Plasma Beta-endorphin Levels Research Articles

Dexamethasone alters plasma levels of beta-endorphin and postoperative pain : Hargreaves KM, Schmidt EA, et al. Clin Pharmacol Ther 42:601, 1987

Dexamethasone alters plasma levels of beta-endorphin and postoperative pain : Hargreaves KM, Schmidt EA, et al. Clin Pharmacol Ther 42:601, 1987

Plasma levels of beta-endorphin, cortisol, prolactin and growth hormone in depressed patients.

Basal serum cortisol, growth hormone, prolactin and immunoreactive (IR) plasma beta-endorphin levels were measured in 31 depressed patients (14 endogenous, 17 nonendogenous) undergoing the dexamethasone suppression test. The endogenously depressed patients had significantly higher (22.55 +/- 1.34 micrograms/dl) predexamethasone cortisol levels than the nonendogenous patients (16.34 +/- 1.93 micrograms/dl). The mean serum prolactin and growth hormone values of these two groups were not significantly different, while plasma IR-beta-endorphin levels of the endogenous group (40.11 +/- 3.57 pg/ml) were significantly lower than those of the nonendogenous group (120.33 +/- 27.98 pg/ml). Neither group showed a significant correlation between plasma IR-beta-endorphin and serum cortisol values. These results indicate that measurement of predexamethasone serum cortisol values and plasma IR-beta-endorphin could be valuable laboratory tests in the diagnosis of depression.

Alteration of opioid peptide circadian rhythm in cancer patients.

Endogenous opioid peptides have been seen to play a role in regulating immunity and tumor growth. This study was carried out to investigate opioid activity in human cancer. We evaluated by radioimmunoassay beta-endorphin plasma levels on blood samples collected at 9.00 a.m. from 121 cancer patients and 42 healthy subjects. In 22 cancer patients and in 12 controls, beta-endorphin circadian rhythm was also investigated. Finally, in 14 cancer patients and in 10 controls GH, PRL, FSH, LH and cortisol serum levels were measured after the administration of a metenkephalin analogue, FK 33-824 (0.3 mg i.v.). No significant differences were seen in beta-endorphin mean levels between cancer patients and normal subjects. Moreover, no differences were found between patients with or without metastases, nor between those with or without chronic pain. beta-Endorphin circadian rhythm appeared to be altered in 16/22 cancer patients, and anomalous hormonal responses to FK 33-824 were seen in 13/14 patients. This study shows an altered opioid activity in human neoplasms, whose clinical significance remains to be determined.

Psychologic stress increases plasma levels of prolactin, cortisol, and POMC-derived peptides in man.

Stressful social interactions have been shown to elicit increases in heart rate as well as in plasma levels of epinephrine, norepinephrine, and cortisol in humans. We sought to determine whether a competitive oral examination would affect plasma levels of the pituitary hormones ACTH, beta-endorphin, beta-lipotrophic hormone, and prolactin in a group of healthy young males. Seven min after beginning the examination, heart rate increased 27% and plasma levels of ACTH, beta-endorphin, beta-lipotropic hormone and prolactin rose 59%, 79%, 42%, and 46%, respectively, compared to values shortly before the examination. These hormone values returned to initial levels after the subjects returned to the waiting room. Plasma cortisol changes were similar in direction to those of ACTH but occurred about 15 min later. The present study demonstrates that a stressful social interaction can elicit rapid increases in plasma levels of the proopiomelanocortin derived peptide hormones and prolactin in man.

Correlation between beta-endorphin plasma levels and anginal symptoms in patients with coronary artery disease

To verify whether beta-endorphin plasma levels influence the presence of anginal symptoms. 74 consecutive male patients were studied. All patients had previously documented coronary artery disease and reproducible exerciseinduced myocardial ischemia. Thirty-five patients (Group I) had a history of angina and reported anginal symptoms during exercise stress testing; 39 patients (Group II) were asymptomatic and had documented silent myocardial ischemia during exercise. Baseline beta-endorphin plasma levels were measured in blood ramples taken before exercise stress testing and analyzed by beta-endorphin-I125-RIA Kit-NEN (a radioimmunoassay method).The mean baseline beta-eadorphin plasma level was 22.5 ± 19 pg/ml in patients with anginal symptoms compared with 43.7 ± 28 pg/ml in asymptomatic patients (p < 0.001). Baseline blood pressure and heart rate-systolic pressure (rate-pressure) product at baseline and at ischemia threshold (1 mm ST segment depression) were similar in the two groups, Group II patients had a longer exercise duration p < 0.01), more pronounced ST segment depression (p < 0.001) and a higher peak rate-pressure product (p < 0.01). The extent of coronary artery disease, ejection fraction and left ventricular end-diastolic pressure were similar in the two groups.These data suggest that higher baseline bata-endorphin plasma levels may play a role in the decreased sensitevity to pain in patients with slient myocardial ischemia. In addition, different beta-endorphin levels can be associated with a different sensitivity to pain.

Differential effects of cisterna magna cannulation on beta-endorphin levels in rat plasma and cerebrospinal fluid.

The concentration of beta-endorphin-like immunoreactivity (beta-ELIR) was determined in plasma and cerebrospinal fluid (CSF) of rats at various times following the implantation under Hypnorm anesthesia of a permanent cannula into the cisterna magna. Plasma beta-ELIR levels were highly increased immediately after the operation, and gradually returned to basal within 6 h. The beta-ELIR concentration in CSF followed a completely different pattern. It appeared to be rather stable during the first hour after the operation, was decreased at 2 h, and showed a marked increase 24 h after surgery. Two days after the surgery, beta-ELIR levels in CSF had decreased to a stable basal level which was maintained for at least 7 days. When at this stage animals were treated with Hypnorm, plasma beta-ELIR was again highly increased 30 min and not 24 h after injection, but no changes were found in the beta-ELIR concentration in CSF. These data indicate that implantation of a cannula into the cisterna magna induces postoperative changes in the CSF levels of beta-endorphin that are detectable up to at least 24 h later. Moreover, the lack of correlation between CSF and plasma levels of beta-ELIR points towards differences in the regulation of brain and pituitary pro-opiomelanocortin cells.

Plasma levels of beta-endorphin, prolactin and gonadotropins in male athletes after an international nordic ski race.

Plasma beta-endorphin, prolactin (PRL), FSH and LH were measured in 17 volunteer male subjects at rest and under the stress caused by a long-distance nordic ski race. The race induced increased levels of beta-endorphin and PRL in all skiers. The changes in PRL with exercise were significantly related to the changes in beta-endorphin (r = 0.69, p less than 0.001). Furthermore, the highly trained skiers training over 150 km.week-1 of nordic ski showed consistently higher post-exercise beta-endorphin and PRL levels than the moderately trained skiers who trained for 20 km.week-1. In addition the race induced slight falls in FSH and LH; however plasma gonadotropin levels did not show any correlation with plasma beta-endorphin concentrations and did not differ between the two groups of skiers. These results suggest that endogenous opioid peptides may modulate PRL secretion in heavy exercise, since they are of minor importance in the release of FSH and LH in such a situation. The observations also suggest that the degree of previous training and the exercise intensity do seem to be responsible for the hormonal changes.

Differences in the plasma betaendorphin levels of bulimics

We previously reported that the plasma beta-endorphin of bulimics who vomit was higher than in normal controls. In this report data are presented which show that bulimics who do not vomit have plasma beta-endorphin levels similar to controls. It is postulated that the increased levels of plasma beta-endorphin in the bulimics who vomit is due to the stress of vomiting or to increased caloric intake.

Acute Effect of Inragastric Ethanol Administration on Plasma Levels of Stress Hormones

We have previously demonstrated that single-dose ethanol administration enhanced plasma levels of ACTH, beta-endorphin, corticosterone (CS) and catecholamines. Since the secretion of proopiomelanocortin-derived peptides (e.g., ACTH, beta-endorphin) can be influenced by catecholamines and vasopressin in addition to the primary physiological regulator, corticotrophin-releasing hormone, we have attempted to determine whether or not the ethanol-induced activation of the hypothalamic-pituitary-adrenal axis (HPAA) could in part be mediated via either epinephrine or vasopressin (AVP) secretion. The selective neutralization of AVP through the administration of AVP antiserum failed to block the ethanol-induced secretion of either ACTH or CS. In addition, adrenal demedullation did not significantly attenuate the ethanol-induced increase of ACTH and CS. It would appear that neither adrenal medulla-derived epinephrine nor median eminence-derived AVP mediates ethanol's activation of the HPAA.

POSTPARTUM PLASMA ADH AND BETA ENDORPHIN LEVELS FOLLOWING DURAMORPH

POSTPARTUM PLASMA ADH AND BETA ENDORPHIN LEVELS FOLLOWING DURAMORPH

Plasma levels and diurnal variation of β-endorphin, β-lipotropin and corticotropin during pregnancy and early puerperium

Using a specific radioimmunoassay the concentrations of beta-endorphin, beta-lipotropin and corticotropin in maternal plasma were studied during pregnancy and in the early puerperium. Compared with the values in nonpregnant women, levels of beta-endorphin and beta-lipotropin were slightly lower in the first and second trimesters; corticotropin showed no difference in the first trimester. The concentrations of all these peptides increased towards term, most markedly in the case of corticotropin. The diurnal variation was studied near term and again in the early puerperium. beta-Endorphin and corticotropin showed a parallel diurnal variation. The values in the morning and during the day were slightly higher during pregnancy than in the puerperium, whereas the values at midnight were similar. After vaginal delivery, a rapid and parallel decrease in the plasma levels of beta-endorphin, beta-lipotropin and corticotropin was found. In elective cesarean section, the values were highest 30 min after delivery, reflecting surgical stress, and then the decrease was similar to that after vaginal delivery. Thus parallel changes in the plasma levels of beta-endorphin, beta-lipotropin and corticotropin during pregnancy and in the early puerperium were found, which can be explained by their origin from a common precursor peptide, pro-opiomelanocortin. The rise in the plasma levels of corticotropin and endorphins near term and the exaggerated diurnal variation is probably a reflection of a maternal adaptation to stress.

Relationship between pain sensitivity, cardiovascular reactivity to cold pressor test and indexes of activity of the adrenergic and opioid system.

An association between increased blood pressure levels and hypoalgesia has been reported in the experimental animal and in man. The relation between pain perception and cardiovascular function is however still obscure. In order to gain some insight into this aspect, normotensive subjects with low and high tolerance to pain, as assessed by tooth pulp stimulation, were compared for blood pressure and heart rate during cold pressor test, 24 hr urinary catecholamines, supine and upright PRA and plasma beta-endorphin levels. No significant difference was observed between the two groups for casual blood pressure, heart rate and PRA. Compared to subjects with low tolerance to pain, those with high tolerance to pain were significantly older and had: 1) significantly higher levels of diastolic blood pressure and of beta endorphin levels during cold pressor test; 2) significantly higher beta-endorphin levels after cold pressor test; 3) a significantly higher excretion of noradrenaline (but not of adrenaline and dopamine).

Neuroendocrinological function in Alzheimer's disease.

The neuroendocrine function is regulated by several neurotransmitters (acetylcholine, dopamine, somatostatin and noradrenaline) known to be reduced in brains of patients with Alzheimer's disease (AD). Moreover, the hypothalamus also has pathological changes. In spite of these findings suggesting neuroendocrine dysfunctions, this function has seldom been investigated in AD patients so far. We have compared patients with clinically 'probable' AD of mild-to-moderate severity with nondemented age- and sex-matched controls. Plasma levels of prolactin (PRL), growth hormone (GH) and thyroid-stimulating hormone (TSH) were measured by commercially available radioimmunoassays (RIA) before and after stimulation with metoclopramide, l-dopa or thyrotropin-releasing hormone. Basal plasma levels of beta-endorphin and beta-lipotropin were measured by RIA after high-performances liquid chromatography. Basal and stimulated plasma levels of PRL, GH, TSH and beta-lipotropin were similar in the two groups. Basal lamina levels of beta-endorphin were significantly higher in the patient group. Of doubtful clinical importance, this might be attributed to decreased tuberoinfundibular dopaminergic activity and has also been seen in patients with Parkinson's disease.

Rise in plasma beta-endorphin, ACTH, and cortisol in cancer patients undergoing whole body hyperthermia.

It has been previously reported that sauna-induced fevers (approximately 39 degrees C) result in rises of beta-endorphins in normal volunteers. This report describes changes in plasma beta-endorphins in cancer patients undergoing whole body hyperthermia (40.5 degrees C to 41.8 degrees C). Results presented show that there is a linear relationship between thermal stress, defined in terms of core temperature and/or duration of hyperthermia, and the quantitative rise in plasma beta-endorphin levels. Data relating to changes in ACTH and cortisol levels are in a single temperature range (41.5 degrees C--41.8 degrees C) are also reported.

Beta endorphin levels in CSF during methadone maintenance

Recent studies have shown that plasma beta endorphin levels of patients on methadone maintenance are comparable to controls. Furthermore, CSF levels of related peptides in methadone patients also do not differ from controls, although CSF levels of beta endorphin have not been specifically measured. In the current study we compared both CSF and plasma levels of beta endorphin in 11 patients on methadone maintenance for at least 10 months to levels in 13 controls getting spinal anesthesia for surgery. The CSF beta endorphin levels of the methadone maintained patients were significantly higher than the controls (52.3 vs 21.7 pg/ml), while plasma levels of beta endorphin (29.6 vs 31.1 pg/ml) and cortisol (13.8 vs 12.6 mg/ml) did not differ. Covarying for age differences between the samples, slightly increased the magnitude of this difference in CSF beta endorphin levels. Plasma levels of beta endorphin did not correlate with CSF levels, but did correlate with plasma levels of cortisol (r=0.51, P<0.02). These findings supported previous studies of plasma beta endorphin levels. However, the dissociation of beta endorphin levels in plasma and CSF within this patient population was a new finding.

Plasma beta-endorphin in response to oral glucose tolerance test in obese patients.

In order to clarify the possible interaction between endogenous opioids and glucose homeostasis in obesity we studied Beta-Endorphin (B-Ep), ACTH, cortisol and insulin plasma levels in response to an oral glucose tolerance test (OGTT) in 8 females suffering from uncomplicated obesity and in 6 healthy volunteers of normal weight. Results were evaluated in terms of secretion areas subtracted from basal value. Basal glucose, insulin and B-Ep levels were significantly higher in the obese patients compared to controls, cortisol levels and ACTH were not statistically different between obese and normal subjects. During OGTT total areas of insulin secretion were significantly higher in the obese patients; cortisol, ACTH, B-Ep plasma levels did not change in controls, whereas obese patients showed a response to B-Ep which reached a peak at 60 minutes. The area of B-Ep response to OGTT in obese patients was significantly higher than in controls. On the basis of these results we may suggest that the opioid system belongs to the chain of neuroendocrine and metabolic events responsible for the origin and the growth of overweight. But the possibility exists that obesity itself can enhance the B-Ep secretion above all through overeating. In this regard it is to stress that glucose ingestion induces in obese patients, differently from normal subjects, insulin hypersecretion and the B-Ep secretion, possibly from gastro-enteric tract and/or pancreatic isles.

Beta-endorphin and ACTH in plasma: Effects of physical and psychological stress

The effects of the expectancy of an official race (22000 m) and the performance of this last event on plasma levels of beta-Endorphin (B-End) and ACTH have been assessed. In a group of nine athletes, samples were obtained first in basal conditions; second in the day of the run before the warming up period and third after running. B-End immunoactivity was increased from 15.7 ± 2.0 pg/ml to 23.4 ± 2.5 pg/ml before the run and up to 30.6 ± 2.9 pg/ml after the trial. ACTH levels were increased from 8.4 ± 1.2 pg/ml to 17.9 ± 2.3 pg/ml before running and up to 36.2 ± 3.9 pg/ml after running. The results suggest that psychological and physical stress act synergically to increase the levels of B-End and ACTH during the practice of physical exercise.

Plasma beta-endorphin levels in silent myocardial ischemia induced by exercise

Although silent myocardial ischemia is a well recognized phenomenon, the reasons for the lack of symptoms in patients with coronary artery disease (CAD) is unclear. Because the endogenous opioid β-endorphin has been related to pain modulation, plasma β-endorphin levels were studied before, during and after exercise-induced ischemia in symptomatic and asymptomatic men. Because β-endorphin responses have been closely linked to adrenocorticotropic hormone (ACTH) and cortisol responses, these hormones also were measured. Nine symptomatic and 12 asymptomatic patients with a high probability (at least 95%) of CAD and 8 apparently healthy men completed a Bruce protocol treadmill test. Blood samples were drawn before, during and 10 minutes after exercise. During exercise the measured hormones showed no significant increases from basal levels. However, plasma β-endorphin, ACTH and cortisol levels were significantly elevated (p ≤0.01) 10 minutes after exercise in all 3 groups. There was no significant difference in plasma β-endorphin levels curing or after exercise between the symptomatic and asymptomatic patients with CAD. Thus, differences in circulating levels of β-endorphin, ACTH and cortisol are not associated with the presence or absence of pain during exercise-induced myocardial ischemia.

Beta-endorphin secretion in rams related to season and photoperiod.

A newly established RIA was used to measure changes in the concentration of beta-endorphin in peripheral blood and pituitary tissue from adult Soay rams living outside under natural conditions and housed indoors under artificial photoperiods. A pronounced seasonal cycle in plasma beta-endorphin immunoreactivity occurred in the outdoor animals, with low levels in spring and early summer (February-May; less than 200 pg/ml plasma) and maximal levels 10-20 times higher in late summer and autumn (July-October). Seasonal changes in plasma levels of PRL, FSH, and cortisol, testis size, and body weight were also monitored; the seasonal cycle in the levels of immunoreactive beta-endorphin occurred in parallel with the cycle in plasma FSH and body weight. There were no significant seasonal changes in plasma cortisol concentrations. Marked changes in the plasma levels of beta-endorphin were also seen in rams kept under the artificial photoperiod regimen of alternating 12- to 16-week periods of long days (16 h of light and 8 h of darkness; 16L:8D) and short days (8L:16D). Transfer from long days to short days led to a greater than 20-fold increase in the levels of beta-endorphin, reaching a maximum after 4-8 weeks; the reverse switch in photoperiod led to a rapid decrease in the levels. There was no diurnal rhythm in the plasma levels of beta-endorphin based on hourly samples collected for 24 h under long and short days. The total content of immunoreactive beta-endorphin in the pituitary gland was lower in rams under short days than under long days, converse to the pattern in the blood. Sephadex chromatography of the plasma samples revealed that most of the beta-endorphin immunoreactivity coeluted with synthetic beta-endorphin-(1-31), and a small amount of activity eluted with beta-lipotropin. The seasonal and photoperiod-induced changes were largely due to changes in the levels of beta-endorphin. Extracts of pituitary tissue revealed a large proportion of beta-lipotropin to beta-endorphin compared to plasma, with no consistent change in ratio related to the photoperiod. The overall results illustrate that there are pronounced seasonal and photoperiod-induced changes in immunoreactive plasma beta-endorphin levels in the ram. Under artificial photoperiods, long days inhibit and short days stimulate beta-endorphin secretion. Under natural conditions, the development of refractoriness to both the inhibitory effects of long days and the stimulatory effects of short days may explain the timing of the annual cycle of beta-endorphin secretion.

Cardiorespiratory depression and plasma beta-endorphin levels in low-birth-weight infants during the first day of life.

Twenty-nine premature infants were studied to determine whether neonatal asphyxia, apnea, and low blood pressure in the first day of life are associated with elevated plasma beta-endorphin concentrations. Plasma beta-endorphin levels were determined at 0.5 to 2, 4 to 6, and 18 to 24 hours of life, using radioimmunoassay. Premature infants with moderate or severe asphyxia (n = 19) had higher levels at 0.5 to 2 hours of age (32.1 +/- 6.7 vs 16.4 +/- 7.4 pmol/L) and significantly higher levels at 4 to 6 hours of age (50.4 +/- 10.0 vs 22.9 +/- 9.2 pmol/L) compared with the ten nonasphyxiated premature infants. A significant elevation in levels at age 0.5 to 2 hours (39.4 +/- 9.9 vs 17.7 +/- 4.4 pmol/L) and age 4 to 6 hours (59.3 +/- 13.8 vs 27.1 +/- 17.1 pmol/L) was observed in premature infants with low blood pressure or impaired perfusion (n = 12) who required the administration of volume expanders. No differences were observed in premature infants with and without apnea. It may be speculated that the increased endogenous release of beta-endorphins in response to perinatal asphyxia may play a role in the pathogenesis of shock observed in the first day of life.