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)

In 32P incorporation experiments with intact adrenocortical cells, adrenocorticotropin (ACTH) or adenosine 3',5'-cyclic monophosphate (cAMP) induced a rapid and transient increase of approximately 300-500% in the phosphorylation of a 32P-containing cytoplasmic protein of about 150,000 daltons (APS150). Half-maximal stimulation of APS150 phosphorylation was observed with about 3 pM ACTH. Receptor-bound cAMP, corticosterone production, and the appearance of phosphorylated APS150 increased in parallel with respect to both time and ACTH concentration. All three responses were dependent on extracellular calcium. Inhibition of protein synthesis with cycloheximide suggested a half-life of APS150 of about 10 min. The time course of 32P incorporation into ACTH-induced APS150 in the absence and presence of nonradioactive phosphate shows that the phosphorylation of APS150 is under simultaneous control of cAMP-dependent protein kinase and of phosphoatase activity. Thus a rapid ACTH-dependent and cAMP-dependent protein phosphorylation in intact adrenocortical cells within steroidogenic ACTH concentrations has now been demonstrated.
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PMID:Adrenocorticotropin (ACTH) induces phosphorylation of a cytoplasmic protein in intact isolated adrenocortical cells. 22 81

A 64-yr-old female presented with severe osteoporosis and easy bruisability of over 2-yr duration. Biopsy of a neck mass revealed medullary carcinoma of the thyroid. Subsequently, lymphangitic pulmonary metastases were demonstrated which had been present radiographically for at least 4 yr. Basal serum calcitonin was markedly elevated and increased during calcium infusion. The diagnosis of ectopic ACTH syndrome was first entertained when hypokalemic alkalosis was observed during evaluation of her carcinoma. Elevated urinary 17-hydroxycorticosteroids, 17-ketosteroids, plasma cortisol, and immunoreactive plasma ACTH levels were documented. Adrenal steroidogenesis seemed to suppress on high dose dexamethasone. The primary tumor and its metastases contained high concentrations of immunoreactive ACTH and beta-melanocyte-stimulating hormone. Hepatic metastases contained extremely high concentrations of calcitonin. In contrast to the usual presentation of the ectopic ACTH syndrome as primarily hypokalemic alkalosis and glucose intolerance, patients with relatively benign and indolent ACTH-secreting tumors, such as certain cases of medullary carcinoma of the thyroid, may present with more typical signs and symptoms of Cushing's syndrome. The more pronounced cushingoid features in this latter group presumably reflects a more prolonged period of exposure to elevated glucocorticoid levels. Ten cases of ACTH-secreting medullary carcinoma of the thyroid from the literature are discussed. Extopic ACTH production by such tumors should be considered in the evaluation of patients with Cushing's syndrome or unexplained severe osteopenia.
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PMID:ACTH-secreting medullary carcinoma of the thyroid presenting a severe idiopathic osteoporosis and senile purpura: report of a case and review of the literature. 23 64

Methionine-enkephalin, leucine-enkephalin and beta-endorphin were applied in known concentrations to an in vitro preparation of myenteric neurons from the guinea-pig ileum. All 3 substances caused a rapid, reversible and dose related inhibition of the firing of myenteric neurons induced and recorded with extracellular suction electrodes. This inhibition of firing occurred at low agonist concentrations (1-300 nM) and was reversed by naloxone and a benzomorphan narcotic antagonist. The inhibition persisted in solutions which were completely free of calcium ions -- thus indicating that the observed effect is taking place directly on the neuron from which the recording is made, and that calcium ions are not required for this inhibitory action of endorphins on neuronal firing.
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PMID:Effects of endorphins on single myenteric neurons. 42 87

Somatostatin (SS) inhibits in a dose-dependent manner electrically evoked contractions in the rat vas deferens. This action was not modified by yohimbine, naloxone or a mixture of antagonists containing atropine, phentolamine, methysergide, burimamide, propranolol and indomethacin, but was markedly potentiated by reducing the Ca2+ concentration of the medium from 2.5 to 1.25 mM and greatly inhibited when increasing the Ca2+ concentration of the medium from 2.5 to 5.0 mM. Clonidine (CLO), but not beta-endorphin (ENDO) was affected similarly to SS by changing the Ca2+ concentration of the medium. The contractile effect of norepinephrine in unstimulated rat vas deferens was not altered by SS. These results were taken as an indication that SS produces its inhibitory action in the rat vas deferens by interacting with specific SS and its receptors presumably located in the cell membranes of adrenergic nerve terminals. The interaction between SS and its receptors may provoke a decreased diffusion of Ca2+ ions into the nerve terminals and/or a decreased mobilisation of Ca2+ ions from intraneuronal stores thus leading to a reduction in electrically evoked release of norepinephrine.
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PMID:Studies on the inhibitory action of somatostatin in the electrically stimulated rat vas deferens. 46 93

The rate of release of beta-endorphin-like immunoreactivity (beta-EI) from rat hypothalamic slices was increased 3- to 4-fold over the spontaneous release during exposure to a depolarizing concentration of potassium ions. This augmented outflow was abolished in the absence of calcium. The amount of beta-EI released from slices exposed to a second pulse of potassium was reduced by approximately 50% compared to that in the first. 70% of the potassium-induced released immunoreactive material migrated on a calibrated Sephadex G-50 column like synthetic human beta-endorphin. These findings are discussed in terms of a neuronal release of beta-endorphin and may be taken as supportive evidence for a neurotransmitter and/or neurohormonal role of beta-endorphin in the hypothalamus.
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PMID:Release of beta-endorphin from rat hypothalamus in vitro. 46 98

Immunoreactive alpha-melanocyte-stimulating hormone (alpha-MSH) was found to be concentrated in a synaptosome-enriched fraction prepared by differential centrifugation of rat hypothalamic homogenates. The release of the hormone from this preparation was investigated. After incubation, the synaptosomes were isolated by ultrafiltration and alpha-MSH in the ultrafiltrate was determined by radioimmunoassay. Particle-bound alpha-MSH, recovered by extraction with acid ethanol, and alpha-MSH released from the synaptosome preparation, were immunologically similar to synthetic alpha-MSH and had an accompanying melanotropic activity. Less than 10% of the particle-bound alpha-MSH was released during incubation in 0.32 M sucrose. However, in the presence of 2 mM Ca2+, alpha-MSH release increased with increasing concentrations (30-150 mM) of K+. The stimulatory effect of 60 mM K+ was complete within 2 min and was potentiated by increasing Ca2+ concentrations over the range of 0 to 2 mM. K+-induced release of alpha-MSH was independent of temperature from 1 to 30 degrees C, and neither glucose (10 mM) nor dopamine (10(-10)-10(-2) M) had any effect on the release of the peptide. It is concluded that a synaptosome-enriched fraction from the hypothalamus contains a releasable pool of immunoreactive alpha-MSH that is mobilized by depolarizing concentrations of K+ in a Ca2+-dependent manner.
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PMID:Release of immunoreactive alpha-MSH by synaptosome-enriched fractions of homogenates of hypothalami. 48 55

A characteristic feature of induced pinocytosis in Amoeba proteus is the formation of broad channels by invagination of the cell membrane. This process, which requires Ca2+, occurs in response to depolarising cations. High Ca2+ levels reduce pinocytosis induced by cations such as Na+ and Tris+, whereas pinocytosis induced by K+ is less affected by Ca2+ (ref. 4). Agents which interfere with the calcium metabolism of the amoeba will therefore either stimulate or inhibit pinocytosis induced by Na+ (ref. 5). Among the agents which are supposed to reduce Ca2+ influx across cell membranes or otherwise decrease cellular availability of Ca2+ are the opiates and opioid peptides, high doses of which have been reported to affect the amoeba. Accordingly, Met-enkephalin, morphine and codeine potentiate the inhibition of pinocytosis caused by Ca2+-binding agents and reverse the calcium blockade of pinocytosis mediated by caffeine. In this report we show that pinocytosis induced by Na+ or Tris+ is suppressed by beta-endorphin, Metenkephalin and morphine. These effects were abolished or diminished by an opiate receptor antagonist, (-)naloxone, by increasing the Na+ concentration, or by addition of Ca2+.
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PMID:Naloxone-reversible effect of opioids on pinocytosis in Amoeba proteus. 50 90

The guinea-pig myenteric plexus-longitudinal muscle (MPLM) preparation electrically stimulated at 0.1 Hz is very sensitive to the inhibitory effects of opiates. We used this preparation to detect an inhibitory response (IR) which was produced by electrical stimulation at 5 to 20 Hz. The magnitude and duration of the IR are determined by the parameters of the stimulation, mainly by the frequency and duration of the period of stimulation. Maximal IR is obtained with symmetrical biphasic stimuli of 2 msec duration and supramaximal voltage at 20 Hz applied for a period of about 5 min. The IR is calcium-dependent, cannot be attenuated by washing and is mediated by several components. About 55 to 70% of the IR can be reversed by specific narcotic antagonists and therefore it is considered to be produced by the release of endorphins. There are at least two additional components, one small, adrenergic in nature, and a third one which has not been identified. The offset rate of the IR is measured in minutes, while enkephalin and human beta-endorphin have half-lives of 10 and 85 sec, respectively, after washing. This suggests that the endorphin that mediates the opiate component of the IR may be a different one with slower offset rates. Myenteric plexus-longitudinal muscle strips obtained from guinea pigs which were made tolerant to morphine by subcutaneous implantation of three pellets were cross-tolerant to the opiate component of the IR elicited by electrical stimulation.
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PMID:Electrically induced opiate-like inhibition of the guinea-pig ileum: cross-tolerance to morphine. 68 13

The rate of release of beta-endorphin immunoreactivity from the anterior lobe of the rat pituitary in vitro increased in respone to potassium-induced depolarization in a calcium-dependent manner. Potassium-induced depolarization did not, however, change the rate of release from intermediate/posterior lobe. These findings provide support for the view that beta-endorphin may have a humoral function and suggest that beta-endorphin stores in discrete pituitary areas are regulated by different release mechanisms.
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PMID:Release of beta-endorphin from rat pituitary in vitro. 69 83

An important factor in regulating secretion from endocrine cells is the cytoplasmic concentration of cyclic-AMP. Many regulatory substances are known to either stimulate or inhibit the production of this second messenger through activation of their receptors. In the present study, we have monitored changes in cyclic-AMP efflux from melanotrope cells of Xenopus laevis in response to established neurochemical regulators of alpha-MSH secretion. In vitro superfusion of neurointermediate lobes allows for a dynamic recording of cyclic-AMP production in relation to hormone secretion. Unlike alpha-MSH secretion, the efflux of cyclic-AMP was not dependent on the concentration of extracellular calcium, indicating that hormone release and cyclic-AMP efflux are mediated by different mechanisms. The phosphodiesterase inhibitor IBMX and the adenylate cyclase activator forskolin stimulated cyclic-AMP efflux, but had no stimulatory effect on alpha-MSH release. This indicates that an increase in cyclic-AMP production in melanotrope cells is not necessarily accompanied by an increase in the rate of alpha-MSH release. Corticotropin-releasing factor stimulated cyclic-AMP efflux with dynamics similar to that induced by the amphibian peptide sauvagine. Dopamine and the GABAB receptor agonist baclofen both inhibited cyclic-AMP efflux and alpha-MSH release, with similar dynamics of inhibition and similar dose-response relationships. It is proposed that an inhibition of cyclic-AMP efflux is coupled to an inhibition of alpha-MSH secretion.
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PMID:Dynamics of cyclic-AMP efflux in relation to alpha-MSH secretion from melanotrope cells of Xenopus laevis. 127 39


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