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 effects of synthetic enkephalin analog (KF 33-824) and beta-endorphin on growth hormone (GH) secretion and their interaction with brain monoamines were investigated in unanesthetized male rats. Blood samples (0.4 ml each) were withdrawn every 10-20 min for 6 h from a catheter chronically implanted in the right atrium. In all control rats, immunoreactive GH secretion was pulsatile in nature and two major GH bursts were found to occur around 12.00 and 15.30. The opioid peptides were injected between bursts at 14.00. Following an intravenous administration of FK 33-824 (10 microgram/100 g b.w.), there was an abrupt increase in plasma GH, which was significantly suppressed by naloxone (125 microgram/100 g b.w., i.v.), a specific opiate antagonist. Pretreatment with reserpine (1 mg/100 g b.w., i.p.) abolished not only the natural GH burst but also the GH response to FK 33-824. Pretreatment with dopamine-beta-hydroxylase inhibitors, diethyldithiocarbamate (DDC, 100 mg/100 g b.w., i.v.) and fusarate (10 mg/100 g b.w., i.v.) also inhibited the natural GH burst and GH rise induced by FK 33-824. Intravenous injection of clonidine (15 microgram/100 g b.w.), an alpha-adrenergic stimulant, resulted in an increase in plasma GH in the rats pretreated with reserpine, DDC or fusarate. Phenoxybenzamine (1 mg/100 g b.w., i.v.), an alpha-adrenergic blocking agent, inhibited the GH response to KF 33-824. On the other hand, GH release induced by FK 33-824 was not influenced by propranolol (1 mg/100 g b.w., i.v.), a beta-adrenergic blocking agent, nor pimozide (0.1 mg/100 g b.w., i.v.), a dopamine antagonist. Intraventricular administration of beta-endorphin (5 microgram/rat) also increased the plasma GH levels which were lowered by phenoxybenzamine. These findings suggest that alpha-adrenergic mechanisms are involved in GH release induced by opioid peptides in the rat.
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PMID:Involvement of alpha-adrenergic mechanisms in growth hormone release induced by opioid peptides in conscious rats. 611 22

A solution synthesis of human beta-endorphin (beta-EP) was carried out by condensation of protected peptide segments bearing N alpha-tert.-butyloxycarbonyl groups and benzyl-derived groups for the protection of functionalities in amino acid side chains. Five intermediate segments were assembled in a stepwise manner starting at the carboxyl terminus. Thus, the segment of sequence region (27-31) was coupled to segment (22-26) by the azide method. Segment (19-21) was incorporated into the growing chain by azide coupling, and segment (10-18) by dicyclohexylcarbodiimide coupling in the presence of 1-hydroxybenzotriazole (DDC-HOBt). Solubility problems in condensing the ensuing 22-peptide with segment (1-9) by DDC-HOBt were overcome by using a dimethylformamidephenol mixture as a solvent. Protecting group cleavage by Na in liquid NH3 was much superior to liquid HF which gave rise to many decomposition products. Homogeneous betah-EP indistinguishable from authentic material in physiochemical and biological properties, was obtained in a single preparative reversed phase liquid chromatographic step after protecting group cleavage.
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PMID:Synthesis of human beta-endorphin in solution using benzyl-type side chain protective groups. 625 7

A variety of neuropeptides, such as TRH, somatostatin, VIP, Substance P, neurotensin, CCK, gastrin, and opioid peptides, alter secretion of GH and PRL from the pituitary. These actions differ according to the route of administration or with experimental conditions, especially anesthesia. Among these peptides, the most consistent results have been obtained with opioid peptides, which stimulate GH and PRL release. Both beta-endorphin and enkephalins are capable of stimulating GH and PRL release in anesthetized and unanesthetized, freely moving rats. The effect is blocked by naloxone, an opiate receptor antagonist. GH secretion induced by opioid peptides seems to be mediated by an alpha-adrenergic mechanism, since treatment with DDC and fusaric acid, which are dopamine-beta-hydroxylase inhibitors, reserpine, and phenoxybenzamine which is an alpha-adrenergic blocking agent, blunted GH secretion. However, pimozide, a dopamine receptor antagonist, and propranolol, a beta-adrenergic blocking agent, were without effect. On the other hand, basal PRL secretion was augmented by pimozide, suggesting the possible involvement of dopamine. It is also possible that serotonin is involved in the GH and PRL release induced by opioid peptides. The physiological significance of opioid peptides in regulating GH and PRL secretion is still unclear. Contradictory results (12,25) have been obtained concerning the effect of naloxone on basal or stimulated GH and PRL secretion in rats, monkeys and humans when tested by the continuous blood sampling method, which rules out the erroneous evaluation of results caused by episodicity of plasma hormone levels. Further studies should clarify the physiological role of opioid peptides in regulating pituitary function.
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PMID:Effect of CNS peptides on hypothalamic regulation of pituitary secretion. 701 Sep 47