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)

We examined the effects of cholinergic, peptidergic and GABAergic agents on secretin secretion from canine duodenal mucosal explants incubated in organ culture media. Carbachol (10(-12) to 10(-4) M), atropine (10(-6) to 10(-4) M), hexamethonium (10(-6) to 10(-4) M), and somatostatin did not alter basal secretion of secretin. Somatostatin (10(-7) to 10(-8) M) inhibited secretin secretion stimulated by pH 4.5. Met, Leu and their D-ala2-analogs inhibited both basal and pH 4.5-stimulated secretin. Naloxone reversed the inhibition caused by met-enkephalin at pH 7.4. GABA (10(-9) to 10(-6) M) stimulated both basal and pH 4.5-stimulated secretin secretion. GABA-stimulated secretin secretion was neuronal in nature, bicuculline sensitive and was mediated via post ganglionic cholinergic neurons. GABA-stimulated secretin secretion was inhibited by both somatostatin and metenkephalin, suggesting that GABA-stimulated secretin secretion may be under the inhibitory control of peptidergic agents as well.
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PMID:Neurohormonal regulation of secretin secretion in canine duodenal mucosa in vitro. 287 46

The influence of naturally occurring opioid peptides (Met-enkephalin (Met-Enk), dynorphin (DYN), beta-endorphin (beta-EP)) as well as morphine and the opiate antagonist naloxone and specific antisera on cerebral blood flow autoregulation was studied in anesthetized, artificially ventilated rats. Local hypothalamic blood flow (CBF, H2-gas clearance technique) and total cerebral blood volume (CBV, photoelectric method) were simultaneously recorded. Autoregulation was tested by determining CBF and CBV during consecutive stepwise lowering of the systemic mean arterial pressure to 80, 60 and 40 mm Hg, by hemorrhage. Resting CBF decreased following Met-Enk, DYN, beta-EP or morphine administration without simultaneous changes in CBV. Naloxone administration, on the contrary, increased CBV without affecting local CBF. Autoregulation of cerebral blood flow was maintained until 80 mm Hg, but not completely at 60 and 40 mm Hg arterial pressure in the control group. General opiate receptor blockade by 1 mg/kg s.c. naloxone abolished autoregulation at all levels, since CBF and CBV passively followed the arterial pressure changes. Intracerebroventricularly injected naloxone (1 microgram/kg) as well as a specific antiserum against beta-EP, but not against Met-Enk or DYN, resulted in the very same effect as peripherally injected naloxone. The present findings suggest that central, periventricular beta-endorphinergic mechanisms might play a major role in CBF autoregulation.
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PMID:Endorphinergic mechanisms in cerebral blood flow autoregulation. 287 14

Opioid peptides and opioid receptors are found in the hearts of various species. Opioid peptides were also shown to modulate norepinephrine inducing changes in atrial rate, in vitro. Since we have recently shown a predominance of kappa and delta receptors in the rat atria, we found it of interest to study the role of highly selective opioid agonists on spontaneous and sympathetically stimulated heart rate. The pithed, artificially ventillated rat was used in these studies. D-Ala2-D-Leu5-enkephalin (DADL), was used as an delta-agonist, D-Ala2-MePhe4-Gly-ol5-enkephalin (DAGO) as a highly selective mu-agonist; Dynorphin A (1-17) as a kappa-agonist and beta-endorphin (beta-END) as a mixed epsilon-delta-mu agonist. Naloxone was used as an opiate antagonist. None of the above opioid peptides changed the basal blood pressure and heart rate at 1-100 nmol/kg except Dyn A-(1-17) which produced a brief depressor response (-15 +/- 2 mmHg, p less than 0.01). Stimulation of the spinal cord (50 v, 1 msec, 1 Hz, 30 sec) produced consistant pressor and cardiac accelerating responses. None of the opioid peptides studied blocked or enhanced the increase in blood pressure or heart rate produced by spinal cord stimulation. The depressor effect of the high dose of Dyn A-(1-17) was not blocked by naloxone. These results suggest that mu, delta or kappa opioid receptors in the rat heart have no role in the regulation of basal or sympathetically driven heart rate. Our data also suggest no role for these opioid receptors in modulation of basal arterial tone or norepinephrine-induced arteriolar constriction.
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PMID:The effect of mu, delta, kappa and epsilon opioid receptor agonists on heart rate and blood pressure of the pithed rat. 288 Dec 24

The blood-brain barrier is capable of transporting peptides with anti-opiate (Tyr-MIF-1) and opiate (enkephalins) activity out of the central nervous system. The relationship of this transport system to the various actions of opiates remains unexplored. This study examined the relationship between the rate of transport and opiate-induced analgesia. Both restraint, a stress that provokes an opiate-mediated analgesia, and the administration of morphine (12 mg/kg, i.p.) each induced an inhibition in the rate of transport. Such inhibition exhibited specificity, since the saturable, brain to blood transport of iodide remained unaltered. However, it was possible to dissociate analgesia and inhibition of transport. The onset and peak of analgesia, as measured by tail-flick latency induced by morphine, preceded the onset and peak of the inhibition of transport. Naltrexone, which blocks opiate-mediated analgesia, also induced inhibition of transport without any significant effect on tail-flick latency. (-) Naloxone but not (+) naloxone also weakly inhibited transport. Deprivation of food and water, associated with analgesia possibly mediated by the opiate, beta-endorphin, which is not transported out of the brain by this system, did not alter transport. These results suggest that while inhibition of transport and analgesia may occur together, these events probably represent two separate aspects of the action of opiates, that may even be mediated by separate receptor sites or peptides in the opiate family.
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PMID:Analgesia and the blood-brain barrier transport system for Tyr-MIF-1/enkephalins: evidence for a dissociation. 289 31

The present study was aimed at characterizing the effects of beta-endorphin on plasma glucose, insulin and glucagon plasma levels in subjects with type-2 diabetes mellitus. Infusion of 0.5 mg/h human beta-endorphin produced significant and simultaneous increments in both insulin and glucagon concentrations and decreased plasma glucose levels (-18 +/- 4 mg/dl, 60 min level, p less than 0.01). When the same diabetics were rendered euglycemic by an insulin infusion (1 mU/kg/min), beta-endorphin did not produce the expected decrease in plasma glucose concentrations nor raise plasma insulin levels; only the response of glucagon was preserved. Normal subjects were rendered hyperglycemic by an intravenous glucose infusion to match the plasma glucose levels of diabetic subjects. In this condition, beta-endorphin produced a significant increase of insulin concentrations, whereas glucagon remained suppressed. The intravenous administration of the long-acting met-enkephalin analogue DAMME (0.25 mg) blunted the hormonal responses to the subsequent beta-endorphin infusion in diabetic patients, although the inhibition was short-lived (30-40 min). Naloxone (5 mg), an opiate antagonist, did not produce any significant change in the insulin and glucagon responses to beta-endorphin, while somatostatin (0.25 mg/h) completely abolished the hormonal responses to the opioid.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Beta-endorphin and islet hormone release in type-2 diabetes mellitus the effects of normoglycemia, enkephalin, naloxone and somatostatin. 289 34

Using a rat tail-flick analgesic assay that uses a cold water-ethylene glycol mixture (-10 degrees C) as the noxious stimulus, we have been able to demonstrate a dose-related, naloxone-reversible analgesic effect for dynorphin A (1-17), the proposed endogenous ligand for the kappa receptor. Male Sprague-Dawley rats were implanted surgically with cannulas in the right lateral ventricle at least 1 week before testing. Five microliters of either drug or saline, followed by a 3-microliter saline flush, were administered. Nociceptive threshold was measured as the latency for the rat to flick or remove its tail from the bath solution after immersion. Dynorphin produced a dose-related analgesia at doses of 1 to 50 micrograms i.c.v., reaching 100% maximum possible analgesia (compared to predrug base line) at the highest dose. We found similar dose-related analgesia when we tested the selective mu agonist [Try-D-Ala-Gly-NMe-Phe-Gly-ol] (0.01-1 microgram), the selective kappa receptor ligand U-50,488H (100-500 micrograms), the selective delta agonist [D-Pen2,5]-enkephalin (50-200 micrograms) and beta-endorphin (0.1-10 micrograms). Naloxone (1.0 mg/kg) was able to block the antinociceptive effect of all but the highest doses of dynorphin, which required 10.0 mg/kg of naloxone. When we compared the same dosages of dynorphin using hot water (55 degrees C) as the noxious stimulus, no antinociception was observed. Although we do not known the mechanisms responsible for the differences between the hot and cold water tests, it may be that the cold water tail-flick test, which is able to assess the antinociceptive activity of both opioid agonists and mixed agonist-antagonists, is a more sensitive measure of the type of analgesia mediated by kappa receptors.
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PMID:Antinociceptive action of intracerebroventricularly administered dynorphin and other opioid peptides in the rat. 290 Mar 24

Plasma levels of some hormones, implicated in the pathogenesis of hypovolemic shock (ACTH, corticosterone, plasma renin activity, aldosterone, prostaglandins, vasopressin and beta-endorphin) were examined on rats with hemorrhagic shock. The animals were treated with the specific opioid antagonist, naloxone (1 mg/kg body weight, i. v.). The results demonstrated that during the first, compensated stage of hypovolemic shock, an increase of ACTH, corticosterone, vasopressin, and stimulation of renin-angiotensin-aldosterone system was evident, that is, an activation of hormonal mechanisms responsible for blood pressure and blood volume restoration occurred. beta-Endorphin and prostaglandin E-release during hemorrhagic shock might contribute to the cardiodepressor changes. Naloxone treatment prevented the development of shock into a progressive stage by several eventual mechanisms: An antagonism of opiate receptors. Stimulation of ACTH secretion, followed by an increased secretion of glucocorticoids or a direct effect on adrenocortical function. Stimulation of aldosterone secretion by ACTH or directly.
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PMID:Hormone changes and beta-endorphin in the pathogenesis of hemorrhagic shock. 293 Sep 96

A 0.01 and 0.1-mg/kg dose of iv naloxone was administered to seven patients in septic shock, in order to evaluate naloxone's hemodynamic effect and possible relation to changes in plasma beta-endorphin and catecholamine levels. Naloxone failed to modify cardiac index, blood pressure, heart rate, and systemic vascular resistance. Plasma beta-endorphin, norepinephrine, and epinephrine were elevated but did not change after naloxone administration. These results suggest that beta-endorphin release is a consequence but not a cause of shock, and that the beneficial hemodynamic effects of naloxone in animal studies could be related to species differences or nociceptive stimulations.
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PMID:Naloxone therapy of human septic shock. 293 1

HCO3- secretion by surface epithelium in duodenum devoid of Brunner's glands was titrated in situ in anesthetized rats. Intravenous injection of small amounts (20 ng/kg) of the endogenous opioid peptide beta-endorphin significantly increased secretion. Naloxone prevented this effect, suggesting that stimulation is mediated by mu-opiate receptors. Morphine 50 microgram/kg had a similar stimulatory action. Vasoactive intestinal peptide (VIP) 0.5-100 microgram/kg dose-dependently increased secretion and this response was independent of simultaneous cholinergic stimulation. The HCO3- secretion maintained pH in the mucus gel adherent to the luminal surface at neutrality for long periods of time (greater than or equal to 60 min); even when the pH in the terminal bulk solution was as low as 2.0. Mucosal HCO3- secretion is thus very probably important in mucosal protection and VIP and endogenous opioid peptides may have a role in its control.
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PMID:Gastroduodenal bicarbonate secretion in mucosal protection. Possible role of vasoactive intestinal peptide and opiates. 293 24

The present experiments assessed the involvement of endogenous opioids in the inhibition of FSH and LH release, ovulation and continuous sexual receptivity following exposure to constant illumination. In the first experiment, exposure to constant illumination resulted in persistent vaginal oestrus in all rats. The injection of naloxone resulted in marked elevations in serum FSH and LH, induced ovulation and increased the frequency of lordosis behaviour. It was concluded that endogenous opioid(s) participate in these effects. In Experiment 2, levels of beta-endorphin were found to be elevated in anterior pituitary and neurointermediate lobe tissue extracts from rats exposed to constant illumination, compared to levels in pro-oestrus rats. Naloxone injection into those rats exposed to constant illumination significantly increased hypothalamic levels of beta-endorphin compared to saline injected controls. This suggests that the blockade of opiate receptors increases beta-endorphin production, uptake and/or decreases its release from the hypothalamus. These results, and the known inhibitory action of beta-endorphin on LH release suggest that it may be this opioid, perhaps in conjunction with pineal products, which is responsible for the observed anti-reproductive effects of constant illumination.
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PMID:The role of endogenous opioid peptides in the effects of constant illumination on reproductive function in the rat. 293 50


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