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)

Herpes simplex viruses (HSV) remain latent in sensory and peripheral ganglia and can be reactivated to cause recurrent HSV infections. Recent evidence has suggested that stress can induce an immunosuppressive state and increase the frequency and severity of recurrent herpes infections. Because macrophages play a central role in the host defense against HSV, the effects of stress-related neuroendocrine hormones on macrophage-HSV interactions were examined. Norepinephrine and epinephrine blocked the capacity of recombinant interferon-gamma (IFN-gamma) to activate murine macrophages to a cytotoxic state capable of selectively killing HSV-infected cells. In contrast, ACTH, dopamine, serotonin, and beta-endorphin had no effect. The suppression of IFN-gamma-induced, macrophage-mediated lysis of HSV-infected cells occurred concomitantly with a marked increase in macrophage intracellular cyclic AMP levels. Moreover, exogenous administration of dibutyryl cyclic AMP blocked induction of macrophage-mediated cytotoxicity, suggesting that the neurohormones were modulating macrophage function via an adrenergic receptor-mediated system. These findings demonstrate that selective stress-related neurohormones modify the cytolytic activity of macrophages against virus-infected cells and suggest a possible neuroendocrine-immunologic basis for the recurrence of HSV infection.
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PMID:Neuroendocrine hormones suppress macrophage-mediated lysis of herpes simplex virus-infected cells. 300 Nov 83

Hemorrhages of various magnitudes were performed on conscious rats, and arterial pressure, heart rate, and plasma levels of adrenocorticotropin hormone (ACTH), epinephrine, and norepinephrine were measured. Eight rats were prepared with chronic femoral arterial cannulas and received a 10, 15, or 20 ml/kg X 3 min hemorrhage in random order on day 4, 7, or 10 after surgery. Mean arterial blood pressure, heart rate, and plasma ACTH, epinephrine, and norepinephrine concentrations were determined before and 20 min after hemorrhage. Arterial blood pressure decreased significantly immediately after each hemorrhage and slowly recovered over the next 20 min. Heart rate did not change during the 10 ml/kg X 3 min hemorrhage but decreased significantly after 15 and 20 ml/kg X 3 min hemorrhages. Plasma ACTH and epinephrine levels increased significantly 20 min after the 15 and 20 ml/kg X 3 min hemorrhages but not after 10 ml/kg X 3 min hemorrhage. Norepinephrine increased significantly 20 min after the 20 ml/kg X 3 min hemorrhage but not after the 10 or 15 ml/kg X 3 min hemorrhage. There was no significant effect of time and repeated hemorrhages on resting levels of plasma ACTH, epinephrine, norepinephrine, osmolality, or proteins. Since hemorrhage leads to a fall in arterial pressure and a subsequent rise in plasma ACTH, the relationship between plasma ACTH and mean arterial blood pressure during hemorrhage was examined in both conscious and acutely prepared pentobarbital sodium-anesthetized rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Responses of ACTH, epinephrine, norepinephrine, and cardiovascular system to hemorrhage. 301 62

A large body of evidences has suggested the role of adrenergic, opioidergic and other peptidergic receptors in the mediation of animal vas deferens motility. Different animal species showed different neurochemical patterns, so it is to be expected that human vas deferens has its own specific response to several substances, in relation to its peculiar function. In this study we report on the effects of monoaminergic (norepinephrine, dopamine, serotonin, isoproterenol, cholinomimetic drugs) and opioidergic (morphine, buprenorphin, beta-endorphin, met-enkephalin and dynorphin) agonists on isolated human vas deferens motility. Norepinephrine and dopamine provoked complex patterns of motility while opioids did not affect the field electroinduced contractions. The implications of this finding are discussed in relation to human vas deferens function.
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PMID:Receptors mediating contraction of isolated human vas deferens. 302 96

Mediobasal hypothalamus tissue (MBH) from adult male rats was incubated in Krebs-Ringer bicarbonate medium (KRB). KRB was changed at 15 min intervals and the concentration of immunoreactive beta-endorphin (beta-ENDi) in the medium was measured by radioimmunoassay. Incubation of MBH tissue in normal KRB resulted in a constant release rate of beta-ENDi of approximately 1% of the tissue content per h. KRB containing 45 mM K+ causes a two fold increase in the release rate of beta-ENDi which was Ca2+ dependent. Dopamine (0.01-1.0 microM) inhibits both the spontaneous and the K+-stimulated release of beta-ENDi in a dose related manner. The dopamine receptor blocking agent haloperidol prevents this inhibitory effect of dopamine. The selective D-1 receptor agonist SKF 38393 does not affect the release rate of beta-ENDi; whereas the selective D-2 receptor agonist LY 141865 inhibits both the spontaneous and K+-stimulated release of beta-ENDi. The effects of LY 141865 can be blocked by (-)-sulpiride, a selective D-2 receptor antagonist. Norepinephrine only weakly inhibits the K+-stimulated release of beta-ENDi, an effect that can be blocked by haloperidol but not by the alpha-adrenoceptor blocker phentolamine. At concentrations tested (0.01-1.0 microM), isoproterenol, 5-hydroxytryptamine, carbachol and 8-Br-cAMP (1.0 microM) do not affect beta-ENDi release. It is concluded that dopamine can inhibit the release of beta-ENDi from hypothalamic neurons via a D-2 receptor mechanism.
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PMID:Dopamine inhibits the release of immunoreactive beta-endorphin from rat hypothalamus in vitro. 315 84

The sauna induces changes in the secretion of hormones, some similar to changes induced in any other stress situation and others characteristic of exposure to the sauna. Noradrenaline is usually the only catecholamine raised by the sauna in people accustomed to it. The secretion of the antidiuretic hormone is increased and the renin-angiotensin-aldosterone system is activated. The concentrations of the growth hormone and prolactin, in particular, secreted from the anterior pituitary are increased in the circulation. The concentration of the immunoreactive beta-endorphin in blood may also increase which may reflect the feeling of pleasure or, on the other hand, discomfort induced by the sauna. The views on the effects of the sauna on the secretion of the ACTH and cortisol are partly contradictory, probably due to differing ways of taking the sauna bath. In Finnish sauna takers the concentration of cortisol in blood is not usually increased. The changes induced by the sauna in various hormone concentrations in the circulation are, however, normalized within a couple of hours after the heat stress.
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PMID:How the sauna affects the endocrine system. 321 98

The central biochemical pathology of anorexia and the natural aging of the brain is similar. Biochemical models for drug withdrawal and depression may also assist in understanding geriatric anorexia. Norepinephrine, corticotropin releasing factor and beta-endorphin may key neurotransmitters in all of these conditions.
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PMID:Drug abuse and depression: possible models for geriatric anorexia. 326 10

The development of shock initiates a cascade of responses in an effort to reestablish homeostasis. Three of the most important hormonal and neurohumoral changes are the secretion of glucocorticoids, catecholamines, and vasopressin. Regulation of adrenal function is much more complex than originally thought. Hemorrhage is a potent stimulus for cortisol release, and both ACTH and ACTH-independent mechanisms have been described. The ACTH response to its releasing hormone, corticotropin releasing hormone (CRF), is itself amplified by vasopressin, which appears to have intrinsic CRF properties. Because ACTH is synthesized as part of a large precursor molecule (pro-opiomelanocortin) containing the amino acid sequences for several important proteins, stimulation of ACTH release has far-ranging effects, the specifics of which are just being clarified. Norepinephrine and epinephrine levels increase manyfold above baseline within minutes of the onset of hemorrhagic shock. Only patients experiencing cardiac arrest or the rare patient with a very active pheochromocytoma have higher concentrations. The levels reached are far in excess of those required to cause both cardiovascular and metabolic alterations. Because of the presence of the endogenous opiates leucine and methionine enkephalin in the neurosecretory granule, it is very likely that the enkephalins are coreleased with the catecholamines, modifying their cardiovascular effects and producing analgesia. Hypovolemia is also a potent stimulus for vasopressin secretion, which overrides hypotonicity, presenting a clinical picture quite compatible with the syndrome of inappropriate antidiuretic hormone secretion, from which it must be differentiated. Vasopressin also is released by pain, nausea, and hypoxia, all of which are likely to be present in the patient with shock.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endocrinology of shock. 353 88

The possible inotropic effects of all three classes of endogenous opioids were tested alone or in combination with noradrenaline, adrenaline, or carbachol on electrically stimulated atria isolated from male Sprague-Dawley rats. Noradrenaline (6.0 and 12 microM) and adrenaline (4.0 and 8.0 microM) injections caused marked but transient (5 min) dose-related increases in atrial tension compared with preinjection control values, whereas carbachol (0.14 and 1.4 microM) caused a more potent and prolonged (over 15 min) dose-related decrease in atrial tension development. Adrenal enkephalins (0.3-4.0 microM) of methionine enkephalin, leucine enkephalin, Met-enkephalin-Arg6-Phe7, and Met-enkephalin-Arg6-Gly7-Leu8, beta-endorphin (0.2-2.0 microM), or dynorphin A(1-13) (0.2-2.0 microM) did not change atrial tension for a 15-min postadministration test period. In addition, these opioids did not affect the positive inotropic effects of noradrenaline (12 microM) or adrenaline (8.0 microM) or the negative inotropic actions of carbachol (1.4 microM) when the same doses of noradrenaline, adrenaline, or carbachol were given alone. These data indicate that endogenous opioids given in micromolar concentrations tested did not affect atrial tension development of electrically stimulated rat atria. Comparing these data with those of past literature, it is suggested that circulating endogenous opioids probably do not have any direct effects on the rat myocardium to affect myocardial contractility.
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PMID:The effects of endogenous opioids on tension development of isolated, electrically stimulated rat atria. 362 Oct 71

Opioid peptides including met- and leu-enkephalins are co-stored with catecholamines at similar concentrations in highly purified chromaffin granule fractions from bovine adrenal medulla and large dense cored vesicle (LDV) fractions from bovine splenic nerve. An initial attempt was made to test the universality of the co-storage of enkephalins in LDVs of sympathetic nerves. Based on a number of practical considerations, vasa deferentia were chosen from seven species. Leu-and met-enkephalin contents were quantitated by radio-immunoassays and norepinephrine by HPLC with electrochemical detection. Norepinephrine contents varied 11-fold and generally paralleled the density of sympathetic innervation among the species as reported in the literature. Leu-enkephalin contents varied 26-fold, generally paralleling the percentage composition of LDVs in the respective terminal varicosities among the species and animal size (axonal length). Met-enkephalin contents varied 20-fold, generally paralleling the density of sympathetic innervation, but not the percentage LDVs. Various amounts of met-enkephalin were also likely stored in cells other than sympathetic nerves, including chromaffin-like cells, the incidence of which varied according to species. Thus, the met- to leu-enkephalin ratios varied from 1.2:1 in dog; 1.7-1.9:1 in rabbit, cat and bull; 2.9:1 in man; 8.2:1 in rat; and essentially only met-enkephalin in guinea pig. The data imply differences in the processing of preproenkephalins in the same tissue of different species as well as in different cells of that tissue.
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PMID:Enkephalin contents reflect noradrenergic large dense cored vesicle populations in vasa deferentia. 372 73

Forty-eight patients received either naloxone (10 mg), fentanyl (0.1 mg), diazepam (0.3 mg/kg), or saline solution placebo, and then underwent surgical removal of impacted third molars under local anesthesia. Placebo resulted in significantly elevated levels of immunoreactive beta-endorphin (i beta-END), norepinephrine, and anxiety during surgery. Patients receiving naloxone had significantly greater intraoperative i beta-END and pain as compared with those receiving placebo. The naloxone effect on intraoperative pain was a result of a difference in perceived unpleasantness. Both the fentanyl and diazepam groups had significantly lower intraoperative i beta-END and anxiety levels as compared with the placebo group. Norepinephrine levels increased significantly in response to surgical stress in all groups except the diazepam group. Postoperative circulating levels of i beta-END and norepinephrine and pain increased significantly from the 1 to 3-hour postoperative period for all groups, with the exception of stable norepinephrine levels observed in patients receiving diazepam. Results indicate that opiate antagonists stimulate and agonists suppress the release of i beta-END, possibly by affecting the patient's perceived level of pain and anxiety. In addition, the association of intraoperative hyperalgesia with naloxone predosing suggests that endogenous opioid peptides inhibit the perception of intraoperative pain even in the presence of concurrent local anesthesia.
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PMID:Naloxone, fentanyl, and diazepam modify plasma beta-endorphin levels during surgery. 373 80


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