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)

Cortisol administered at a dose of 25 mg/kg 24 h before measurements decreased the prolactin secretion induced by intraventricularly given opioids (dynorphin, beta-endorphin, Met-enkephalin or D-Met-Pro-enkephalinamide). The effect of cortisol was depressed by actinomycin D pretreatment. The cortisol-induced inhibition of the action of morphine was facilitated in adrenalectomized animals; measuring the effects of increasing doses of cortisol a maximal inhibition was obtained at a dose of 5 mg/kg. The opioid-induced corticosterone secretion was not affected 24 h after a single administration of cortisol. The present results show that the cortisol-induced inhibition of opioid-induced prolactin secretion is dependent on protein synthesis and independent of changes in drug metabolism, and of the type of opiate receptor preferentially affected by the opiate agonists employed.
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PMID:Prolactin release induced by opiate agonists, effect of glucocorticoid pretreatment in intact and adrenalectomized rats. 290 15

To study the role of opioid peptides in human obesity, plasma beta-endorphin (beta EP), beta-lipotropin (beta LPH), and cortisol resting values, circadian rhythms, and responses to hypoglycemia were studied in 6 prepubertal and 6 pubertal obese adolescents (at least 40% above ideal body weight) and in 10 normal subjects matched for age, sex, and pubertal development. Baseline plasma beta LPH and beta EP concentrations in both obese children and adolescents were twice as high as those in normal controls, while cortisol levels were not different. Cortisol, beta EP, and beta LPH levels had a clear circadian rhythmicity in all subjects, with the exception of obese pubertal boys whose plasma beta EP concentrations were constant throughout the day. After insulin administration, the fall in blood sugar was similar in all groups. Plasma cortisol and beta EP responses were similar in both obese and normal prepubertal subjects. In obese pubertal adolescents, beta EP did not increase significantly after hypoglycemia, although it did increase in normal weight pubertal subjects. In normal prepubertal subjects, the circadian rhythms of beta EP and beta LPH secretion and release induced by hypoglycemia suggest the presence of a well developed neuroendocrine control of proopiomelanocortin-related peptide secretion. In prepubertal obese children, the increased plasma beta EP and beta LPH levels with the maintenance of their circadian rhythm and responsivity to hypoglycemia suggest overactivity of anterior pituitary secretion. In obese adolescents, in spite of the normal rhythm of beta LPH and cortisol, beta EP levels did not change throughout the day, thus suggesting beta EP secretion from nonpituitary sources in these subjects. The present study indicates a possible direct role for hyperendorphinemia in the induction of overeating in obese children and adolescents.
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PMID:Hyperendorphinemia in obese children and adolescents. 293 22

Plasma beta-endorphin, human growth hormone (hGH) and cortisol were measured concomitantly during insulin hypoglycemia (0.1 u/kg i.v.) or clonidine administration (0.075 mg/m2 orally) in children with idiopathic short stature. Whereas hypoglycemia raised plasma beta-endorphin levels, clonidine slightly decreased beta-endorphin in six subjects and had no effect in four. Cortisol levels increased following hypoglycemia and decreased markedly after clonidine. hGH increased to greater than 20 ng/ml in all but one subject. The findings are interpreted as further evidence that the hGH stimulation of clonidine is not stress-mediated.
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PMID:Comparison of the effect of insulin hypoglycemia and clonidine on secretion of growth hormone, cortisol and beta-endorphin in children and adolescents. 293 51

The goal of this study was to evaluate the effects of menstrual cyclicity on plasma beta-endorphin (beta-EP) levels. For this purpose, beta-EP and cortisol plasma concentrations were measured during the menstrual cycle in healthy control subjects (n = 12), in patients affected by anovulatory syndrome (n = 6), and in amenorrheic patients (n = 8). In the same patients, beta-EP and cortisol were also measured under treatment for the induction of ovulation with pulsatile luteinizing hormone-releasing hormone or human menopausal gonadotropin plus human chorionic gonadotropin administration. In spontaneous and pharmacologically induced ovulatory cycles, a significant preovulatory rise of plasma beta-EP levels was always evident. Constant levels were found in the other periods of ovulatory cycles and in the patients affected by anovulatory syndrome and primary amenorrhea. Cortisol levels did not show any significant change throughout the cycle, either in controls or in patients before or after treatment. This result suggests that when ovulation occurs, plasma beta-EP levels show a relevant rise, the physiologic significance of which remains to be elucidated.
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PMID:Plasma beta-endorphin levels in anovulatory states: changes after treatments for the induction of ovulation. 293 25

There is growing experimental evidence that beta-endorphin immunoreactivity is raised by surgical stress in patients undergoing general anesthesia. As the assay methods employed to date did not allow to fully discriminate between beta-endorphin and its immediate precursor, beta-lipotropin, we have investigated in the present study plasma levels of these two peptides by separating them by chromatography on plasma extracts prior to radioimmunoassay in eighteen surgical patients under general anesthesia and eight under spinal anesthesia. Beta-lipotropin, but not beta-endorphin, plasma levels were found to be significantly elevated during surgery in the general anesthesia group, while no change was found in either peptide concentration in the spinal one. Cortisol plasma levels also increased significantly 90 minutes after the beginning of surgery, when they were positively correlated to beta-lipotropin ones. Although the sampling time we adopted may have prevented us from detecting an early peak of beta-endorphin during the first 30 minutes of surgery, the major component of the pituitary opioid response to surgical stress appears to be related to beta-lipotropin. This is in agreement with results of experimental work on various kinds of stress in animals and humans and seems to rule out a role for plasma beta-endorphin in post-operative analgesia.
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PMID:Beta-lipotropin is the major component of the plasma opioid response to surgical stress in humans. 296 Aug 67

Synthetic ovine corticotropin releasing factor (o-CRF) was administered as an intravenous bolus (100 micrograms) to eight patients suffering from a major depressive disorder, endogenous subtype. All patients showed inadequately suppressed cortisol levels after 1 mg dexamethasone. After clinical remission and normalized dexamethasone responses, these patients were reinvestigated with o-CRF stimulation. The mean adrenocorticotropic hormone (ACTH) release from the pituitary corticotroph cells was indiscriminate at both test sessions. Cortisol and corticosterone output after o-CRF tended to be higher during depression than after recovery. The o-CRF-induced increments observed with corticosterone were more marked in comparison with cortisol. Within the limitations of the current protocol, our preliminary data lend support to the view that an increased pituitary ACTH reserve or adrenocortical steroid reserve is not likely to be responsible for the defective pituitary-adrenal regulation in some dexamethasone-resistant depressives.
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PMID:ACTH, cortisol, and corticosterone output after ovine corticotropin-releasing factor challenge during depression and after recovery. 298 88

Effects of N-terminal peptide of salmon proopiocortin (salmon NPP-I) on cortisol secretion was examined in vitro using diced interrenal tissue from the rainbow trout, Salmo gairdneri. ACTH(1-24) at concentrations of 1 to 50 nM stimulated cortisol secretion in dose-dependent manner, whereas salmon NPP-I had no effect over a range of 50 pM to 500 nM. Cortisol secretion in response to various doses of ACTH(1-24) was modified slightly when 1 to 100 nM of salmon NPP-I was added to the incubation medium together with ACTH. An augmentation of in vitro secretion of cortisol in response to ACTH(1-24) was observed when the interrenal was removed from the trout pretreated with one IU of porcine ACTH but not with 10 micrograms of salmon NPP-I. A slight but significant potentiating effect of salmon NPP-I (10 or 100 nM) on the ACTH-induced cortisol secretion was observed when the trout was sensitized to ACTH by porcine ACTH pretreatment. Furthermore, six daily injections of salmon NPP-I into the trout induced hyperplasia of interrenal tissue. These findings suggest that NPP-I, together with ACTH, may be involved in controlling interrenal function in the trout. Such activities could be due to conservative region in the N-terminal portion of NPP.
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PMID:Effects of N-terminal peptide of salmon proopiocortin on interrenal function of the rainbow trout. 298 83

We administered ovine corticotropin-releasing hormone (CRH) as a bolus iv injection (1 microgram/kg) to 21 normal boys and girls, aged 6-15 yr. CRH stimulated release of immunoreactive ACTH and cortisol in all children. The peak plasma ACTH and cortisol levels after CRH were 15.7 +/- 9.4 (SD) pg/ml and 14.3 +/- 3.6 micrograms/dl, respectively, in the girls, and 20.7 +/- 9.7 pg/ml and 16.6 +/- 3.3 micrograms/dl, respectively, in the boys. Plasma ACTH and cortisol responsiveness to CRH did not differ between girls or boys, or between children and adults. Cortisol-binding globulin concentrations in plasma did not change with age. We conclude that CRH provides a safe means of stimulating the pituitary-adrenal axis in children.
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PMID:Ovine corticotropin-releasing hormone stimulation test in normal children. 300 Nov 26

The effect of rate of blood loss by acute hemorrhage (H) on adrenocorticotropin (ACTH) and cortisol plasma concentrations was assessed in anesthetized cats. Arterial blood was withdrawn at a rapid rate (10% blood vol/min) or at a slow rate (2%/min), and responses were compared across three volumes of H (10, 20, and 30% of blood vol). After rapid rate of H, ACTH increased in proportion to volume of H (r = 0.669, P less than 0.001) with a mean elevation of 124 +/- 27, 267 +/- 102, and 950 +/- 195 pg/ml for 10, 20, and 30% H, respectively. Slow rate of H evoked a significant increase in ACTH that was not proportional to volume of H (r = 0.314, P greater than 0.10), and the mean change during the post-H sampling period was 611 +/- 166, 828 +/- 302, and 1,070 +/- 239 pg/ml for 10, 20, and 30% H, respectively. Control animals showed no change in ACTH to the repeated sampling paradigm. Rapid H evoked an immediate decrease in mean arterial pressure (MAP) with a post-H recovery of MAP inversely proportionate to volume of H (r = -0.552, P less than 0.01). Slow H caused a progressive decrease in MAP with no significant post-H recovery of MAP at any volume of H. Cortisol concentration increased in proportion to volume of H after rapid H (r = 0.515, P less than 0.025), but not after slow H.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of rate of hemorrhage on release of ACTH in cats. 300 90

Fetal adrenocorticotropin (ACTH) and renin secretion are increased by a variety of stimuli and decreased by cortisol negative feedback inhibition. However, the time courses of these interactions are unknown. The present studies were designed to test for rapid feedback negative suppression of ACTH and renin secretion in fetal and adult sheep. In chronically catheterized fetal sheep, ACTH and renin secretion were stimulated by intravenous infusion of sodium nitroprusside, a vasodilator drug. Vehicle or cortisol, infused at rates of 1, 2, or 4 micrograms/min for 2 min before and during the infusion of nitroprusside did not significantly alter the fetal ACTH or renin responses to nitroprusside. In five nonpregnant ewes, chronically prepared with skin loops containing the carotid arteries, nitroprusside (20 micrograms X kg-1 X min-1) was infused beginning 2 min after infusion of vehicle or cortisol (3.5 or 7 micrograms X kg-1 X min-1). Cortisol infusion produced a rising plasma cortisol concentration similar to that after stress but did not alter the magnitude of the ACTH response to nitroprusside. The results indicate that cortisol-induced suppression of ACTH secretion does not occur rapidly in the fetal or adult sheep and that the cortisol-induced suppression of fetal plasma renin activity is a slow process.
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PMID:Absence of fast negative feedback control of ACTH and renin in fetal and adult sheep. 300 21


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