Β-endorphin Concentrations Research Articles

Notes on the use of sodium hyaluronate in thoroughbreds

In this study, circulating β-endorphin, ACTH and cortisol concentrations were chosen as physiological markers of the hypothalamic-pituitary-adrenal (HPA) stress-related response in Therapeutic Riding Horses (TRHs). The aim of this research was to investigate HPA axis hormonal response in TRHs and check the effects of different kind of riders (mentally-impaired and able-minded riders). The main hypothesis was that, in TRHs, the HPA axis reaction would be less responsive to mentally-impaired than to able-minded riders, due to increasing levels of horse control by the able-minded riders. 6 TRHs were randomly ridden in the same setting by 2 groups of riders, adult mentally-impaired riders (Treatment Group A) and able-minded adult riders (Treatment Group B). Both groups consisted of inexperienced riders. Each rider rode 2 times a week for 6 consecutive weeks. The horses performed the same gaits and exercises at all sessions, with both Treatment Group A and Treatment Group B riders. All hormones’ concentrations were determined on a resting day (baseline, T0), before the session (T1), and at 5 min (T2) and 30 min (T3) after each session. Statistical analysis showed significant effects of the different Treatment Groups on the cortisol concentrations only, with lower cortisol concentrations both at T2 and at T3 in Treatment Group A than in Treatment Group B. Related to changes over the sampling time, ccortisol concentrations in horses were significantly higher at T1 than at T0 in Treatment Group A, and at T1, T2 and T3 than at T0, in Treatment Group B. ACTH concentrations were significantly higher at T1, T2 and T3 than at T0, only in Treatment Group B. β-endorphin concentrations at T3 were significantly higher than at T0, only in Treatment Group B. Results showed differences in the TRHs' stress levels between rider groups, with significantly lower cortisol concentrations in Treatment Group A than in Treatment Group B. Thus, although sessions’ workload stress was equivalent, the minor response of HPA axis could be related to different effects of horse-human interaction.

Streptozotocin-Induced Diabetes Is Associated with Reduced Immunoreactive Beta-Endorphin Concentrations in Neurointermediate Pituitary Lobe and with Disrupted Circadian Periodicity of Plasma Corticosterone Levels

Lower concentrations of immunoreactive (IR) beta-endorphin were present in the neurointermediate pituitary lobes of streptozocin-induced diabetic versus control animals at both 2 and 4 weeks after the onset of diabetes. The forms of beta-endorphin-like material present appeared to be similar in both groups when studied with cation-exchange chromatography. Insulin therapy via minipump for 2 weeks did not alter this finding of lowered beta-endorphin concentrations in diabetic animals, despite normalization of blood glucose levels and body weight gain. Lower IR beta-endorphin levels were also found in neurointermediate lobes of weight-restricted rats, but this group had increased plasma IR beta-endorphin concentrations compared to diabetic animals. Concentrations of IR beta-endorphin in microdissected brain regions and in anterior pituitaries of the diabetic animals failed to show consistent changes; in addition, ACTH concentrations in pituitary lobes and plasma did not differ among groups. Circadian rhythmicity of plasma insulin and corticosterone concentrations was absent in the diabetic animals, although food and water intake, while elevated, showed the normal nocturnal pattern of increased ingestion. Furthermore, adrenal hypertrophy was present in the diabetic animals and was accompanied by an elevation of mean plasma corticosterone levels. The present findings indicate that diabetes is associated with a decrease of neurointermediate pituitary lobe synthesis of beta-endorphin, while not affecting the processing of the peptide in this lobe, and confirm previous reports of altered adrenal function in diabetic animals.

Effects of Acute Behavioral Stress on Plasma and Cerebrospinal Fluid ACTH and β-Endorphin in Rhesus Monkeys

To elucidate the effect of acute behavioral stress on plasma and cerebrospinal fluid (CSF) concentrations of adrenocorticotropic hormone (ACTH) and beta-endorphin, rhesus monkeys were subjected to 30 min of confinement stress. Simultaneous plasma and CSF samples revealed no significant change in CSF ACTH or beta-endorphin up to 120 min after the onset of the stress despite significant elevations in plasma cortisol, ACTH, and beta-endorphin. It is suggested that acute behavioral stress does not alter CSF ACTH or beta-endorphin, and that this information may be clinically useful for future human studies of CSF ACTH and beta-endorphin in neuropsychiatric illnesses.

Term and preterm umbilical artery levels of β-endorphin and ACTH and their significance in the development of respiratory distress syndrome

SummaryUmbilical artery concentrations of adrenocorticotrophic hormone (ACTH), β-endorphin and pH values were measured in term and preterm babies. There was a strong correlation between acidosis and elevated ACTH and β-endorphin levels. Those preterm infants who developed severe respiratory distress syndrome had the highest ACTH and β-endorphin values and the lowest pH. Fetal antepartum stress was found to be associated with severe rather than mild respiratory distress syndrome and may in fact cause exacerbation.

Plasma immunoreactive β-endorphin in the early puerperium and during suckling

SummaryChanges in the plasma levels of β-endorphin and prolactin were studied in the early puerperium and during breast feeding. The mean plasma concentration of immunoreactive β-endorphin decreased from the maximum value of 282 pg/ml at the time of delivery to 72 pg/ml at 10 min, 51 pg/ml at 30 min and 19 pg/ml at 60 min after the delivery of the newborn. Still the mean β-endorphin level was higher during the first 6 days of the puerperium (23.4 ± 3.8 pg/ml) than was found in non-pregnant healthy women (12.4 ± 0.8 pg/ml; P> 0–01), suggesting that β-endorphin secretion from the maternal hypophysis remains increased in the early puerperium. The effect of suckling stimulus on the plasma level of β-endorphin was studied for 3–6 days after labour when breast feeding had already been established. The mean plasma level of β-endorphin did not change during suckling. There was no correlation between the plasma levels of β-endorphin and prolactin during or after delivery or during suckling. Thus β-endorphin does not seem to regulate prolactin secretion in the puerperium. The rapid withdrawal of β-endorphin from maternal circulation after delivery might predispose to the development of various psychic symptoms common in the early puerperium.

6-methoxy-tetrahydro-β-carboline (pinoline): effects on plasma renin activity and aldosterone, TSH, LH and β-endorphin levels in rats

Plasma renin activity and the plasma concentrations of aldosterone, TSH, LH and beta-endorphin were radioimmunologically determined in rats after ip administration of 15 mg/kg of 6-methoxy-tetrahydro-beta-carboline (6-MeO-THBC, pinoline), a compound found to occur normally in mammalian and avian pineal gland. A 2.6-fold increase of plasma aldosterone concentration was found and it was preceded by increase of plasma renin activity. An increase was also found in beta-endorphin/beta-lipotrophin concentration while TSH and LH concentrations did not change significantly. The present results do not prove nor exclude the concept that 6-MeO-THBC is the 'adrenoglomerulotropin'. The effects of 6-MeO-THBC on plasma beta-endorphin/beta-lipotrophin levels may be mediated by the dopaminergic or 5-HT-neurones.

Plasma β-endorphin concentrations prior to and during pregnancy, in labor, and after delivery

Beta-Endorphin was measured by radioimmunoassay in peripheral plasma of nonpregnant women (58 +/- 2.4 pg/ml, n = 17, mean +/- SE), during the first trimester (47 +/- 2.4 pg/ml, n = 11), the second trimester (33 +/- 1.9, n = 11), and the third trimester (49 +/- 2.7 pg/ml, n = 10) of pregnancy, during early (202 +/- 32 pg/ml, n = 12) and advanced labor (389 +/- 78 pg/ml, n = 10), and 30 to 60 minutes post partum (177 +/- 22 pg/ml, n = 12). Mean plasma levels of beta-endorphin were significantly lower in each trimester of gestation than the levels in nonpregnant control subjects. During labor and the early postpartum period, maternal plasma levels of beta-endorphin were significantly elevated. Furthermore, peripheral plasma levels of beta-endorphin during labor fell from 189 +/- 31 to 97.6 +/- 12 pg/ml (n = 13, p = 0.015) in response to epidural anesthesia, as compared to peripheral plasma concentrations of beta-endorphin of 223 +/- 71 and 193 +/- 47 pg/ml prior to and after injection of saline solution into epidural catheters, respectively, in 10 control subjects. Mean plasma levels of beta-endorphin in patients immediately prior to elective repeat cesarean section who were not in labor (151 +/- 23 pg/ml, n = 15) were significantly higher (p less than 0.005) than the levels in third-trimester control subjects. These data indicate that the pain associated with labor and the psychological stress of anticipating an operation are potent stimuli for the pituitary release of beta-endorphin.

Central acth deficit in degenerative and vascular demetria

Cerebrospinal fluid (CSF) concentrations of ACTH, β-lipotropin (β-LPH) and β-endorphin (β-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 < 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 β-LPH and β-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 β-LPH and β-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).

Effect of hypoglycemic stress on plasma and cerebrospinal fluid immunoreactive β-endorphin in conscious sheep

The effect of insulin-induced hypoglycemic stress on the concentrations of immunoreactive β-endorphin (ir β-EP) in plasma and cerebrospinal fluid (CSF) was examined in conscious non-pregnant ewes in which the cisterna magna and a jugular vein had been previously catheterized. In control experiments, no significant changes were observed in plasma cortisol or ir β-EP and CSF ir β-EP concentrations. During hypoglycemia induced by intravenous injection of 20 units of insulin, plasma cortisol concentrations rose significantly, reaching a peak 1.5 h after injection. The changes in plasma ir β-EP concentration were significantly different between hypoglycemic and normoglycemic sheep (analysis of variance, P = 0.0089). Following insulin injection, mean plasma ir β-EP rose by 100% within 0.75 h, continued to rise six-fold over initial concentrations by 2.25 h, and remained elevated for 3.75 h. The CSF ir β-EP concentrations following insulin injection were not significantly different from those observed in controls. These results suggest that if β-endorphin mediates hypoglycemic stress-induced analgesia, its actions may be peripheral, not central.

Rapid extraction and separation of plasma β-endorphin by cation-exchange high-performance liquid chromatography

Cation-exchange high-performance liquid chromatography (HPLC) was used to increase the sensitivity and specificity of the radioimmunoassay of plasma β-endorphin. Proteins were precipitated from a 0.5 to 2.5 ml sample of plasma with 60% acetonitrile at pH 4.7. The supernatant was subjected to cation-exchange HPLC. Gradient elution with volatile buffers was used to separate β-endorphin from β-lipotropin. The β-endorphin fraction (1.8 ml) was concentrated by lyophilization and subjected to radioimmunoassay. In healthy pregnant women at labour plasma concentration of β-endorphin varied from 105 to 403 pg/ml. In healthy non-pregnant women plasma concentration of β-endorphin was low, exceeding the detection limit (4 pg/ml) of the assay in only one of the 7 subjects studied.

Human neutrophil migration is enhanced by beta-endorphin

Using a serum-free chemotaxis-under-agarose assay, we measured the effect of β-endorphin on directed migration of human neutrophils toward 10 −7 M N-formyl-methionyl-leucyl-phenylalanine (FMLP). Neutrophils were pre-incubated with a range of β-endorphin concentrations. β-endorphin enhanced migration of neutrophils towards FMLP. This effect was maximal at 10 −9 M β-endorphin. Naloxone inhibited the β-endorphin effect, suggesting that enhanced migration is mediated via an opiate receptor.

β- Endorphin contributes to the antihypertensive effect of clonidine in a subset of patients with essential hypertension

Naloxone [0.4 mg iv.] increased blood pressure and heart rate of 13 clonidine-treated [0.3 mg per os for 3 days] patients with essential hypertension [reacting group] while it has no such effect in 11 clonidine-treated patients [non-reacting gr.] Clonidine increased plasma β-endorphin concentration of the reacting patients by 17.53 ± 1.68 pM/l and in the non-reacting ones by 5.91 ±0.88 pM/l. Significant linear correlation was found between the clonidine-induced increase in plasma β-endorphin level and the naloxone-induced change in mean blood pressure [r=0.9572,n:24, p<0.001]. In another group of 8 patients clonidine [0.15 mg iv.] decreased mean blood pressure but naloxone, 30 min after the clonidine injection, did not reverse the clonidine hypotension. We suggest that β-endorphin, released by chr.clonidine therapy, contributes to the antihypertensive effect only in the reacting group.

Clearance from Cerebrospinal Fluid of Intrathecally Administered ??-Endorphin in Monkeys

Five adult male monkeys (Macaca mulatta) weighing 7.1-9.9 kg were given synthetic human beta-endorphin (800 micrograms) and [14C]methoxy-inulin (50 microCi) in 400 microliters of normal saline intrathecally. Serial samples of cerebrospinal fluid were drawn through a previously positioned indwelling spinal catheter and were assayed for concentrations of beta-endorphin (determined by radioimmunoassay) and inulin (determined by liquid scintillation counter). Spinal fluid concentrations of beta-endorphin and inulin peaked and declined in a parallel manner. The clearance ratio (calculated from the reciprocal of the ratio of the areas under the respective curves of elimination of the two species) remained remarkably similar from animal to animal, giving a mean value of 1.060 +/- 0.090 (SEM). This ratio, being near unity, suggests that beta-endorphin is eliminated from spinal fluid in a fashion similar to that of inulin, which is removed exclusively by bulk absorption.

The effects of chronic naloxone on pituitary hormone secretion in female rats

The effects of a sustained-release implant for naloxone (NAL) on serum concentrations of prolactin (PRL), immunoreactive β-endorphin (IR-β-ENDO), growth hormone (GH) and thyroid stimulating hormone (TSH) were evaluated in ovariectomized female rats. After 9 days of exposure to NAL, serum levels of none of these 4 pituitary hormones were altered. However, the NAL implant antagonized the stimulatory effects of morphine (15 and 30 mg/kg body weight) on PRL and IR-β-ENDO secretion, enhanced the stimulatory effects of morphine on GH secretion, and had no effect on morphine-induced suppression of TSH secretion. These results indicate that while chronic NAL exposure does not, by itself, persistently alter pituitary hormone secretion, it differentially effects the response of these hormones to morphine exposure. These data suggest that chronic treatment with narcotic antagonists may invoke differential compensatory mechanisms to maintain normal hormone secretion.

β-endorphin and sprint training

Male, Wistar rats were sprint trained using a high intensity, interval type, treadmill running protocol. Sprint training produced a significant decrease in plasma β-endorphin levels. Conversely, animals who performed a high intensity acute run displayed significant increases in the concentration of plasma β-endorphin which may be stress-related. Neither training nor acute running had any significant effect on the β-endorphin levels of the pituitrary, cortex, posterior or anterior hypothalamus.

Fentanyl Preloading for Rapid-Sequence Induction of Anesthesia

Protecting the patient's airway is of paramount importance in the induction of general anesthesia. For the patient at risk of regurgitation of stomach contents, the rapid-sequence (crash) induction provides protection, but at the expense of increased stress response to laryngoscopy and intubation. This stress response is especially dangerous for the patient at risk for myocardial ischemia. The purpose of this study was to examine the efficacy of using low-dose fentanyl (5 μg/kg) to reduce cardiovascular and neuroendocrine stress responses to rapid-sequence induction. Thirty patients were randomly assigned to a rapid-sequence induction protocol either with or without fentanyl preloading. Fentanyl-preloaded patients (fentanyl group) received 2 mg/kg of thiopental whereas patients who were not preloaded with fentanyl (control group) received 4 mg/kg of thiopental. Data collected as indices of the stress response included heart rate, systolic, diastolic, and mean blood pressures, and plasma concentrations of catecholamines (epinephrine, norepinephrine, dopamine) and β-endorphin. Electrocardiograms (modified V5 lead) were monitored for dysrhythmias and ST segment depression. Control patients had higher systolic, diastolic, and mean blood pressures after intubation than did patients given fentanyl (P < 0.05). Although the incidence of dysrhythmias was decreased by fentanyl (20% vs 42%), this difference was not statistically significant. Plasma concentrations of β-endorphin and norepinephrine increased significantly in control patients but not in patients given fentanyl (P < 0.05). Low-dose fentanyl (5 μg/kg) reduces some aspects of the stress response to rapid-sequence induction of anesthesia.

Evidence that chronic hyperprolactinemia effects skin temperature regulation through an opioid mechanism.

Studies were undertaken to evaluate the effects of chronic hyperprolactinemia (HYP) induced by the MtTW15 tumor on the thermoregulatory response of female rats to blockade of opiate receptors with naloxone. Both chronic administration of morphine and HYP cause a mild hyperthermia as evidenced by a 0.8-1.0 degrees C elevation in rectal temperature (Tr). Naloxone-precipitated morphine withdrawal caused a prompt increase (4.9 +/- 0.76 degrees C) in tail skin temperature (TST) and a subsequent decline in Tr (-2.8 degrees C). Similarly, naloxone administration to HYP rats caused a dramatic TST response which was coincident with the onset of severe HYP. This effect of naloxone was maximal at 7 weeks of tumor growth when a TST response of 4.8 +/- 0.3 degrees C was observed but was not evident prior to or 1 week following tumor inoculation, when serum prolactin levels were low. The TST response to naloxone in chronic HYP exhibited distinct pulses with an amplitude of 3.4 +/- 0.4 degrees C and a frequency of 2.2 +/- 0.5 pulses per 120 min. It appears that blockade of opiate receptors in HYP rats induces instability in the regulation of skin temperature as evident by recurrent episodes of TST surges. These effects of chronic HYP on the TST response to naloxone were not influenced by ovariectomy, suggesting that changes in ovarian secretions were not involved in the response. At 4 weeks of tumor growth, immunoreactive beta-endorphin concentrations in the medial basal hypothalamus, preoptic area-anterior hypothalamus and the neurointermediate lobe of the pituitary were decreased by 59, 28 and 47%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of dopaminergic drugs on hypothalamic and pituitary immunoreactive β-endorphin concentrations in the rat

β-endorphin concentrations have been evaluated in the hypothalamus, pituitary lobes and plasma after 1-and 3-week treatment with 2-Br-α-ergocriptine or lisuride, two potent dopaminergic drugs. Hypothalamic β-endorphin concentrations were significantly decreased after the administration of the dopaminergic agents for 1 or 3 weeks. Similarly, β-endorphin concentrations decreased in the neurointermediate lobe and plasma. After gel chromatography, it appeared that in the anterior pituitary, β-lipotropin concentrations were unchanged or lightly increased concomitantly with a decrease of β-endorphin. Our data indicate that, both in the hypothalamus and the neurointermediate pituitary lobe, β-endorphin is under an inhibitory dopaminergic tone. The latter may also play a role in inhibiting β-endorphin cleavage from β-lipotropin in the anterior pituitary.

Changes in beta-endorphin content in discrete areas of the hypothalmus throughout proestrus and diestrus of the rat

The aim of the present study is to investigate changes in β-endorphin content in the hypothalamus during different stages of the estrous cycle. Groups of 9 to 10 Sprague-Dawley rats were sacrificed every two hours on proestrus from 8.00 to 18.00 h and groups of 7 to 8 rats were sacrificed on diestrus at 8.00, 12.00, 14.00 and 18.00 h. Preoptic suprachiasmatic region, posterior hypothalamus, arcuate nucleus and median eminence were dissected and assayed for β-endorphin. A significant increase in β-endorphin content was detected in the arcuate nucleus during proestrus (9.00 h: 1.76 ± .31; 14.00 h: 4.10 ± .85 μg/g tissue wet weight). Levels did not change during diestrus (1.18 ± .06 μg/g). The increase caused significant differences in β-endorphin values between both days at 12.00, 14.00 and 18.00 h, while the concentrations at 8.00 h were similar. The opposite pattern was observed in the median eminence with significantly higher proestrous β-endorphin levels at 8.00 h (11.24 ± 3.1 vs 3.52 ± .64 μg/g) and nonsignificant differences for the rest of the day. No significant change in β-endorphin concentration was seen in the preoptic suprachiasmatic region over the day of proestrus (1.35 ± .09 μg/g). Diestrous β-endorphin concentrations in this region were higher during the morning (2.60 ± .65 μg/g) and lower at 18.00 h (0.94 ± .12 μg/g) when compared to proestrous values. This pattern was caused by a 50% increase in β-endorphin during the afternoon of diestrus. No changes were observed in the posterior hypothalamus on either day with comparable levels of β-endorphin except at 18.00 h, when values were significantly higher on proestrus (1.66 ± .30 vs 0.83 ± .06 μg/g).

Changes of beta-endorphin and somatostatin concentrations in different hypothalamic areas of female rats after chronic starvation

To study the effect of starvation on hypothalamic β-endorphin and somatostatin (SRIF) concentrations in relation to starvation induced anestrus, groups of 8 rats were fed 50% of their normal daily chow consumption. Rats were sacrificed after 4, 8, 12, and 16 days during diestrus or anestrus. β-endorphin concentrations decreased in the preoptic suprachiasmatic area (0.52 ± 0.13 vs 0.21 ± 0.05 ng/mg tissue wet weight) and increased in the posterior hypothalamus (0.31 ± 0.06 vs 0.57 ± 0.11 ng/mg) after 4 days of starvation. No significant change occurred in the arcuate nucleus or in the median eminence. On day 8 and 12 of starvation, β-endorphin was unaltered in all areas compared to controls. Vaginal smears showed constant diestrus in a significant number of rats (5 out of 8) after 12 days. β-endorphin concentrations in the arcuate nuclei of these rats were significantly reduced on day 16 (1.00 ± 0.33 vs 0.30 ± 0.11 ng/mg). The SRIF levels changed only in the median eminence with increased concentrations on day 12 (45.2 ± 8.4 vs 79.5 ± 14.8 ng/mg). At this time serum levels of luteinizing hormone (LH), prolactin (PRL), and growth hormone (GH) were significantly reduced. The results indicate that changes in hypothalamic β-endorphin accompany the events leading to starvation induced anestrus.