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 effect of hypoxia on plasma met-enkephalin and catecholamine levels was studied in chronically catheterized fetal sheep. Maternal and fetal hypoxia was maintained for 20 min. We found hypoxia significantly increased the plasma levels of large mol wt met-enkephalin containing peptides from 1755 +/- 229 pg/mL during baseline to 4408 +/- 1426 pg/mL by 15 minutes of hypoxia. The levels of the met-enkephalin pentapeptide were unchanged during hypoxia from a baseline value of 168 +/- 56 pg/mL. Norepinephrine and epinephrine levels increased 5- and 10-fold, respectively, by 15 min of hypoxia. These observations suggest cosecretion of the large mol wt met-enkephalin peptides with catecholamines during stress in developing animals.
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PMID:The effects of hypoxia on (methionine) enkephalin peptide and catecholamine release in fetal sheep. 229 72

The effects of a vegetarian low-protein, low-phosphorus diet supplemented with essential amino acids and ketoanalogues, on the serum beta-endorphin, growth hormone, parathyroid hormone, thyroid hormones (T3 and T4), pituitary TSH and total cortisol were studied in 12 male chronic uremics. beta-Endorphin decreased, as well as growth hormone. Parathyroid hormone and T3 improved significantly, reaching almost normal values. It is hypothesized that the correction of the beta-endorphin excess may account in part for the improvement of some endocrinological and metabolic effects exerted by this dietary treatment. The possible pathophysiological mechanisms which could explain the antiendorphinic action of this treatment in uremic patients are discussed, as well as the possible beneficial endocrine and metabolic effects exerted by the fall in circulating beta-endorphin.
Nephron 1989
PMID:Effects of a low-phosphorus, low-nitrogen diet supplemented with essential amino acids and ketoanalogues on serum beta-endorphin in chronic renal failure. 253 Apr 57

During a 5 month, double blind crossover study of the clinical effect of cyclobenzaprine on 7 patients with fibrositis, weekly measurements were done of plasma beta-endorphin (endorphin, prostaglandin E (PGE) and catecholamines). Endorphin levels were normal but varied with tender point tenderness. Mean plasma dopamine and PGE were elevated. Norepinephrine was normal to very high while epinephrine levels were continuously low to normal. We conclude that patients with fibrositis have a neurotransmitter plasma profile like other chronic pain states having stress and increased vasomotor activity with the possible exception of having low circulating epinephrine. This disparity may mark a failure of central nervous system pain modulation in fibrositis.
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PMID:The plasma endorphin, prostaglandin and catecholamine profile of patients with fibrositis treated with cyclobenzaprine and placebo: a 5-month study. 253 82

The dog pituitary pars intermedia (PI) appears to consist of relative large numbers of ACTH-containing cells in addition to the more abundant alpha MSH-containing cells. Since regulation of PI secretion probably varies across mammalian species, this study was undertaken to identify substances potentially involved in the control of dog PI POMC peptide secretion and to determine if these substances altered the secretion of immunoreactive (IR) ACTH and IR-alpha MSH in a parallel fashion. Pituitary neurointermediate lobes from dogs were collected and dispersed, and the PI cells obtained were perifused. For comparison, rat PI and pars distalis (PD) cells as well as dog PD cells were similarly collected and perifused. Dog PI cells secreted IR-alpha MSH at a basal rate of 125 +/- 59 (mean +/- SD) pg/min.10(5) cells and IR-ACTH at a rate of 40 +/- 9 pg/min.10(5) cells (molar IR-alpha MSH/IR-ACTH = 10). In contrast, secretion rates for IR-alpha MSH and IR-ACTH from perifused rat PI cells were 171 +/- 108 and 3 +/- 2 pg/min.10(5) cells, respectively (molar IR-alpha MSH/IR-ACTH = 179). Using Sephadex G-50 gel filtration chromatography, virtually all of the IR-beta-endorphin secreted by dog PI cells eluted near beta-endorphin (1-31). In addition, all of the IR-alpha MSH secreted by dog PI cells coeluted with synthetic alpha MSH on the G-50 column, but IR-ACTH appeared in two peaks, one eluting near porcine ACTH-(1-39) and another, apparently larger mol wt species. Dopamine and somatostatin were found to inhibit the secretion of IR-alpha MSH and IR-ACTH from perifused dog PI cells in a parallel and dose-dependent fashion. Norepinephrine and epinephrine similarly inhibited POMC peptide secretion, but this effect was blocked by haloperidol, suggesting that it was mediated through a dopamine receptor. CRF stimulated the secretion of both hormones from dog PI, and this effect was abolished by treatment of the cells with either dopamine or somatostatin. Cortisol had no effect on either basal or CRF-stimulated secretion of IR-alpha MSH or IR-ACTH from dog PI cells, but it did inhibit CRF-stimulated IR-ACTH from perifused dog PD. These results suggest that 1) dog PI secretes considerably more IR-ACTH than that in the rat; 2) the probable separate cell sources of IR-alpha MSH and IR-ACTH in dog PI are regulated in an identical fashion; and 3) dopamine, somatostatin, and CRF may function in the physiological or pathophysiological regulation of dog PI.
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PMID:Regulation and secretion of proopiomelanocortin peptides from isolated perifused dog pituitary pars intermedia cells. 253 71

In 24 patients with a functioning kidney transplant, hypoglycemia-induced somatotropin (STH), adreno-corticotropin and cortisol secretion was studied. In a further 24 transplanted patients, secretion of lutropin, follitropin and testosterone after the intravenous administration of luliberin was assessed. Data obtained in this paper suggest the presence of abnormal function of the pituitary-adrenal and pituitary-gonadal axis and abnormal STH secretion in patients with a functioning transplant. Type and duration of immunosuppressive therapy seem to influence the intensity of the above-mentioned endocrine abnormalities.
Nephron 1989
PMID:Influence of type of immunosuppressive therapy on secretion of somatotropin and function of the pituitary-adrenal and pituitary-gonadal axis in patients with a kidney transplant. 207 24

To further our understanding of the functional role of catecholaminergic systems in regulating hypothalamic corticotropin-releasing hormone (CRH) secretion, we assessed the direct effects of a multiplicity of catecholamine agonists and antagonists on hypothalamic CRH secretion. To accomplish this, we used an in vitro rat hypothalamic organ culture system in which CRH secretion from single explants was evaluated by a specific RIA (IR-rCRH). Norepinephrine (NE) stimulated IR-rCRH secretion dose dependently, with peak effects in the nanomolar range. The effect of NE was antagonized by the mixed alpha antagonist phentolamine, the alpha 1 antagonist prazosin, and the alpha 2 antagonist yohimbine, but not by the beta blocker, L-propanolol. Compatible with these data were the findings that the alpha 1 agonist phenylephrine and the alpha 2 agonist clonidine both stimulated IR-rCRH secretion in a dose-dependent fashion. On the other hand, whereas the beta agonist, isoproterenol, caused a weak, non-dose-dependent increase in IR-rCRH secretion, this effect could not be antagonized by L-propanolol. Despite pretreatment with serotonin and acetylcholine antagonists, the effect of NE upon IR-rCRH secretion was undiminished, suggesting that NE-induced CRH secretion is not mediated by either neurotransmitter. On the other hand, pretreatment with gamma-aminobutyric acid (GABA) attenuated NE-induced IR-rCRH secretion. Whereas epinephrine (E) stimulated IR-rCRH secretion, this occurred only at higher concentrations, and was antagonized by phentolamine, but not by L-propanolol. Dopamine (DA) had a weak stimulatory effect that could be antagonized by the DA1 receptor antagonist, SCH 23390, but not by phentolamine. We conclude that NE and E stimulate hypothalamic IR-rCRH secretion via alpha 1 and alpha 2 receptors. The effect of NE upon IR-rCRH secretion is not apparently mediated by serotonergic or cholinergic interneurons, but is modulated by the inhibitory neurotransmitter, GABA. These data support the idea that the central catecholaminergic systems are excitatory rather than inhibitory upon CRH secretion when acting directly at the hypothalamic level.
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PMID:Catecholamine effects upon rat hypothalamic corticotropin-releasing hormone secretion in vitro. 290 33

The effect of hemodialysis on the plasma concentration of beta-endorphin (beta-EP) and beta-lipotropin (beta-LPH) was studied in 11 patients with end-stage renal disease (ESRD). The plasma beta-EP/beta-LPH concentrations measured at 13.00 h were not significantly different in the patients compared to age-matched controls. Furthermore, hemodialysis produced no change in the plasma concentrations of beta-EP/beta-LPH. The elevated levels of beta-EP/LPH previously reported are most likely a reflection of the measurement of these peptides at a time of peak diurnal secretion compounded by a fall in the metabolic clearance rate of the endogenous opioids in ESRD. It remains to be established whether measurement of adronocorticotropic hormone or beta-EP/beta-LPH is more accurate an indicator of the integrity of the hypothalamic-pituitary-adrenal axis in patients with ESRD.
Nephron 1986
PMID:Plasma beta-endorphin and beta-lipotropin in patients with end-stage renal disease--effects of hemodialysis. 294 91

Circulating opioids were studied in insulin-dependent diabetics with renal haemodynamic alterations. Higher circulating beta-endorphin (beta-EP) and lower beta-lipotropin (beta-LPH) levels were found in patients with glomerular hyperfiltration than in diabetics with normal glomerular filtration rate (GFR) and controls. Moreover, significantly positive correlations between beta-EP and GFR, and between beta-EP and renal plasma flow were demonstrated in these patients. On the contrary, reduced beta-EP levels were observed in diabetics with impaired GFR and overt nephropathy. Plasma renin activity was increased in diabetics with glomerular hyperfiltration and reduced in diabetics with overt nephropathy. Circulating opioids might, therefore, play a role in renal haemodynamic alterations, both in patients with early and advanced glomerular changes.
Nephron 1987
PMID:Circulating opioids and plasma renin activity in insulin-dependent diabetics with renal haemodynamic alterations. 295 38

Studies of the roles played by neurotransmitters in the development of hypertension in the spontaneously hypertensive (SHR) rat are complicated by the presence of genetic differences between SHR and normotensive control rats, which are not related to differences in blood pressure. One approach that may be used in an attempt to overcome this difficulty is to study the manner in which neurotransmitter and metabolite levels change with age, and to relate these changes to alterations in blood pressure with ageing. Noradrenaline (NA) levels in the brainstem and spinal cord of SHR and Wistar Kyoto rats fell with age, while 3,4-dihydroxyphenylethyleneglycol (DHPG) levels (a neuronal metabolite of noradrenaline) remained constant. Similar changes were seen when NA and DHPG levels were measured in the discrete brainstem A1, A2, and C2 region, and when adrenaline, NA, and DHPG levels were examined in the C1 region. Differences in age-related changes of neuropeptide Y (NPY) levels were also found in the ventromedial nucleus of the hypothalamus and the locus coeruleus, and of beta-endorphin in the anterior hypothalamic nucleus, the paragigantocellular nucleus of the brainstem, and the locus coeruleus. These changes may indicate either a progressive increase in the activity of neurons in the sympathoexcitatory C1 region or a progressive reduction in the activity of vasodepressor A1, A2, and C2 regions with ageing, or both. However, changes in catecholamines and metabolites with age were similar in both strains and therefore cannot readily explain the more rapid rise in blood pressure with ageing in SHR rats.
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PMID:Neurotransmitters and neuropeptides in blood pressure regulation in the spontaneously hypertensive rat. 296 19

Ten men and 10 women exercised on a bicycle ergometer for 20 min at 40, 60, and 80% maximal oxygen uptake (VO2max) to determine the relationship between plasma beta-endorphin, catecholamines, and exercise intensity. Compared to rest, plasma beta-endorphins were not significantly elevated during the 40 and 60% workloads (4.8 +/- 1.0 pmol.l-1 vs 3.8 +/- 0.7 and 6.3 +/- 0.9, respectively). In contrast, the 80% exercise significantly elevated endorphins to 16.1 +/- 4.0 pmol.l-1. Plasma norepinephrine concentrations were 0.30 +/- 0.04 ng.ml-1 at rest and increased with exercise intensity (40% = 0.60 +/- 0.05, 60% = 0.93 +/- 0.07, 80% = 2.00 +/- 0.14, VO2max = 2.55 +/- 0.14 ng.ml-1). Plasma epinephrine followed the same trend (rest = 0.07 +/- 0.01, 40% = 0.33 +/- 0.03, 60% = 0.49 +/- 0.02, 80% = 0.88 +/- 0.07, VO2max = 0.95 +/- 0.06 ng.ml-1). Norepinephrine was found to significantly correlate to endorphins (r = 0.499; P less than 0.02). Conversely, epinephrine was not correlated with beta-endorphin (r = 0.309; P greater than 0.05). The low correlation suggests a weak relationship between beta-endorphin and catecholamine responses during exercise. The results of this investigation suggest that the relationship between beta-endorphin and exercise intensity is curvilinear, with anaerobic activity producing the most significant endorphin response. It was also noted that the beta-endorphin response was not related to gender, but the amine response to exercise was gender-related, being greater for the men.
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PMID:Exercise intensity-related responses of beta-endorphin and catecholamines. 296 88


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