands at 64, 58 and 56 kDa. In summary, antibodies selective for C'-peptide displaced beta-endorphin from the naloxone-insensitive receptor on U937 cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Characterization of antisera to the naloxone-insensitive receptor for beta-endorphin on U937 cells generated by using the complementary peptide strategy. 133 18

The affinity cross-linking of the delta-opioid receptor in neuroblastoma x glioma NG108-15 cells was undertaken using (3-[125I]iodotyrosyl27)human-beta-endorphin ([125I]beta-endorphin) and disuccinimidyl suberate (DSS) or bis(sulfosuccinimidyl) suberate (BS3) in order to estimate molecular size. Following sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) analysis, two radioactive bands were observed. Labeling of a major band of 29 kDa diminished in the presence of unlabeled selective delta-opioid agonist, [D-Pen2,D-Pen5]enkephalin (DPDPE), in a concentration-dependent manner, while labeling of a minor band of 58 kDa was hardly affected. The labeling intensity of the 29 kDa band decreased by addition of guanosine 5'-(3-o-thio)triphosphate (GTP gamma S) or by pretreatment of cells with pertussis toxin. These results, taking the molecular weight of covalently bound beta-endorphin (3.6 kDa) into consideration, suggest that the delta-opioid receptor in NG108-15 cell membrane is a 25 kDa protein which is coupled to pertussis toxin-sensitive guanosine triphosphate-binding proteins (G-proteins).
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PMID:Affinity cross-linked delta-opioid receptor in NG108-15 cells is low molecular weight (25 kDa) and coupled to GTP-binding proteins. 133 16

Acute unilateral nephrectomy (AUN) causes natriuresis from the contralateral kidney through neurohumoral reflex pathways that involve an increase in the plasma of peptides derived from the N-terminal region of the adrenocorticotropic hormone (ACTH)/beta-endorphin precursor proopiomelanocortin (POMC). To determine the specificity of these humoral changes, the concentrations in plasma of ACTH and two peptides arising from the N-terminal fragment (NTF) of POMC, NTF32-49 and gamma-melanocyte-stimulating hormone (gamma-MSH), and of another natriuretic peptide, atrial natriuretic peptide (ANP), were measured by RIA with highly specific antisera to these epitopes. Group I experiments followed the course of sodium excretion (UNaV) for 120 min after AUN or sham nephrectomy. UNaV more than doubled within 60 min of AUN, and this natriuresis was maintained for the remainder of the experiment, whereas UNaV in sham rats did not change. There was no difference in plasma immunoreactive (ir) ACTH or ir-ANP concentrations between sham and AUN rats 120 min after the procedure, but plasma ir-NTF concentration was double in AUN rats compared with sham (P < 0.03). In Group II experiments, animals were killed 30, 60, 90, or 120 min after AUN and the urinary response related to peptide concentrations in plasma. UNaV rose rapidly after AUN, reaching a maximum value within 45 min that again was double the control value and remained stable for the duration of the experiment, up to 120 min after AUN. There was no significant change in ir-ACTH or ir-ANP at any point after AUN compared with values in sham AUN rats. However, plasma concentrations of both ir-NTF and ir-gamma-MSH were elevated 30 min after AUN and reached values at 120 min that were again double the values in sham rats (P < 0.05 for both).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute unilateral nephrectomy elicits a specific increase in plasma of peptides derived from the N-terminal region of proopiomelanocortin. 133 5

Hypertension was induced by chronic foot-shock and noise stress in adult male Sprague-Dawley rats. Microinjection of 0.3 microliters (150 mmol) sodium glutamate (Glu) into the nucleus arcuatus (ARC) elicited a significant depressor effect in rats with chronic stress-induced hypertension. The depressor effect induced by excitation of ARC neurons was attenuated significantly by microinjection of 0.3 microliters beta-endorphin antiserum (beta-EPAS) into the dorso-medial periaqueductal gray (PAG) or 0.1 microliters into the area of locus coeruleus (LC) due to blockage of beta-endorphinergic fibres from ARC to PAG or LC.
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PMID:[Depressor effect of nucleus arcuatus stimulation in chronic stress-induced hypertensive rat]. 162 Nov 6

To identify the dynamic response of hormones after burns with special reference to ANP during shock and the subsequent period, plasma concentrations of atrial natriuretic peptide (ANP), aldosterone, cortisol, arginine vasopressin (AVP), corticotropin, (ACTH), plasma renin activities (PRA), norepinephrine (NE) and epinephrine (E) were measured from the day of ICU admission and for 7 days following burn injury. Plasma AVP levels were highest on ICU admission and correlated with size of the burn injury ranged from 20-60 percent of the total body surface area. Between the 5th and 6th postburn day plasma ANP levels elevated while plasma AVP levels returned to normal. Urine sodium concentrations decreased from the 3rd day. Plasma aldosterone levels declined after the 2nd day. Mean epinephrine (E) and norepinephrine (NE) levels elevated on admission and remained elevated throughout the study. These results suggest that ANP plays important role for restoring fluid homeostasis by improving edema in burned tissues during refilling periods in burns.
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PMID:The endocrine response after burns. 165 90

We found symptomatic hyponatremia in four elderly patients in which serum sodium (Na) levels ranged from 101 to 122 mEq/l. All 4 patients had low levels of plasma adrenocorticotropic hormone (ACTH), serum cortisol, and urinary excretion of 17-OHCS, and poor responses of ACTH to exogenous insulin and antidiuretic hormone (ADH). Other pituitary hormones were all normal. They were therefore diagnosed as having isolated ACTH deficiency. Plasma ADH was relatively high despite hypoosmolality which was associated with the hyponatremia. Water loading test revealed impaired water excretion and poor suppression of plasma ADH. Replacement with 20-30 mg hydrocortisone completely restored the serum Na level and restored the plasma ADH level to the normal range in all 4 patients. Other factors such as decreased glomerular filtration, enhanced urinary Na loss and decreased Na intake were also included. These results indicate that there is marked hyponatremia and that in the presence of hypoosmolality the sustained secretion of ADH is the key factor in causing the impaired water excretion and hyponatremia in isolated ACTH deficiency.
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PMID:Role of antidiuretic hormone in hyponatremia in patients with isolated adrenocorticotropic hormone deficiency. 166 14

In fetal sheep, plasma concentrations of both adrenocorticotropic hormone (ACTH) and cortisol increase at the end of gestation. The increase in fetal plasma cortisol concentration induces placental 17 alpha-hydroxylase and 17, 20 lyase activities and therefore stimulates the placenta to secrete relatively more estrogen and relatively less progesterone. The resultant increase in the estrogen-to-progesterone ratio is thought to increase uterine contractility and initiate labour. We had previously demonstrated that the efficacy of cortisol-induced suppression of ACTH secretion at the end of gestation was reduced. We hypothesized that cortisol-induced stimulation of placental steroidogenesis promoted the secretion of a steroid hormone which reduced negative feedback efficacy, and therefore allowed both ACTH and cortisol secretion to increase simultaneously. Others had proposed that cortisol stimulates the placental secretion of corticotrophin releasing factor, which might also stimulate fetal ACTH secretion. This study was designed to test the hypotheses that cortisol reduces its own feedback efficacy or stimulates CRF secretion. Five pregnant ewes with twin pregnancies were studied after chronic catheterization. One fetus was subjected to infusion of hydrocortisone sodium succinate (10 micrograms/min, iv) and the other to infusion of saline. After 5 and 53 h of infusion, each fetus was subjected to a period of hypotension produced by infusion of sodium nitroprusside. The infusion of hydrocortisone sodium succinate decreased plasma progesterone concentrations in the fetal circulation into which the steroid was infused, and in the maternal circulation. Fetal plasma CRF concentrations were increased on the third day of infusion, the day in which the fetuses went into labour.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Induction of parturition by cortisol: effects on negative feedback sensitivity and plasma CRF. 166 56

The present study evaluated the effects of high K+ and four excitatory amino acids (EAAs) on the release of met-enkephalin-like immunoreactivity (ME-i.r.) from slices of the rat striatum and globus pallidus. High K+ (15-50 mM) increased the release of ME-i.r. in a concentration-dependent manner in both regions, the release response in the globus pallidus being consistently greater than in the striatum. This release was highly Ca(++)-dependent and was significantly enhanced in the absence of external Mg++. D-2-Amino-7-phosphonoheptanoic acid (0.5 mM), a competitive N-methyl-D-aspartate (NMDA) receptor antagonist, did not alter this enhanced action of K+, suggesting that the activation of NMDA receptors by an endogenous agonist did not contribute to the enhancement. Exposure of pallidal or striatal slices to four EAA receptor agonists, NMDA, L-glutamate, kainate (KA) and quisqualate, increased the release of ME-i.r. above the base line, an effect that was Ca(++)-dependent. Both L-glutamate and NMDA, at concentrations of 1 and 5 mM, produced a graded increase in the ME-i.r. release, but a higher concentration (10 mM) produced a lower release. In both regions the NMDA (5 mM)-evoked release was effectively inhibited by Mg++ (1.2 mM), 3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP) (5 microM), a competitive NMDA receptor antagonist and thienylcyclohexylpiperidine (10 microM), a noncompetitive NMDA receptor antagonist. Tetrodotoxin (0.3 microM), a Na+ channel blocker, did not affect the NMDA-evoked release of ME-i.r. in the striatum, but decreased it by 52% in the globus pallidus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Met-enkephalin release from slices of the rat striatum and globus pallidus: stimulation by excitatory amino acids. 167 84

The identification of multiple opioid receptors and opioid peptides in the 1970 was the starting point of an increasing knowledge on opioid physiology and pharmacology. The mechanisms of action of spinally supraspinal levels. At the spinal level, opioids act by a modulation of specific supraspinal effect is the consequence of the migration of opioids, other in the bloodstream or in the cerebrospinal fluid, towards the encephalon. This action involve complex systems of inhibitory control on spinal structures. Opioids act on specific receptors which have a broad distribution in the central nervous system. the classification of opioid receptors is based on the activity of specific ligands: mu (morphine), kappa (ketocyclazocine), sigma (SKF 10047), delta (leu-enkephalin) and epsilon (beta-endorphin). Evidence for the existence of different isoreceptors for each type has been given by experimental studies. At the receptor level, opioid agonists act, hypothetically via the system of adenylcylase, more certainly via a modulation of membrane tonic channels. Thus, opioids modify sodium, calcium and potassium currents, and modify the successives phases of the membrane action potential. The result is an hyperpolarization which is responsible of an inhibition of the release of various neurotransmitters such as P substance.
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PMID:[Opioids by the perimedullary route: mechanisms of opioid analgesia]. 167 76


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