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)

Catheterization of the portal vein and stereotaxic implantation of electrodes in the lateral hypothalamic area (LHA) were performed in normal rats after thiopental anesthesia. Immunoreactive glucagon (IRG) and insulin (IRI), glucose, catecholamines, and beta-endorphin were monitored in portal and peripheral plasma, before and during electrical stimulation of the LHA. The influences on glucose and hormone concentrations of propranolol, phentolamine, atropine, and naloxone infusions were also investigated in similar rats. A basal portoperipheral concentration gradient was found for IRG, IRI, and catecholamines, but not for beta-endorphin. The LHA stimulation induced a significant rise in portal catecholamine, IRG, and glucose concentrations; IRI remained unchanged; the portoperipheral catecholamine gradient was augmented. These alterations were not observed after bilateral splanchnicectomy. Propranolol infusion abolished the LHA-dependent IRG and glucose rises. Naloxone reduced the IRG rise significantly. Phentolamine and atropine did not modify the LHA-induced reactions. These results suggest that the glucagon release which follows LHA electrical stimulation depends mainly on beta-adrenergic transmission by the splanchnic nerves. Opioid peptide receptors may modulate this effect.
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PMID:Glucagon release after stimulation of the lateral hypothalamic area in rats: predominant beta-adrenergic transmission and involvement of endorphin pathways. 630 29

A series of studies were conducted to determine the effects of leucine-(leu-) enkephalin and methionine-(met-) enkephalin on perfusion pressure. These experiments utilized isolated perfused femoral arterial preparations in pentobarbital-anesthetized cats. The enkephalins were administered intraarterially into the femoral artery and changes in perfusion pressure recorded. Leu-enkephalin in doses of 1 microgram to 320 micrograms produced significant dose-dependent decreases in perfusion pressure (4.0 +/- 1.3% with 1 microgram to 19.1 +/- 2.1% with 320 microgram). Similar declines in perfusion pressure (5.2 +/- 2.4% with 1 microgram to 21.7 +/- 4.1% with 320 micrograms) were observed following the administration of met-enkephalin. Pretreatment with naloxone (3 mg/kg) antagonized the effects of both enkephalins. Diphenhydramine (2 mg/kg) effectively antagonized the leu-enkephalin elicited decline in perfusion pressure but blocked the effects of met-enkephalin only at lower agonist doses. Propranolol treatment (4 mg/kg) did not alter the pressure responses to either enkephalin. The results of the study show that intraarterially administered enkephalins exert a vasodilatory effect on vasculature in skeletal muscle which may be direct, indirect or both. The differential antagonism of the effects of the two enkephalins suggest that the two opioids act through different receptors or multiple receptors.
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PMID:Effects of enkephalins on perfusion pressure in isolated hindlimb preparations. 714 40

In several animal species the catecholamines stimulate the release of alpha-MSH from the melanotrope cells of the pituitary neurointermediate lobe through beta-receptors. The human hypophysis does not include a well-defined intermediate lobe and the methods for measuring alpha-MSH are often poorly sensitive. Neuroregulation of this hormone in man has thus received little attention. To see whether the adrenergic system is involved in the control of alpha-MSH secretion and whether the latter is independent of that of other peptides derived from proopiomelanocortin, such as ACTH, we studied the effects on plasma alpha-MSH-like immunoreactivity (alpha-MSH-LI), ACTH, and cortisol of some adrenergic drugs active on the beta-receptors. Six normal volunteers underwent the infusion of the following drugs: isoproterenol (0.03 microgram.kg-1.min-1 for 60 min), propranolol (1 mg.min-1 for 5 min followed by 0.1 mg.min-1 for 115 min), propranolol+isoproterenol (infused between 30 and 90 min of propranolol infusion), placebo (saline solution). Isoproterenol increased alpha-MSH-LI at 15 min (p < 0.001). Propranolol induced a fall of alpha-MSH-LI between 30 and 60 min (p < 0.001), followed by a return to preinfusion concentrations beginning at 75 min, and completely prevented the stimulatory effect of isoproterenol. Plasma ACTH and serum cortisol were always unaffected. These results indicate that in man the adrenergic system stimulates alpha-MSH-LI release through beta-receptors, and that alpha-MSH-LI secretion is dissociated from that of ACTH and cortisol. This in turn suggests that separate neuroregulatory mechanisms exist for the melanotrope and corticotrope cells.
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PMID:Adrenergic regulation of alpha-MSH secretion in man: evidence for a stimulatory role of beta-receptors. 838 4

The significance of enkephalins for the function of the hypothalamic-pituitary-adrenal (HPA) axis, in spite of many efforts, is still elusive. We investigated the effect of leucine- and methionine-enkephalin on the HPA activity in conscious rats. These enkephalins, given intracerebroventricularly (i.c.v.) increased dose-dependently the activity of the HPA axis, measured indirectly through serum corticosterone levels. On a molar basis, leu-enkephalin exerted a stronger effect that met-enkephalin. Naloxone, an opioid receptor antagonist, given i.c.v. prior to enkephalins almost abolished the corticosterone response to met-enkephalin and significantly impaired the response to leu-enkephalin. Prazosin, an alpha 1-adrenergic antagonist, considerably reduced the increase in serum corticosterone levels induced by both enkephalins. Pretreatment of rats with yohimbine, an alpha 2-adrenergic antagonist, also considerably reduced the corticosterone response to met-enkephalin and significantly diminished the response induced by leu-enkephalin. Naloxone and yohimbine inhibited to the same extent the corticosterone response to met- and leu-enkephalin. This suggests an interaction between presynaptic opioid and alpha 2-receptors in regulation of the HPA function. Propranolol, a beta-adrenergic antagonist, given i.c.v. did not alter the corticosterone levels raised by met- and leu-enkephalin. These results indicate that both met- and leu-enkephalin increase the activity of the HPA axis in rats and both central opioid and adrenergic alpha-receptors are involved in this stimulation.
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PMID:Stimulatory effect of intracerebroventricular met- and leu-enkephalin on corticosterone secretion in rats. 926 23


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