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)

Beta-endorphin has been implicated in the cardiovascular depression that occurs in shock. While pharmacologic doses of beta-endorphin cause hypotension, physiologic doses of beta-endorphin have not been studied. In this study, six dogs (group I) were given IV beta-endorphin (peak concentrations previously determined in canine shock, 3,200 pg/ml); 5 minutes prior to beta-endorphin infusion, four dogs (group II) were given naloxone, 2 mg/kg bolus, and continuous infusion, 2 mg/kg/hr. In group I, beta-endorphin decreased stroke volume (from 0.99 +/- .12 to 0.57 +/- .08 ml/kg), dP/dt (from 3,167 +/- 140 to 2,875 +/- 412 mmHg X sec), and coronary blood flow (from 2.5 +/- .47 to .68 +/- .11 ml/min/gm), while heart rate rose significantly. Naloxone pretreatment maintained dP/dt, stroke volume, and coronary blood flow with no change in heart rate or mean arterial pressure. This study confirms that beta-endorphin depresses contractility and coronary blood flow in normovolemic nonstressed dogs, suggesting that beta-endorphin is in part responsible for cardiovascular depression in shock.
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PMID:Cardiocirculatory effects of physiological doses of beta-endorphin. 293 43

The involvement of endogenous opioid peptides in the antihypertensive action of acutely administered clonidine, a centrally acting adrenergic agonist, was studied in humans. Eight hypertensive subjects received clonidine 0.2 mg orally, naloxone 8 mg i.v. followed by a 0.13 mg/min infusion, and both drugs together on separate days. Clonidine resulted in a significant decrease in mean blood pressure, which was not affected by concomitant treatment with naloxone. Naloxone alone or with clonidine caused significant elevations in plasma aldosterone, not mediated by increased plasma renin activity. Plasma beta-endorphin was not increased after clonidine administration. In humans, the antihypertensive effects of acute clonidine administration do not appear to be mediated by the release or action of endogenous opioids.
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PMID:Endogenous opioid peptides: do they mediate the acute antihypertensive action of clonidine in humans? 293 15

Caerulein has been shown to possess a long-lasting antagonistic effect on amphetamine hyperactivity in rats when given in combination with haloperidol. We found that this effect of caerulein involved beta-endorphin. Naloxone pretreatment and hypophysectomy abolished the caerulein effect, while intracerebroventricular or intra-nucleus accumbens injection of beta-endorphin together with haloperidol administration produced an effect similar to that of caerulein. The results suggest that the long-term antagonism of the amphetamine effect of caerulein is mediated by the endogenous opioid beta-endorphin.
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PMID:beta-Endorphin involvement in the antidopaminergic effect of caerulein. 294 Mar 95

Ornithine decarboxlyase (ODC) catalyzes the initial step in the bio-synthesis of the polyamines spermidine and spermine, which are key regulators of cell growth, proliferation and differentiation. Intracisternal administration of beta-endorphin (1 microgram) to 6 day-old rats markedly decreased brain, liver, heart and kidney ODC activity. Conversely, subcutaneous administration of beta-endorphin increased ODC activity in the heart and liver. Thus, ODC inhibition in peripheral organs in rat pups given beta-endorphin intracisternally appears to reflect central effects of this neuropeptide. Experiments were also carried out to test whether opioid receptors are involved in these tissue ODC responses. Naloxone prevented the decreases in brain ODC indicating the participation of opioid receptors in that process. In contrast, naloxone did not alter ODC responses in peripheral organs in rat pups given beta-endorphin intracisternally, indicating that these effects are independent of its classical opioid character. These results support the view that endogenous beta-endorphin may play an important role in organogenesis by modulating the growth-related enzyme ODC. The data also suggest that the regulation of peripheral organ development by beta-endorphin may be mediated through the release of growth regulatory substances from the CNS.
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PMID:Effects of beta-endorphin on ornithine decarboxylase in tissues of developing rats: a potential role for this endogenous neuropeptide in the modulation of tissue growth. 294 33

In humans, plasma beta-endorphin levels rise during application of acute stressful stimuli (vertigo, cold pain, and transcutaneous electrical stimulation) that induce gut motor disturbances. Whereas it is possible that circulating beta-endorphin participates in the mediation of these central effects on gut motility, its role cannot be established solely on the basis of changes in plasma levels. Therefore, we designed the present study to investigate 1) the dose-related effects of intravenous synthetic human beta-endorphin and naloxone on gastrointestinal pressure activity in fed healthy individuals; and 2) the interactions of the opiate agonist and antagonist. Infusion of beta-endorphin increased pyloric phasic pressure activity (P less than 0.001) and induced intestinal bursts of rhythmic activity (P less than 0.05) which interrupted normal fed motility. These effects were dose related, with the pyloric dose-response profile being essentially linear. The effects in the proximal intestine were obtained with doses of beta-endorphin at 250 ng X kg-1 X min-1 or greater. In the antrum, there was an overall reduction in phasic pressure activity (P less than 0.02), which was predominantly an effect of the highest dose of beta-endorphin infused (2,500 ng X kg-1 X min-1). Naloxone by itself had no significant effect on fed upper gut motility. However, naloxone significantly inhibited the effect of the lower doses of beta-endorphin on the pylorus. In addition, naloxone significantly reduced the probability of beta-endorphin, triggering intestinal bursts of rhythmic activity. These data suggest that beta-endorphin may play a humoral role in the stimulation of fed pyloric contraction at physiological levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dose-related effects of synthetic human beta-endorphin and naloxone on fed gastrointestinal motility. 294 39

To investigate the possibility of a direct effect of morphine on the pars intermedia cells of the pituitary gland, rat neurointermediate lobes (NIL) were transplanted under the kidney capsule. At 2 and 8 days posttransplantation the NIL transplant had maintained its morphological integrity. However, at 15 days posttransplantation the morphological integrity of the NIL transplant had started to deteriorate. The NIL transplant contained, synthesized, and released beta-endorphin-like peptides. It was noticed that there was very little beta-endorphin in the radiolabelled biosynthesized products, suggesting that either the maturation processing of proopiomelanocortin was modified, or that beta-endorphin was released immediately as soon as it was formed and did not accumulate in the tissue. In support of the latter possibility was the elevated content of beta-endorphin-like immunoreactivity in the sera of rats with a NIL under the kidney capsule. Furthermore, the NIL transplant seemed to produce a substance or substances which could decrease the content, the biosynthesis and the release of beta-endorphin-like peptides by the NIL in situ. Treatment with either morphine or naloxone for 5 days did not change the beta-endorphin-like immunoreactivity content in the NIL transplanted under the kidney capsule. However, a distinct decrease in the beta-endorphin-like immunoreactivity in the NIL in situ of animals with or without a NIL transplant was observed following the morphine treatment. Naloxone treatment induced a decrease in the beta-endorphin-like immunoreactivity content in the hypothalamus, but had no effect on the beta-endorphin-like immunoreactivity content in the anterior lobe and NIL of the pituitary gland in situ or in the NIL transplant.
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PMID:Neurointermediate lobe transplanted under the kidney capsule modifies the activity of the neurointermediate lobe in situ, but does not respond to opiate treatment. 294 31

Serotonin (5-hydroxytryptamine) and beta-endorphin administered into the third ventricle of the hen blocked normal and progesterone-induced ovulation, and suppressed the release of LH in normal and progesterone-injected hens. p-Chlorophenylalanine, an inhibitor of serotonin synthesis, caused the release of LH and diminished the effect of beta-endorphin. Naloxone, an antagonist of opiate peptides, diminished the effect of beta-endorphin but not the effect of serotonin. The results suggest that both serotonin and beta-endorphin are involved in the control of LH release in the hen as an inhibitory agent, and serotonin is predominant while beta-endorphin is subsidiary to the inhibition of the LH release.
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PMID:Effect of serotonin and beta-endorphin on the release of luteinizing hormone in the hen (Gallus domesticus). 294 59

Chemical antagonists were used to assess the role of beta-endorphin and arginine-vasopressin (AVP) in canine endotoxin shock. Fifteen awake dogs were given Escherichia coli endotoxin IV. Within 5 min, CO decreased to 28%, LV dP/dt to 46%, and MAP to 52% baseline. Fifteen minutes after endotoxin, five dogs each received naloxone, AVP antagonist, or no treatment. Control (untreated) animals exhibited persistent cardiovascular depression, with CO 49%, LV dP/dt 69%, and MAP 91% of baseline after 45 min. Naloxone improved CO to 69%, LV dP/dt to 94%, and MAP to 91% by 30 min after treatment. AVP blockade improved CO to 105%, LV dP/dt to 107%, and MAP to 95% of baseline by 30 min after treatment, and caused significant tachycardia. Plasma cortisol and AVP increased markedly in all groups after endotoxin administration. AVP antagonist treatment increased mean survival from 1.4 to 4 days. These data suggest that abnormally elevated AVP contributes to cardiovascular depression in canine endotoxin shock and that AVP blockade is therapeutic in the animal model studied.
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PMID:The role of endorphins and vasopressin in canine endotoxin shock. 294 95

beta-Endorphin was measured in the plasma of control subjects and 12 chronic alcoholics in the acute stage of ethanol intoxication. Naloxone was administered and the level of beta-endorphin was compared before and after treatment. The increased level of beta-endorphin in the intoxicated subjects supports the presence of ethanol interactions with the opioid system, since pituitary secretion does not seem to be involved. Furthermore, the coexistence of high levels of beta-endorphin and an effective naloxone response suggest a possible link between the two.
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PMID:Determination of beta-endorphin in alcoholic patients in the acute stage of intoxication: relation with naloxone therapy. 294 52

The cardiovascular effects of beta-endorphin [beta-LPH-(61-91)] were investigated after systemic (i.v.) and central (third ventricle and right lateral ventricle) administration in urethane-anesthetized rats. beta-Endorphin (10 and 100 micrograms/kg i.v. or 40 micrograms into the third ventricle or into the lateral ventricle) in normotensive animals induced a decrease in blood pressure and bradycardia. The same dose of beta-endorphin by systemic and central administration induced much more pronounced cardiovascular effects in spontaneously hypertensive rats and in rats rendered hypertensive by DOCA administration than in normotensive rats. Naloxone i.v. pretreatment reduced the cardiovascular effects induced by beta-endorphin.
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PMID:Central and peripheral cardiovascular effects of beta-endorphin in normotensive and spontaneously hypertensive rats and in rats rendered hypertensive by deoxycorticosterone acetate administration. 295 May 76


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