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)

Both respiratory and metabolic acidemia stimulate the secretion of adrenocorticotropic hormone (ACTH), vasopressin, and renin. The present study was designed to test the blood pressure, heart rate, and endocrine responses of conscious sheep to low-rate infusions of H+. We infused HCl and lactic acid at a rate of 500 mueq/min into the inferior vena cava of seven chronically catheterized adult sheep. Control experiments in six sheep consisted of infusion of HCl at a rate of 100 mueq/min. Only the 500 mueq/min infusion of HCl stimulated reflex responses. This infusion increased mean arterial blood pressure and plasma ACTH concentration but transiently decreased blood pH only after the onset of the reflex responses. Heart rate appeared to increase initially but then decreased. Overall, the apparent changes in heart rate were not statistically significant. None of the infusions significantly altered plasma renin activity or vasopressin concentration. We speculate that heart rate, plasma renin activity, and vasopressin may have been partially inhibited by the increase in blood pressure. However, the lack of effect of lactic acid suggests that the HCl stimulated reflex ACTH and blood pressure responses via a mechanism not related to the concentration of the acid in the infusate or to the total amount of acid infused. It is possible that HCl, but not lactic acid, stimulated release of a humoral agent that stimulated ACTH secretion directly or reflexly. The results do not appear consistent with the stimulation of a venous chemoreceptor sensitive to H+.
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PMID:Intravenous acid infusion stimulates ACTH secretion in sheep. 184 73

1. Heart tissues of several rodent species including the rat, gerbil (Meriones unguiculatus), hamster (Mesocricetus auratus) and guinea pig (Cavia porcellus) were extracted with an acetone-water-HCl mixture. An acid acetone powder was obtained by adding a copious volume of acetone to the extract. 2. Rat heart acid acetone powder was subjected to ion exchange chromatography on CM-cellulose. Gerbil heart acid acetone powder was subjected to salt fractionation, gel filtration on Sephadex G-10 and then ion exchange chromatography on CM-cellulose. Hamster and guinea pig heart acid acetone powders were subjected to gel filtration on Sephadex G-25. 3. The fractions were assayed for the ability to stimulate corticosterone production in isolated rat adrenal decapsular (zona fasciculata, zona reticularis and medulla) cells, to displace D-ala2-D-leu5-(tyrosyl-3,5-3H) enkephalin from binding to rat brain membranes, and to inhibit 125I-human beta-endorphin from binding to its antibodies. 4. The widespread occurrence of beta-endorphin-like immunoreactivity among the rat heart CM-cellulose fractions may reflect different species of beta-endorphin. The fraction with the highest beta-endorphin-like immunoreactivity and opiate receptor binding activity was strongly adsorbed on CM-cellulose. 5. In hamster and guinea pig hearts, beta-endorphin-like immunoreactivity and opiate receptor binding activity were distributed among high molecular weight and low molecular weight fractions. 6. In gerbil hearts, opiate receptor binding activity was present in fractions unretarded on Sephadex G-10 (i.e. with a molecular weight greater than 700) as well as in the retarded fractions (i.e. with a molecular weight smaller than 700).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Beta-endorphin-like and adrenocorticotropin-like materials in heart tissues of the rat, gerbil, hamster and guinea pig. 197 55

1. Turtle heart and intestine acetone powders were extracted with an acetone-water-HCl mixture. An acid acetone powder resulted by adding a copious volume of acetone to the extract. The powder was subjected to gel filtration on Sephadex G-25 and ion exchange chromatography on CM-cellulose. 2. In turtle heart, corticotropin-like bioactivity was distributed among chromatographic fractions (derived from material unretarded on Sephadex G-25) unadsorbed and adsorbed on CM-cellulose. The highest opiate receptor binding activity and beta-endorphin-like immunoreactivity were adsorbed on CM-cellulose. 3. In turtle intestine, corticotropin-like bioactivity was absent. Opiate receptor binding activity was present in fractions unretarded as well as in fractions retarded on Sephadex G-25, indicating a molecular weight of greater and smaller than 5000 respectively. 4. The highest opiate receptor binding activity and beta-endorphin-like immunoreactivity were found in a fraction adsorbed on CM-cellulose.
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PMID:Beta-endorphin-like and adrenocorticotropin-like materials in turtle heart and intestine. 198 Apr 47

Serotonin (5-HT) and 5-HT agonists act on multiple 5-HT receptor subtypes to increase corticosterone secretion. The present experiments describe the effects of a highly selective 5-HT2 receptor agonist DOI [(+-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane HCl] on plasma corticosterone in conscious, unrestrained, male rats with indwelling arterial and venous catheters. DOI (500 micrograms/kg, i.v.) increased plasma corticosterone levels 6- to 7-fold from 15 to 60 min. Pretreatment with the central 5-HT2 antagonist LY 53857 (100 micrograms/kg, i.v.) blocked the effect of DOI on corticosterone secretion at all times. The peripheral 5-HT2 antagonist xylamidine (100 micrograms/kg, i.v.) attenuated the corticosterone response elicited 15 min after DOI but did not alter the 60-min response. In contrast, dexamethasone pretreatment (350 micrograms/kg, s.c.) attenuated the corticosterone response to DOI at 15 min, but abolished the response at 60 min. The increase in corticosterone levels elicited 5 min after the nonselective 5-HT agonist quipazine (3 mg/kg, i.v.) was also reduced by xylamidine. These data suggest that 5-HT2 receptor agonists increase corticosterone secretion initially, in part, through a direct adrenal mechanism not entirely dependent on adrenocorticotropin, and at later times via a central, dexamethasone-suppressible mechanism. This raises the possibility that endogenous 5-HT in the adrenal medulla may act as a local paracrine to participate in the regulation of corticosterone secretion from the adrenal cortex.
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PMID:Evidence for central and peripheral serotonergic control of corticosterone secretion in the conscious rat. 210 69

Guinea pig brain membranes depleted of mu and delta receptors by pretreatment with the site-directed acylating agents, 2-(4-ethoxybenzyl)-1- diethylaminoethyl-5-isothiocyanatobenzimidazole.HCl (BIT) and N-phenyl-N-[1-(2-(4-isothiocyanato)phenethyl)-4- piperidinyl]-propanamide.HCl (FIT), were used in this study to test the hypothesis that guinea pig brain possesses subtypes of kappa receptors. Pretreatment of membranes with either (-)-(1S,2S)-U50,488 or the kappa selective acylating agent, (1S,2S)-trans-2-isothiocyanato-N-methyl-N-[2-(1- pyrrolidinyl)cyclohexyl]benzeneacetamide, caused a wash-resistant inhibition of kappa 1 binding sites labeled by [3H]U69,593 binding, but not kappa 2 binding sites labeled by [3H]bremazocine. Binding surface analysis of [3H]bremazocine binding resolved two binding sites, termed kappa 2 and kappa 2b, present at densities of 212 and 225 fmol/mg protein, which had low affinity for (-)-(1S,2S)-U50,488 and U69,593. The kappa 2b site had high affinity for beta-endorphin(1-31) (Kd = 5.5 nM) and [D-Ala2,D-Leu5]enkephalin (Kd = 14 nM), and lower affinity for [D-Ala2-MePhe4,Gly-ol5]enkephalin (Kd = 147 nM) and [Leu5]enkephalin (Kd = 46.0 nM). Binding surface analysis of [3H]U69,593 binding also resolved two binding sites, termed kappa 1a and kappa 1b, present at densities of 6.0 and 40.0 fmol/mg protein. The kappa 1a binding site was characterized by very high affinity for alpha-neoendorphin. Quantitative autoradiographic studies demonstrated that kappa 2a and kappa 2b binding sites are heterogeneously distributed in guinea pig brain, and that the anatomical distribution of kappa 1 binding sites reported in the literature is different from that observed in this study for the kappa 2 binding sites. Viewed collectively, these data provide evidence for four kappa receptor subtypes in guinea pig brain.
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PMID:Interaction of endogenous opioid peptides and other drugs with four kappa opioid binding sites in guinea pig brain. 216 33

Snake (Ptyas mucosa) pituitaries were heated, extracted with an acidic medium, and the extract subsequently chromatographed on carboxymethyl cellulose (CMC). Fractions were assayed for their abilities to displace D-ala2-D-leu5-[tyrosyl, 3,53H] enkephalin from binding to rat brain membranes and 125I-beta-endorphin from binding to its antibody, and to stimulate corticosterone production by isolated rat adrenal cells. The fraction unadsorbed on CMC (having the least basic character) had the lowest opiate receptor binding activity and beta-endorphin-like immunoreactivity. The highest steroidogenic activity, opiate receptor binding activity and beta-endorphin-like immunoreactivity were concentrated in a strongly adsorbed fraction. Snake pituitaries were also extracted with Tris-HCl buffer (pH 7.8). The extract from the second procedure was subsequently chromatographed on ConA-Sepharose, ultrafiltered and dialyzed to obtain a nonglycopeptide fraction with a molecular weight between 1,000 and 10,000. This fraction also exhibited steroidogenic and opiate receptor binding activities.
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PMID:beta-Endorphin-like and adrenocorticotropin-like hormones in the pituitary of the snake Ptyas mucosa. 216 96

Rats were subjected to three consecutive sessions, one session per day, of either a step-down inhibitory avoidance task using a 60-Hz. 0.3-mA footshock, or a two-way active avoidance task using 20 presentations of a 5-s, 1-kHz tone and a 0.3-mA footshock. After either the first or the second training session animals received an intraperitoneal injection of ACTH (0.2 microgram/kg), epinephrine-HCl (5.0 micrograms/kg), or naloxone-HCl (0.8 mg/kg). All these treatments caused memory facilitation on both tasks when administered after the first training session. When administered after the second training session only ACTH and adrenaline were effective, on both tasks. As previous physiological and pharmacological reports point to the activation of the brain beta-endorphin system after the first, but not the second, session of a task, we propose that (a) memory facilitation by naloxone depends on the previous activation of the brain beta-endorphin system; and (b) memory facilitation due to ACTH or epinephrine does not depend on the opioid activity, so their effects are expressed after both the first and the second training sessions. It was also observed that the enhancement of performance in the second training session due to post-training facilitatory treatments carried over to the test session. These results suggest that some form of consolidation occurs both after the first and after the second training session.
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PMID:Distinct mechanisms underlying memory modulation after the first and the second session of two avoidance tasks. 230 39

Administration of 20, 4 or 2.5 micrograms/kg of atriopeptin III (AT III) into the fourth ventricle of the brain of spontaneously hypertensive rats produced a 13, 14 and 7 mm Hg decrease in MAP respectively, while 1 microgram/kg had no effect on MAP and was significantly different from 20 or 4 micrograms/kg (p less than 0.025). In contrast, injection of AT III 20 micrograms/kg into the lateral ventricle did not produce a change in MAP. To examine an interaction of AT III with the opioidergic system, the opiate antagonist, naloxone HCl, 10 micrograms, was given by ICV injection 10 minutes prior to AT III, and significantly prevented the depressor response to AT III (p less than 0.025 compared with AT III alone). Injection of specific anti-sera to beta-endorphin failed to prevent the AT III-induced depressor response. Our results demonstrate that AT III can act within the central nervous system to decrease the MAP of rats, most likely at a locus in proximity to the fourth ventricle of the brain. Further, an interaction with the central opioidergic nervous system underlies the central effects of AT III.
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PMID:Central nervous system mediated vasodepressor action of atrial natriuretic factor. 252 18

Adrenocorticotropic hormone (ACTH), arginine vasopressin (AVP), and renin responses to hemorrhage are highly correlated to the hemorrhage-induced decreases in arterial pH. The present study was designed to test the responses of these three systems to acute fetal acidemia, produced by intravenous infusion of H+. HCl was infused into chronically catheterized fetal sheep at rates of 0.02 (n = 5), 0.10 (n = 6), and 0.50 (n = 5) meq/min. Infusions at rates of 0.10 and 0.50 meq/min significantly decreased fetal arterial pH and increased arterial PCO2. Fetal heart rate and plasma concentrations of ACTH, cortisol, and AVP were significantly increased during infusion of HCl at 0.5 meq/min. Neither fetal plasma renin activity nor fetal arterial blood pressure was significantly altered by any of the infusions. The results of these experiments suggest that fetal ACTH, AVP, and heart rate are stimulated by decreases in arterial pH and/or increases in arterial PCO2. We speculate that these responses are chemoreceptor mediated, although we cannot distinguish the apparent relative roles of peripheral and central chemoreceptors on the basis of the present study.
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PMID:Acidemia stimulates ACTH, vasopressin, and heart rate responses in fetal sheep. 254 8

beta-Endorphin-like immunoreactivity (BE-LI) was measured in 7 brain regions of Swiss-Webster mice after 24, 48 and 72 h of exposure to ethanol vapor following a priming injection of ethanol and daily injections of pyrazole HCl to inhibit ethanol metabolism. Control mice in identical chambers received pyrazole injections but breathed air only. Ethanol dependence was confirmed by scoring additional groups of mice for handling-induced convulsions during withdrawal after each exposure duration. Measurement of anterior and neurointermediate (NIL) pituitary BE-LI, alpha-MSH and ACTH and plasma corticosterone confirmed earlier results showing NIL depletion of all 3 peptides at 24 h and increased plasma corticosterone concentrations at 72 h in ethanol-exposed mice. In brain extracts from ethanol-dependent mice, BE-LI was significantly reduced in the hypothalamus and midbrain with the greatest reduction occurring at 24 h. In forebrain, cerebral cortex, septum and hippocampus, pyrazole treatment significantly reduced BE-LI relative to an unhandled control group, and ethanol exposure tended to reverse this effect. HPLC of hypothalamic extracts revealed no differences in proportions of molecular forms of beta-endorphin-like peptides between 24 h control and ethanol-exposed groups. The predominant BE-LI peak in both groups co-eluted with opiate-active unmodified beta-endorphin. Ethanol dependence in mice is associated with regionally selective decreases in brain beta-endorphin concentration.
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PMID:Influence of ethanol dependence on regional brain content of beta-endorphin in the mouse. 294 58


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