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)

In a previous study we observed that calcitonin increases beta-endorphin, ACTH, and cortisol secretion. We assumed that calcitonin might have a modulatory role on the pituitary function. The present study was initiated to clarify whether this effect is due to a direct pituitary stimulation or to an indirect stimulation through CRF (corticotropin releasing factor). Fourteen healthy subjects, aged 30-60 years were investigated. All the subjects received 100 IU Salmon calcitonin Sandoz i.v. at 8 a.m. (time 0). Plasma beta-endorphin, ACTH and cortisol were estimated every 30 min from -30 to 120 min by specific radioimmunoassay. The same parameters were estimated a second time, at the same intervals, when cyproheptadine 8 mg (7 subjects) and 40 mg propranolol (7 subjects) were given per os at -30 min and calcitonin i.v. at time 0. beta-endorphin, ACTH and cortisol levels (Mean +/- SEM) rose significantly after calcitonin (peak value at 30-90 min) from 5.2 +/- 0.7 to 15.1 +/- 2.6 pmol/l; from 43.0 +/- 2.7 to 70.7 +/- 4.1 pg/ml and from 10.6 +/- 1.5 to 19.6 +/- 2.1 micrograms/100 ml respectively (p less than 0.0001 by analysis of variance and covariance and repeated measures). Propranolol 40 mg (per os) administered at time -30 did not alter the response of beta-endorphin, ACTH and cortisol to calcitonin (infused at time 0). Cyproheptadine, the antiserotonergic substance that inhibits the synthesis and release of CRF completely inhibited the stimulatory effect of calcitonin. We conclude that probably calcitonin has a modulatory role on the hypothalamo-pituitary adrenal axis and that it acts at the hypothalamic level probably by stimulating CRF secretion.
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PMID:Antiserotonergic inhibition of calcitonin-induced increase of beta-endorphin, ACTH, and cortisol secretion. 285 Mar 48

Specific somatostatin (SRIH) receptors on human pituitary adenoma cell membranes were characterized using [125I]Tyr11-SRIH as the radioligand. Specific binding of [125I] Tyr11-SRIH to adenoma cell membranes reached a steady state within 30 min at 25 C, and semilogarithmic analysis of the data revealed that the rate of the binding was linear at 25 C with a t1/2 of 13.2 min. Specific binding increased linearly with 5-160 micrograms plasma membrane protein. SRIH-14 and SRIH-28 inhibited [125I]Tyr11-SRIH binding to adenoma cell membranes with ID50S of 0.32 and 0.50 nM, respectively, while secretin, glucagon, gastrin, cholecystokinin-8, bombesin, TRH, LHRH, human GH-releasing factor-(1-44)-NH2, D-Ala2-met-enkephalin, gamma-aminobutyric acid and taurine did not significantly inhibit binding. All of 13 GH-secreting adenomas investigated had specific and high affinity SRIH receptors, with a dissociation constant (Kd) of 0.80 +/- 0.15 nM (mean +/- SEM) and a maximal binding capacity (Bmax) of 234.2 +/- 86.9 fmol/mg protein (mean +/- SEM). Among five of the nonsecreting pituitary adenomas examined, two had SRIH receptors with Kd values of 0.18 and 0.32 nM and Bmax values of 17.2 and 48.0 fmol/mg protein, respectively. In the remaining three, SRIH receptors were not detected. These results indicate that GH-secreting adenomas as well as some nonfunctioning adenomas have specific SRIH receptors, and hence, the function of the adenomas could be altered by SRIH.
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PMID:Specific somatostatin receptors on human pituitary adenoma cell membranes. 286 81

To determine whether peptides derived from the N-terminus of the corticotropin/melanotropin/endorphin precursor, pro-opiomelanocortin, are released into blood in response to acute haemorrhagic stress, we examined the effect of haemorrhage on plasma concentrations of immunoreactive gamma 3-melanotropin, beta-endorphin and cortisol. Plasma concentrations of immunoreactive gamma 3-melanotropin (mean +/- SEM) increased within 30 min of haemorrhage from 71.1 +/- 10.4 to 106.8 +/- 6.3 fmol/mL (p less than 0.01) and plasma cortisol increased from 16.2 +/- 3.8 to 85.9 +/- 22.4 pmol/mL (p less than 0.025). The changes in plasma immunoreactive gamma 3-melanotropin and beta-endorphin were positively correlated (p less than 0.025). This study shows that peptides derived from the N-terminus of pro-opiomelanocortin are co-secreted with the C-terminal peptide beta-endorphin during acute haemorrhagic stress in sheep.
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PMID:Secretion of N-terminal pro-opiomelanocortin-derived peptides in response to acute haemorrhagic stress in conscious sheep. 293 48

We have investigated the role of adrenal steroids and the opiates in regulating arginine vasopressin (AVP) secretion into the pituitary stalk blood of the rat. The portal plasma concentration of AVP in urethane-anesthetized male rats was 532 +/- 68 pg/ml (mean +/- SEM), while the peripheral plasma AVP concentration in intact urethane-anesthetized rats was 20.7 +/- 5.7 pg/ml. Column chromatography on Sephadex G-25 of an extract of a pool of portal plasma revealed that the material being assayed comigrated with synthetic AVP. Bilateral adrenalectomy (ADX) 5 days before the collection of portal blood elevated portal plasma AVP concentrations approximately 6-fold (655 +/- 124 pg/ml in controls vs. 4090 +/- 504 pg/ml in adrenalectomized animals). Dexamethasone administration (15 micrograms/kg X day) for 5 days prevented the ADX-induced increase in portal plasma AVP concentrations without significantly changing portal plasma AVP concentrations in intact rats. Portal plasma concentrations of beta-endorphin were not changed by ADX or dexamethasone treatment. The iv infusion of morphine sulfate (3 mg/kg) dramatically decreased the concentration of AVP in the portal plasma of the rat (501 +/- 101 pg/ml before morphine vs. 185 +/- 50 pg/ml after morphine). The inhibitory effect of morphine was reversed by naltrexone (1.0 mg/kg), whereas naltrexone alone did not alter AVP secretion. Morphine administration also decreased systemic plasma AVP concentrations in urethane-anesthetized rats (27.1 +/- 6.6 pg/ml in controls vs. 3.3 +/- 1.3 pg/ml in morphine-treated rats). Naltrexone treatment reversed this effect. These results suggest that AVP secretion into pituitary stalk blood is under the inhibitory influence of the adrenal steroids, and the increased concentration of AVP found in portal blood may be partially responsible for the elevated levels of ACTH after ADX. Furthermore, morphine-induced activation of the pituitary-adrenal axis is apparently independent of hypothalamic AVP secretion.
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PMID:The concentration of arginine vasopressin in pituitary stalk plasma of the rat after adrenalectomy or morphine. 293 37

To study the possible role of plasma beta-endorphin in bulimia, we measured plasma beta-endorphin immunoreactivity in 34 female patients with normal-weight bulimia and 34 normal female controls matched for weight as percent of ideal. Plasma beta-endorphin immunoreactivity in bulimics (mean 59.6 pg/ml; SEM 5.6) was significantly lower (p less than 0.05) than in controls (mean 79.5 pg/ml; SEM 8.5). Within the bulimic group, plasma beta-endorphin immunoreactivity correlated inversely with severity of bulimic symptomatology as measured by the Eating Attitudes Test Bulimia Subscale (p less than 0.05). Endorphin level did not correlate with severity of depression or with percent ideal body weight. Abnormalities in opioid metabolism may be implicated in eating disorders and account for the addictive properties of these disorders.
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PMID:Eating behavior and plasma beta-endorphin in bulimia. 294 30

The effect of electroimmobilisation on the plasma concentrations of beta-endorphin/beta-lipotrophin (beta-EP/beta-LPH), cortisol and prolactin (PRL) has been assessed in sheep. Serial blood samples were collected from control and electroimmobilised animals during the first and fourth of a series of four repeated treatments over two days. After electroimmobilisation the mean (+/- SEM) plasma concentrations of beta-EP/beta-LPH increased significantly from 132 +/- 19 pg ml-1 to 545 +/- 111 pg ml-1; the plasma concentrations of cortisol also increased significantly from 22.3 +/- 3.5 ng ml-1 to 108.0 +/- 12.9 ng ml-1. There was no significant change in plasma PRL concentrations after electroimmobilisation and also no significant difference between the plasma concentrations of PRL in the control and electroimmobilised animals. There was no significant difference between the effects of the first and fourth exposure to electroimmobilisation on the plasma concentrations of beta-EP/beta-LPH, cortisol and PRL. These results suggest that the endocrine response to electroimmobilisation may be specific to the pituitary-adrenal axis.
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PMID:Effect of electroimmobilisation on ovine plasma concentrations of beta-endorphin/beta-lipotrophin, cortisol and prolactin. 294 54

The placenta has been shown to contain ACTH and beta-endorphin but the roles of these peptides are unknown. To investigate whether they are released into the maternal circulation from the placenta in response to physiological stimuli the effects of hypoglycaemic stress were investigated. Plasma samples were collected from the femoral artery (FA) and uterovarian (UV) vein of nine pregnant sheep before and during hypoglycaemia induced by intravenous insulin (100U). Plasma concentrations of ovine beta-endorphin (o beta-EP) were measured by radioimmunoassay. Concentrations of o beta-EP rose in both vessels by 60 min after insulin. The peak concentrations of o beta-EP (pmol/l) were 122 +/- 29 (mean +/- SEM, n = 8) in the UV and 96 +/- 24 (n = 9) fmol/ml in the FA 60 min after insulin injection. There was no difference between the concentrations of o beta-EP in the vessels before insulin injection but at 60 and 120 min after insulin the concentrations of o beta-EP were significantly higher in the UV than FA (P less than 0.02, analysis of variance). This indicates that the pregnant uterus or placenta can respond to hypoglycaemia by secreting beta-EP into the maternal circulation. It is therefore possible that placental pro-opiomelanocortin (POMC) peptides may have a role in maternal endocrinology and metabolism.
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PMID:Secretion of beta-endorphin into the maternal circulation by uteroplacental tissues in response to hypoglycaemic stress. 297 50

Vasopressin (VP)-converting aminopeptidase (VP-AP) activity and VP contents were measured in single rat pineal glands during the summer of two successive years. The peptidase activity decreased significantly in August. The lowest activity (+/- SEM) of 0.18 +/- 0.02 pmol.hour-1 was recorded on August 14, compared to the basal activity of 0.25 +/- 0.01 pmol.hour-1 in July and September of 1986. The change with similar percentage occurred in the same period of 1987. The specific activity of the enzyme in the crude homogenate, 15,000 g pellet and supernatant fraction of rat pineal glands, exhibited the same pattern of variations. The decrease in peptidase activity coincided with the previously reported dramatic rise in pineal VP content in early August which was confirmed in this series of experiments. Another peptidase, the so-called gamma-endorphin generating endopeptidase (gamma-EGE) activity, and beta-endorphin-related peptides in the pineal gland did not change in this period. The results show that the variations of pineal VP contents and VP-AP activity during summer are not general for other peptides and peptidases. The coincidence of opposite changes in VP content and VP-AP activity of the pineal gland may indicate a role of the peptidase activity to regulate the VP content.
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PMID:Changes in vasopressin-converting aminopeptidase activity in the rat pineal gland during summer: relationship to vasopressin contents. 297 42

Long term use of ovine corticotropin-releasing hormone (oCRH) requires a convenient route of administration. The effects of 0.3, 3, and 30 micrograms/kg BW synthetic oCRH given as a sc injection and of 10 and 30 micrograms/kg given as an intranasal spray were studied in 10 normal men in the late afternoon. Basal plasma immunoreactive ACTH (IR-ACTH) and IR-cortisol levels were 14 +/- 1.9 pg/ml and 4.3 +/- 0.4 microgram/dl (mean +/- SEM). Peak IR-ACTH levels (mean +/- SEM) were 43 +/- 5.5, 53 +/- 8.1, and 64 +/- 8.9 pg/ml after the 0.3, 3, and 30 micrograms/kg doses of oCRH given sc, respectively, and 23 +/- 4.3 and 36 +/- 4.8 pg/ml after the 10 and 30 micrograms/kg doses of oCRH given intranasally, respectively. The lowest sc dose and both intranasal doses caused only single IR-ACTH peaks. After 3 and 30 micrograms/kg sc oCRH, IR-ACTH rose by 15 min, reached an initial peak at 45-60 min, fell rapidly until 90-120 min, and rose to a second peak at 3-5 h. This biphasic response is similar to that previously found after iv administration. IR-ACTH levels remained elevated for 4, 10, and at least 16 h after 0.3, 3, and 30 micrograms/kg sc oCRH, respectively, and for 1.5 and 3 h after 10 and 30 micrograms/kg intranasal oCRH respectively. The effect on IR-cortisol was similar, but more prolonged. Compared to the iv route, sc oCRH produced similar mean peak IR-ACTH and IR-cortisol levels and had a slightly longer duration of action. Intranasal oCRH was only about 1% as effective. Peak plasma IR-oCRH levels in 2 subjects receiving 3 micrograms/kg sc oCRH were 13 and 17 ng/ml at 90 min. These peaks were lower than those after iv administration of the same dose, but the levels remained elevated longer, probably accounting for the longer duration of action of sc oCRH. Peak plasma IR-oCRH levels in 4 subjects given 10 microgram/kg intranasal oCRH were only 64-122 pg/ml, presumably reflecting poor absorption through the nasal mucosa. These results demonstrate that sc injection of oCRH is at least as effective as the iv route with respect to plasma IR-ACTH and IR-cortisol responses. The convenience of this route of administration and the prolonged duration of action of oCRH suggest the feasibility of long term oCRH use.
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PMID:Effect of subcutaneous and intranasal administration of ovine corticotropin-releasing hormone in man: comparison with intravenous administration. 298 33

To determine whether the plasma immunoreactive ACTH (IR-ACTH) and IR-cortisol responses to ovine corticotropin-releasing hormone (oCRH) depend on the time of day, we administered 1 microgram/kg BW synthetic oCRH as an iv bolus dose to five normal men at their usual time of awakening between 0530-0740 h, at 1600 h, and at 2300 h. Mean basal plasma IR-ACTH and IR-cortisol levels were highest upon awakening, intermediate at 1600 h, and lowest at 2300 h, reflecting the diurnal rhythm of ACTH secretion. There was no significant difference in the plasma IR-ACTH response to oCRH at different times of the day. In contrast, the mean maximum plasma IR-cortisol increment and mean integrated response were 2- and 2.6-fold greater (P less than 0.05), respectively, at 2300 h than upon awakening. In another study, oCRH was given in the morning (0700-0900 h) to 22 normal men and in the late afternoon (1600-1800 h) to 24 normal men. Mean basal plasma IR-ACTH and IR-cortisol levels were significantly higher (P less than 0.001) in the morning [24 +/- 3 pg/ml (mean +/- SEM) and 10.6 +/- 0.8 micrograms/dl, respectively] than in the afternoon (13 +/- 2 pg/ml and 5.6 +/- 0.6 micrograms/dl, respectively). Mean peak plasma IR-ACTH was slightly greater in the morning (60 +/- 5.5 pg/ml) than in the afternoon (47 +/- 5.5 pg/ml), the mean maximum plasma IR-ACTH increments were the same (35 +/- 4 and 34 +/- 5 pg/ml, respectively), and the mean integrated IR-ACTH response was slightly less in the morning (2036 +/- 414 vs. 2365 +/- 358 pg . min/ml), but none of these differences was statistically significant. Mean peak plasma IR-cortisol concentrations in the morning and afternoon were similar (18.7 +/- 0.7 and 17.3 +/- 0.9 micrograms/dl, respectively), but the mean maximum plasma IR-cortisol increments (8.1 +/- 0.8 and 11.7 +/- 0.9 micrograms/dl, respectively; P less than 0.005), and the mean integrated IR-cortisol responses (588 +/- 115 and 976 +/- 95 micrograms . min/dl, respectively; P less than 0.01) were greater in the afternoon. There was an inverse correlation between basal plasma IR-cortisol concentration and the integrated IR-ACTH response (P less than 0.05), the maximum IR-cortisol increment (P less than 0.001), and the integrated IR-cortisol response (P less than 0.001).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Diurnal variation in the response of plasma adrenocorticotropin and cortisol to intravenous ovine corticotropin-releasing hormone. 298 16


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