Plasma and CSF endorphin levels in primary and symptomatic headaches.
Explore the source record for details and available documents.
Adult↗
Biomedical subjects
F Petraglia
Publications and source records attributed to F Petraglia.
Lack of beta-endorphin plasma level rise in oxytocin-induced labor.
beta-Endorphin (beta-EP), beta-lipotropin (beta-LPH) and cortisol plasma levels were measured during labor in 18 pregnant women. In 7 cases labor progressed spontaneously and in 11 cases oxytocin (5 mIU/min) was administered to stimulate uterine contractions. In control and oxytocin-treated subjects hourly blood samples were taken until delivery. In spontaneous labor all three hormones showed a progressive and significant increase until parturition. In oxytocin-treated patients, however, both beta-EP and beta-LPH remained constant until parturition. Cortisol levels in oxytocin-treated patients presented a significant increase but reached values significantly lower than in control patients. These results indicate that women with uterine hypocontractility during labor requiring oxytocin showed no rise in their plasma beta-EP and beta-LPH and a blunted cortisol rise during oxytocin administration.
Adult↗
Central opioid receptor activity in patients affected by puerperal, idiopathic and tumoral hyperprolactinemia.
The aim of our study was to evaluate the activity of opioid receptors involved in the regulation of prolactin secretion in different kinds of hyperprolactinemic states (puerperal, idiopathic and tumoral subjects). Prolactin plasma level changes were measured after the acute administration of a met-enkephalin synthetic analogue. FK 33-824, and placebo. The prolactin-releasing effect of this drug, evident in control subjects, was blunted in patients affected by idiopathic hyperprolactinemia, and absent in puerperal and tumoral patients. These results indicate that hyperprolactinemia affects the activity of central opioid receptors, with the most evident effects in patients with highest prolactin plasma levels.
Adenoma↗
Endorphin patterns within the headache spectrum disorders.
The role of opioid peptides in modulating the nervous system adaptability has been demonstrated recently; proopiomelanocortin (POMC)-related peptides, in particular, serve in pain perception, in adaptation to stress, and in modulating higher brain functions. Primary headaches, besides pain, involve neuroendocrine/autonomic/adaptive processes as well as mood and personality factors. The view that primary headaches can be taken as a possible model of POMC-related peptides dysfunction led us to evaluate the resting plasma and CSF peptide levels and their plasma changes in response to various stimuli affecting their release. The data obtained from basal and dynamic studies agree with the concept that primary headaches are sustained by opioid system disturbance. In particular the reduced release of endogenous opioids by anterior pituitary in response to physical, endocrine or pharmacological stimuli agrees with a weak adaptive ability of headache sufferers. This impairment of endorphin responsiveness could play a key role in headache susceptibility to environmental stimuli. Primary headaches constitute a wide, intriguing field, including several subgroups bordering on "ischemic" and behavioral/affective disorders. The development of neuroendocrine techniques could be a useful means for supporting the clinical criteria identifying subpopulations of headache sufferers.
Adrenocorticotropic Hormone↗
Mainly mu-opiate receptors are involved in luteinizing hormone and prolactin secretion.
We evaluated plasma PRL and LH concentrations in the rat after the administration of drugs that exert a specificity directed mainly, although not absolutely, toward the mu-, delta-, or kappa-opiate receptors, in order to investigate the role of different receptors and thus the respective endogenous ligands in the modulation of the release of these anterior pituitary hormones. LH concentrations were evaluated in prepuberal female rats, in adult male rats, and in ovariectomized, estradiol benzoate-treated rats. PRL concentrations were evaluated in suckling rats, in ovariectomized, estradiol benzoate-treated rats, and in ether-stressed rats. The delta-antagonist ICI 154129 never affected PRL or LH concentrations, whereas both the mu- and kappa-antagonists, naloxone and MR 1452, respectively, seemed to be effective. However, when graded doses of the two classes of antagonists were tested, the mu-antagonist appeared to be effective on both hormones at doses that were one tenth of those of the kappa-antagonist. In conclusion, the mu-receptor seems to be the most profoundly involved in the regulation of PRL and LH secretion.
Animals↗
Dermorphin reduces the metyrapone-evoked release of adrenocorticotropin, beta-endorphin, and beta-lipotropin in man.
The aim of this study was to investigate further the influence of dermorphin (D), a new potent opioid peptide (H-Tyr-D-Ala-Phe-Gly-Tyr-Pro-Ser-NH2), on the functional activity of the pituitary-adrenocortical system in man. Six normal men were treated with oral metyrapone to stimulate the secretion of ACTH, beta-lipotropin, and beta-endorphin. In these subjects, significant suppression of metyrapone-evoked release of ACTH and related peptides occurred during D infusion (5.5 micrograms/kg X min for 30 min) compared with that during saline infusion. These results indicate that D can induce a significant decline in plasma levels of ACTH, beta-lipotropin, and beta-endorphin, the major circulating peptides from the C-terminal part of proopiocortin, and suggest that opioid peptides may be involved in the control of the functional activity of pituitary-adrenocortical activity in man.
Adrenocorticotropic Hormone↗
beta-Endorphin cerebrospinal fluid decrease in untreated parkinsonian patients.
We measured CSF and plasma contents of beta-endorphin (beta-EP), beta-lipotropin (beta-LPH), and ACTH in 24 patients with Parkinson's disease; 14 had not been treated. CSF beta-EP concentrations in untreated patients were lower than in 15 controls (p less than 0.005), but values did not differ significantly in treated and untreated patients. In untreated and treated patients, ACTH and beta-LPH CSF, and beta-EP, beta-LPH, and ACTH plasma concentrations were in the same range as controls. The Parkinson's disease-related decrease of CSF beta-EP levels further supports the concept that there is a generalized brain disorder in Parkinson's disease affecting more than dopaminergic neurons in the substantia nigra.
Adrenocorticotropic Hormone↗
Impairment of adrenergic-induced proopiomelanocortin-related peptide release in heroin addicts.
The effects of iv stimulation with clonidine on plasma levels of beta-lipotropin (beta-LPH), beta-endorphin (beta-EP), cortisol, growth hormone (GH) and adrenocorticotrophic hormone (ACTH) were tested in a group of 10 healthy volunteers and in 8 heroin abusers. Hormones were measured either by direct radioimmunoassay (RIA) (GH, cortisol) or after plasma extraction and Sephadex G-75 column chromatography (beta-LPH and beta-EP) or by immunoradiometric assay (IRMA) (ACTH). Plasma levels of GH increased in a similar fashion in the two groups. In the controls, clonidine induced release of beta-LPH and beta-EP after 30 min (from 8.9 +/- 1.0 to 19.1 +/- 4.6 fmol/ml, P less than 0.01 and from 8.1 +/- 0.6 to 17.9 +/- 4.6, P less than 0.01) and of ACTH after 60 min (from 12.1 +/- 1.8 to 18.1 +/- 1.8, P less than 0.05) while in addicts beta-EP but not beta-LPH showed a significant increase (from 8.5 +/- 0.7 to 19.8 +/- 4.2, P less than 0.05), 90 min after the injection. In heroin addicts, plasma cortisol levels decreased continuously after clonidine stimulation while in controls they showed a biphasic pattern, decreasing until the 60th min (from 135.2 +/- 30.4 ng/ml to 74.0 +/- 13.3, P less than 0.05) and regaining basal levels 1 h later (122.0 +/- 24.8, P less than 0.05 vs 60th min value). These data demonstrate the existence in human beings of noradrenergic control of proopiomelanocortin (POMC)-related peptides and indicate that chronic opiate abuse greatly interferes with this control. Clonidine-induced release of plasma beta-EP may be of importance with regard to its therapeutic effects in detoxification.
Adolescent↗
Opioid peptides of the pituitary and hypothalamus: changes in pregnant and lactating rats.
Immunoreactive (Ir) beta-endorphin concentrations were determined in plasma, anterior pituitary (AP), neurointermediate pituitary lobe (NIL) and mediobasal hypothalamus (MBH) of pregnant (12-14 and 18-20 days) and fertile control rats, during labour and lactation. Immunoreactive Met-enkephalin concentrations were also evaluated in the MBH. Concentrations of Ir beta-endorphin in plasma, AP and NIL of rats during early and late pregnancy were significantly higher than in controls, the plasma and AP contents showing an increasing pattern in the second half of gestation. During labour, Ir beta-endorphin concentrations in plasma and AP reached the highest values, whereas those in NIl remained unchanged. Lactating rats showed Ir beta-endorphin concentrations in NIL and plasma in a range similar to that found in pregnant rats, resulting in concentrations in the AP not significantly different from those of nonpregnant controls. Immunoreactive beta-endorphin and Ir Met-enkephalin concentrations in MBH of pregnant rats were almost twice as high as in controls, rising markedly during labour; during lactation levels were in the same range as in non-pregnant controls. These results indicate that pregnancy and labour are characterized by high plasma, pituitary and hypothalamic concentrations of Ir-beta-endorphin as well as by high hypothalamic Ir Met-enkephalin levels, and that Ir beta-endorphin concentrations vary differently during pregnancy, lactation and labour in the two pituitary lobes, supporting the existence of different control mechanisms in the AP and NIL.
Animals↗
Estrogen changes as a critical factor in modulation of central opioid tonus: possible correlations with post-menopausal migraine.
The effects exerted by ovarian steroids on the modulation of opioid activity were investigated in post-menopausal migraine sufferers and in healthy controls. In order to evaluate central opioid tonus, plasma LH rise after naloxone injection was measured, bearing in mind the tonic inhibition of endogenous opioid on hypothalamic LH-RH. There was no response of plasma LH to naloxone in post-menopausal women or in patients submitted to ovariectomy in fertile life. When the subjects underwent a sequential estrogens + progestagens therapy, such a response was noted from the first month of treatment; progestagens alone were ineffective. The same phenomena were also evident in post-menopausal migraine sufferers. These data indicate that ovarian steroids modulate the activity of opiate receptors in both healthy women and migraine sufferers. Interestingly, replacement therapies through ovarian steroids restored the activity of central opioid tonus in patients affected by migraine.
Adult↗
Central ACTH deficit in degenerative and vascular dementia.
Cerebrospinal fluid (CSF) concentrations of ACTH, beta-lipotropin (beta-LPH) and beta-endorphin (beta-EP) were measured in 15 patients affected by dementia, who underwent also a brain computerized tomography (CT), and in 13 age-matched healthy volunteers. ACTH CSF levels of patients (4.0 +/- 2.4 fmol/ml, M +/- SD) were significantly lower than in controls (9.8 +/- 5.0, P less than 0.01) the lowest values being found in Alzheimer type of dementia (ATD: 3.1 +/- 2.5) and in patients with radiological evidence of cortical atrophy (2.5 +/- 1.2), independently of the probable origin of dementia. Although beta-LPH and beta-EP levels of patients fell within normal range, they were lower in ATD than in dementia sustained on a vascular origin. There was no variation of either peptides concentration in relation to CT findings. These data indicate the ACTH impairment as typical of dementia, supporting in humans the positive role of this peptide on learning and mnesic functions. Moreover, the maintained CSF levels of both beta-LPH and beta-EP in the dementia sustained on a vascular origin, while lower values were found in ATD, could represent a differentiation between vascular and degenerative diseases of the Central Nervous System (CNS).
Adrenocorticotropic Hormone↗
Increase of proopiomelanocortin-related peptides during subjective menopausal flushes.
The present study reports the plasma levels of gonadotropins (luteinizing hormone, follicle-stimulating hormone), proopiomelanocortin-related peptides (adrenocorticotropic hormone, beta-endorphin, and beta-lipotropin), and cortisol in eight menopausal women experiencing frequent hot flushes. beta-Endorphin and beta-lipotropin levels were measured by radioimmunoassay after extraction and Sephadex G-75 column chromatography. Plasma levels of adrenocorticotropic hormone (after extraction), luteinizing hormone, follicle-stimulating hormone, and cortisol were measured by specific radioimmunoassay. All hormone levels showed a prompt and significant rise on occurrence of hot flushes (18 total recordings), remained high for 15 minutes, and decreased to basal levels 35 minutes later. The evaluation of the behavior pattern of single hormone levels revealed a more pronounced increase of proopiomelanocortin-related peptides and cortisol than of gonadotropins (p less than 0.01).
Adrenocorticotropic Hormone↗
Autonomous beta-endorphin secretion from the pituitary neurointermediate lobe: in vivo studies.
The existence of independent control mechanisms of beta-endorphin (beta-EP) secretion from the anterior (AP) and intermediate (NIL) pituitary lobes is now ascertained. The aim of this study was to evaluate the effect of surgical separation from the hypothalamus of the two pituitary lobes on beta-EP secretion. Two experimental models of surgical hypothalamo-pituitary disconnection were used: 1) rats with ablation of the medial basal hypothalamus (MBH); 2) rats bearing two entire ectopic pituitaries or two anterior pituitaries (APs) only, transplanted under the kidney capsule. In rats with MBH-ablation plasma beta-EP levels were significantly higher than in sham-operated controls. Plasma beta-EP levels increased in rats transplanted with entire pituitaries 3 days after surgery and were still elevated after 1 week. In rats transplanted with APs only, no significant beta-EP changes in plasma were evident. In both experimental conditions no significant difference was present in beta-LPH plasma levels. Concentrations of beta-EP in the ectopic NILs decreased gradually after transplantation. In all these results indicate that that NIL but not the AP is capable, when is disconnected from the hypothalamus, or secreting autonomously beta-EP.
Animals↗
Lack of correlation between amniotic fluid and maternal plasma contents of beta-endorphin, beta-lipotropin, and adrenocorticotropic hormone in normal and pathologic pregnancies.
Reported are the concentrations of beta-endorphin, beta-lipotropin, and adrenocorticotropic hormone (ACTH) in the amniotic fluid and plasma of 40 healthy pregnant women at different stages of gestation. Moreover, the amniotic fluid levels of the three peptides were evaluated in 20 other pregnant women affected by different pathologic conditions (Cooley's disease, gestosis, diabetes, placental insufficiency, etc.). A silicic acid extraction procedure was performed on the samples. Each extract was subjected to Sephadex G-75 column chromatography, and the two fractions corresponding to beta-lipotropin and beta-endorphin were collected, freeze-dried, and assayed by two specific radioimmunoassays. Levels of ACTH were measured by radioimmunoassay directly on the extracts. Levels of beta-endorphin in amniotic fluid showed the highest values in the first trimester (173 +/- 30 fmol/ml, mean +/- SEM) but were significantly decreased in the second (75.2 +/- 14) and third trimesters (14.3 +/- 1.8). An inverse trend characterized plasma levels of beta-endorphin, which showed a progressive increase from the first trimester to term (10.4 +/- 11.1). Amniotic fluid levels of beta-lipotropin remained stable during the first (48.6 +/- 6.3) and second (54.6 +/- 11.1) trimesters, but decreased significantly in the third trimester (17.9 +/- 2.3). The plasma concentrations of beta-lipotropin showed the highest levels in the first trimester (10.9 +/- 0.9), and decreased significantly at term (8.9 +/- 1.3). Last, amniotic fluid levels of ACTH decreased from 55.3 +/- 4.75 fmol/ml in the first trimester to 12.5 +/- 1.16 in the second trimester, and rose again in the third trimester to 34.4 +/- 6.6 fmol/ml. Plasma levels of ACTH were characterized in the first two trimesters by values twice those recorded for nonpregnant women, and decreased at term to 8.9 +/- 1.4 fmol/ml. In the pregnant patients with fetuses affected by Cooley's disease (second trimester) and in those with edema-proteinuria-hypertension (EPH) gestosis (third trimester), amniotic fluid levels of beta-endorphin, beta-lipotropin, and ACTH were in the same range as those in healthy pregnant women.
Adrenocorticotropic Hormone↗
Opioid plasma levels in primary affective disorders. Effect of desimipramine therapy.
Mean plasma levels of beta-endorphin (beta EP), beta-lipotropin (beta LPH) and ACTH were significantly higher in 22 patients with primary affective disorders (PAD) and in 2 schizoaffective subjects off therapy since 10 days than in 22 age- and sex-matched healthy controls. Desimipramine therapy (50-100 mg/day per os for 3-5 weeks) induced in parallel psychological improvement and fall in beta LPH-beta EP in 6 of 8 PAD patients treated, and a normalization of beta EP-beta LPH levels with minimal mood improvement in the 2 schizoaffective subjects. These results indicate that the opioid levels are increased in PAD and schizoaffective patients and normalized by the desimipramine therapy in those patients in whom the affective disorders improved.
Adrenocorticotropic Hormone↗
Secretion pattern of endogenous opioids in chronic schizophrenia.
Baseline plasma levels of beta-endorphin, beta-lipotropin, and ACTH were assayed in 37 patients with chronic schizophrenia: 24 men and 13 women, 28 with hebephrenic and nine with paranoid schizophrenia. None of the patients had received any medication for at least 10 days. The mean values of both opioids were significantly higher in the schizophrenic patients than in 21 age- and sex-matched control subjects. Insulin stimulation and dexamethasone suppression tests were given to eight of the patients, and the circadian rhythms of beta-endorphin, beta-lipotropin, ACTH, and cortisol were assayed in the same eight patients. Insulin stimulation, dexamethasone suppression test results, or circadian rhythmicity was impaired in seven of these eight patients.
Adrenocorticotropic Hormone↗
Serotoninergic agonists increase plasma levels of beta-endorphin and beta-lipotropin in humans.
A pharmacological approach was used to investigate the serotoninergic control of plasma levels on beta-endorphin (beta-EP) and beta-lipotropin (beta-LPH) in humans. Acute administration of L5-OH-triptophan, the physiologic precursor of serotonin (SE), induced a significant rise in plasma beta-EP and beta-LPH levels both when injected iv (20 and 40 mg) (four normal men) and when administered orally (200 and 400 mg) (seven normal men) (P less than 0.01 vs. placebo). The iv route of administration induced a prompt (mean peak values after 150 min) dose-dependent increase in beta-EP and beta-LPH levels. The responses evoked by oral administration (mean peak values after 130 and 240 min) were not dose dependent. Fluoxetine (15 and 30 mg orally) a blocker of SE reuptake, induced a significant dose-related rise in plasma beta-EP and beta-LPH levels in a group of seven normal men (P less than 0.01) (mean peak values after 150 min). Pretreatment with methysergide, a SE receptor antagonist (3 X 2.8 mg orally, five men), did not induce any significant changes in plasma beta-EP and beta-LPH levels, but blocked the increase in the two hormones evoked by L5-OH-triptophan (40 mg iv). Plasma cortisol levels changed similarly to those of beta-EP and beta-LPH in all the experiments, indicating that putative serotoninergic drugs exert a positive role on the various corticotropin-releasing hormone-mediated secretions.
5-Hydroxytryptophan↗
Impaired circadian rhythmicity of beta-lipotrophin, beta-endorphin and ACTH in heroin addicts.
The circadian rhythm of plasma proopiocortin-related peptides was studied in 15 heroin addicts and in 6 sex- and age-matched controls. ACTH, beta-lipotrophin, (beta-LPH), beta-endorphin (beta-EP) and cortisol were measured by RIA either directly (cortisol), or after plasma extraction (ACTH) and Sephadex G-75 gel chromatography (beta-LPH and beta-EP) every 4 h from 8 a.m. to 8 p.m. and again at 8 a.m. the next morning. The means of the two 8 a.m. measurements of beta-LPH (2.67 +/- 0.34 fmol/ml, mean +/- SE), ACTH (2.74 +/- 0.71) and cortisol (218 +/- 31 pmol/ml) levels in heroin addicts were significantly lower than those in controls (6.28 +/- 0.61, 10.1 +/- 0.74 and 364 +/- 27, respectively, P less than 0.01) while beta-EP concentrations in heroin addicts (5.1 +/- 0.6) were similar to those of healthy volunteers (6.44 +/- 0.56). In controls, all three peptides and cortisol show a circadian rhythm of secretion, the lowest values being in the evening and the highest ones in the morning. Heroin addicts partially lack this phenomenon showing constant levels of the three proopiocortin-related peptides throughout the day, with a slight but significant decrease of plasma cortisol. In the 7 subjects who took heroin throughout the study, no systematic changes were observed in the three proopiocortin-related peptides, while it seems that this group of addicts shows a cortisol decrease in the evening to a lesser extent than subjects receiving methadone maintenance only.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗