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)

Evidence is presented for a number of events in the fetal hypothalamic-pituitary axis which may play a key role in the onset of labour: (1) In the sheep fetus a progressive rise in the fetal circulating concentrations of corticotropin in the days preceding delivery; (2) In the human fetus a switch from the production of corticotropin-like fragments (melanotropin and corticotropin-like intermediate lobe peptide) to authentic corticotropin in the last weeks of gestation; there is evidence also for a placental origin of corticotropin; (3) In the human fetus, a release of oxytocin and vasopressin associated with the process of spontaneous labour.
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PMID:The fetal hypothalamus and pituitary in the initiation of labour. 20 96

beta-Lipotropin is the predominant opioid peptide of the human pituitary and rat pars distalis and is present in concentrations essentially equimolar with corticotropin. When freshly, obtained nonfrozen rat anterior pituitaries were homogenized with 0.2 M HCl, approximately 98% of the immunoreactivity detected utilizing an antiserum that crossreacts equally with beta-lipotropin and beta-endorphin coeluted with 125I-labeled human beta-lipotropin upon molecular sieve chromatography. The remainder of the activity eluted with synthetic human beta-endorphin. Similar results were obtained for human pituitary. HCl homogenization of thawed tissue or homogenization of fresh tissue with acetic acid yielded substantially greater concentrations of beta-endorphin and decreased concentrations of beta-lipotropin. In human subjects, acute anterior pituitary stimulation using either insulin-induced hypoglycemia or vasopressin administration was associated with increased plasma beta-lipotropin and corticotropin levels. At the time of peak concentrations, no significant levels of beta-endorphin were detectable. These data indicate the lack of significant amounts of beta-endorphin in human pituitary. Additionally, there appears to be no specific intrapituitary conversion of beta-lipotropin to beta-endorphin.
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PMID:beta-Lipotropin is the major opioid-like peptide of human pituitary and rat pars distalis: lack of significant beta-endorphin. 20 78

beta-Endorphin is not detectable in plasma from normal human subjects when measured under baseline conditions or after the subjects have received vasopressin, an agent that elevates beta-lipotropin and adrenocorticotropic hormone (ACTH). Significant amounts of beta-endorphin are present in plasma of patients with endocrine disorders associated with increased ACTH and beta-lipotropin production. Highly purified, natural beta-lipotropin is not peripherally converted to beta-endorphin in vivo in normal subjects.
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PMID:beta-Endorphin is not detectable in plasma from normal human subjects. 21 85

A three dimensional reconstruction of the central neural pathways that appear to mediate release of ACTH in response to hemodynamic change is illustrated in Figure 11. Fibers from receptors in the right atrium and the carotid arteries project to the lateral solitary nucleus and then to the medial and the lateral nucleus intercalatus. A pathway containing projections from these nuclei then converges dominantly in the locus subcoeruleus and locus coeruleus. Multiple pathways then diverge, to travel in part directly to the hypothalamus through dorsal pathways. One pathway inhibits and another facilitates the release of ACTH. Multiple pathways also diverge, to travel in part medially, and then to the hypothalamus through ventral pathways. Again, one pathway inhibits and another facilitates the release of ACTH. The dorsal and ventral inhibitory pathways appear to converge in a region extending from just caudal and ventral to the paraventicular nucleus to the posterior hypothalamic area. Thus, after the coalescences of the various pontine-hypothalamic pathways, three principal pathways remain. These include a posterior inhibitor path, an anterodorsal facilitatory path that terminates in the paraventricular nucleus and that may be mediated through release of vasopressin, and an anteroventral facilitatory path that terminates in the suprachiasmatic and ventromedial nuclei and that is probably mediated through release of corticotropin-releasing hormone. The mode of integration of these pathways has not been defined. The pathways described herein are oligosynaptic: a signal may travel from atrium to hypothalamus over three to seven neurons. The combination of control of input hemodynamic signals and of measurement of ACTH permits quantitation of both sensory and motor events, that inevitably must be embedded in the neuronal pathways described here. The analysis of the input-output relations and their correlation with internal neural events must form the basis of a description of the physiology of the physiology of the system whose central neural anatomy has been defined in part by these studies.
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PMID:Neural control of ACTH release in response to hemorrhage. 21 14

The cerebral uptake of subcutaneously injected [3H]2-deoxy-D-glucose (2DG) in 16 brain regions was examined following 30 noncontingent random footshocks or the acute injection of saline, ACTH1-24 (0.5 microgram/g), ACTH/MSH4-10 (0.25 microgram/g), [D-Phe7]ACTH4-10 (0.25 microgram/g), [Met4SO2,D-Lys8,Phe9]ACTH4-9 (0.01 microgram/g), ALPHA-MSH (0.5 microgram/g), corticosterone (2.5 microgram/g) or lysine vasopressin (0.05 microgram/g). Footshock selectively decreased 2DG uptake in parietal cortex and brain stem, and increased that in the hypothalamus. Whole brain 2DG uptake was decreased by injection of saline or most of the hormones relative to uninjected animals, but this effect was probably peripheral since plasma glucose content was increased by the injections. The only regionally specific effect of the hormones was an increased 2DG uptake in olfactory bulb by saline, ACTH/MSH4-10 And corticosterone relative to uninjected animals. Since alpha-MSH had been reported previously to decrease blood flow (measured by antipyrene uptake) in all brain regions except occipital cortex [5,6], we directly compared antipyrene uptake with 2DG uptake in the same animals using a double-isotope procedure. The results revealed an increase in 2DG uptake relative to antipyrene in cortical regions relative to subcortical regions, contradicting earlier assumptions [19].
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PMID:Mouse brain deoxyglucose uptake after footshock, ACTH analogs, alpha-MSH, corticosterone or lysine vasopressin. 21 66

The hypothalamic pituitary adrenocortical function has been studied in 16 patients operated from pituitary tumors (13 adenomas; 3 craniopharyngiomas). Comparisons have been made between corticotropin and cortisol response to lysine vasopressin, insulin induced-hypoglycemia and metyrapone IV and per os. Among these different stimulating tests, insulin induced hypoglycemia and metyrapone per os seem to give the more accurate informations metyrapone per os being more convenient because harmless. Three different groups of patients have been distinguished : one without adrenocortical deficiency; one with a complete deficiency and a third group with a partial deficiency. Correlations have been studied between the degree of the adrenocortical deficiency, the volume of the tumor and the presence of the absence of other anterior pituitary dysfunctions.
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PMID:[Study of the hypothalamo-pituitary adrenal function in 16 patients after surgery for pituitary tumor (author's transl)]. 21 1

Hypothalamic extract stimulates the release of corticotropin (ACTH) and endorphins 2.5- to 30-fold in mouse pituitary tumor cell cultures (AtT-20/D(16v) line) and primary cell cultures from mouse anterior pituitary. ACTH and endorphin activities were measured by radioimmunoassay and immunoprecipitation. Pretreatment of tumor cell cultures with 1 muM dexamethasone reduced the stimulatory effect of the extract on release of ACTH and endorphins. Pretreatment of primary cell cultures with 10(-6) M dexamethasone reduced the stimulatory effect of both vasopressin and the extract on the release of ACTH and endorphins. Release of ACTH and endorphin was coupled in both kinds of cultures in the basal, stimulated, and inhibited states. The molecular weight forms of ACTH and endorphin in tumor cell culture medium were analyzed by sodium dodecyl sulfate/polyacrylamide gel electrophoresis. Radioimmunoassay and immunoprecipitation show that the 13,000-dalton and 4500-dalton forms of ACTH were present in about equal amounts in medium from cultures incubated with or without hypothalamic extract for 15 min, 30 min, or 2 hr. Smaller amounts of the high molecular weight forms of ACTH (20,000- to 23,000-dalton and 31,000-dalton ACTH) were observed in the culture medium at these times. The predominant forms of endorphin released after 20 min or 3 hr of incubation had molecular weights of 31,000, 11,700 (beta-lipotropic hormone-size material) and 3500 (beta-endorphin-size material). No degradation of the forms of endorphin released into the culture medium was observed after incubating the culture medium for 1.5 hr in the absence of cells. The proportions of the different forms of endorphin and ACTH present in the culture medium resembles that seen in cell extracts.
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PMID:Coordinate control of corticotropin, beta-lipotropin, and beta-endorphin release in mouse pituitary cell cultures. 21 8

Male mice were given a single injection of either adrenocorticotropic hormone (ACTH) or lysine vasopressin immediately after a defeat in an encounter with an aggressive male mouse. The defeated mice were tested for submissiveness at either 24 hours, 48 hours, or 7 days after the initial encounter. Both hormone treatments increased future submissiveness, although the time courses of the effects were different: The effects of ACTH disappeared after 48 hours, whereas those of vasopressin persisted for 7 days. These results suggest that changes in peptide hormone levels following naturally stressful experiences can affect the memory of those experiences, as expressed in future adaptive responses.
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PMID:ACTH and vasopressin treatments immediately after a defeat increase future submissiveness in male mice. 22 73

The capacity which the cells of some tumors have of synthesizing, storing, and releasing hormonal polypetides constitutes the basic characteristic of the neoplasms of the APUD system. On many occasions these polypeptides are released as hormonal precursors of high molecular weight, with a minimal biological action in comparison with the real hormone (big ACTH, big gastrin, etc.), and they have no clinical expressivity. On other occasions they reproduce, however, the clinical syndrome of the hormone released in excess. The production of multiple hormones by a single tumor is not a common event. Here we present the case of a patient with an oat-cell carcinoma of the lung and a carcinoma of the pancreas, both histopathologically primitive. In this patient a syndrome of inadequate secretion of antidiuretic hormone was detected. By means of radioimmunoassay techniques, the existence of antidiuretic hormone, ACTH with a predominance of the components of high molecular weight (big ACTH and beta-LPH) and MSH was demonstrated in the tumoral extracts from the lung, pancreas, and from a mediastinal metastatic lymph node. While the concentrations of ACTH were much greater in the lung than in the pancreas, the opposite occurred for the antidiuretic hormone. The synthesis of MSH by the hypophyseal gland or by tumors is not at present recognized, but rather is considered as a degradation product during the process of extraction. The APUD system makes up the morphologic substrate of the syndromes of familiar multiple endocrine adenomatosis. The present case could represent a variant of sporadic multiple endocrine neoplasms which would have the same anatomical basis.
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PMID:[Hormonal multiplicity of an apudoma of the lung and pancreas. Characterization of the different peptides in the tumoral extracts (author's transl)]. 22 76

The influence of ACTH4-10, a behaviourally active fragment of adrenocorticotropic hormone (ACTH) devoid of endocrine activity, on synaptic transmission in the paravertebral sympathetic ganglion of the frog was investigated. Postsynaptic potentials evoked by electrical stimulation of pregnanglionic nerves were recorded using a sucrose gap method. Fast excitatory postsynaptic potentials (EPSPs), which are mediated via nicotinic cholinergic synapses, were not affected by 10(-6) M ACTH4-10. Application of ACTH4-10 in a concentration as low as 10(-8) M for 60 min caused a marked augmentation of the amplitude of slow inhibitory postsynaptic potentials (IPSPs) which are mediated via dopaminergic synapses. The increase in amplitude developed gradually after a latency of 60--90 min and outlasted the application of the peptide. In addition, ACTH4-10 at 10(-6) M increased the hyperpolarising response of the ganglion to exogenous dopamine, as studied by a micro-application method. There was no significant effect of ACTH4-10 on the muscarinic cholinergic depolarising response of the ganglion towards exogenous acetylcholine. The behaviourally active vasopressin fragment DG-LVP (10(-6) M) had no effect on slow IPSPs. The results demonstrate that ACTH4-10 specifically affects slow synaptic inhibition in frog sympathetic ganglion, probably by acting upon the postsynaptic membrane. The possibility is discussed that ACTH4-10 affects one of the intermediate steps between dopaminergic receptor interaction and generation of the slow IPSP.
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PMID:Effects of ACTH4-10 on synaptic transmission in frog sympathetic ganglion. 22 81


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