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)

The influence of alpha-melanocyte stimulating hormone (alpha-MSH) and beta-endorphin (beta-END) on the secretion of somatostatin (SRIF) from the median eminence (ME) was studied using an in vitro incubation system. The MEs from adult male rats were first preincubated at 37 degrees C for 30 min with constant shaking in 0.4 ml of Krebs-Ringer bicarbonate-glucose buffer (pH 7.4) containing bacitracin in an atmosphere of 95% O2/5% CO2. Medium was discarded and replaced by medium containing different doses of alpha-MSH, beta-END, or a fixed dose of alpha-MSH (10(-7) M or 10(-9) M) plus beta-END at various concentrations. By themselves alpha-MSH and beta-END did not alter basal SRIF release, but in the presence of alpha-MSH (10(-7) M) beta-END stimulated somatostatin release. This effect was significant at concentrations of beta-END of 10(-8) M and higher. The permissive effect of alpha-MSH was observed at a concentration as low as 10(-9) M, but in this case the stimulatory effect of beta-END became evident only at higher doses tested (10(-7) M). It is suggested that alpha-MSH and beta-END participate in the modulation of SRIF release. By themselves beta-END and alpha-MSH did not affect basal release of SRIF but in the presence of alpha-MSH, beta-END had a stimulatory effect on SRIF release. The mechanism for this interaction is unknown. The results are consistent with the possibility that beta-END neurons have stimulatory and inhibitory effects on SRIF release and that alpha-MSH, by blocking the inhibitory components, discloses the stimulatory effect of beta-END on SRIF release.
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PMID:Alpha-melanocyte stimulating hormone discloses a stimulatory effect of beta-endorphin on somatostatin release. 288 55

Cord plasma levels of endorphins and catecholamines were correlated with the values of cord blood gas analysis and with hemodynamic parameters in 11 newborns (group A) delivered by elective cesarean section and in 18 newborns (group B) born spontaneously by vaginal route. All infants were in a good condition. No statistically significant differences were found in the mean cord plasma levels of adrenaline (A), noradrenaline (NA) and immunoreactive beta-endorphin (ir beta-E) between groups A and B. After spontaneous labor in group B a highly significant negative correlation was found between plasma NA level and pH and a positive correlation between NA and carbon dioxide tension in cord arterial blood and between NA and the short-term variability of the fetal heart rate before birth. Cord plasma A and ir beta-E did not show such correlations. These findings show that cord plasma level of NA is a sensitive indicator of minor stress during normal labor. After birth, during the first two hours of life, the mean plasma level of ir beta-E decreased in group B after vaginal delivery, but remained at a higher level in group A after elective cesarean section. This shows that the mode of delivery influences the neonatal endorphin secretion.
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PMID:Stress of delivery and plasma endorphins and catecholamines in the newborn infant. 293 59

Sleep loss impairs ventilatory responsiveness to hypercapnia and hypoxia, and also interferes with performance on spirometry. To test the hypothesis that the decline in hypercapnic drive due to sleep loss is mediated by endorphin production, we measured loaded and unloaded CO2 response after injection of placebo and naloxone in 11 normal subjects who were alternately rested and sleep-deprived. Blood for beta-endorphin and epinephrine assay was drawn before testing each day. Unloaded CO2 response was lower after sleep loss than after sleep restoration; naloxone had no effect on this difference. Likewise, there was no difference between CO2 response after naloxone administration and CO2 response in control subjects. beta-Endorphin activity did not rise after sleep loss. Loaded CO2 response was reduced compared to unloaded response and was not affected by sleep loss or by naloxone. The serum epinephrine level rose significantly with sleep loss. We conclude that naloxone is not a respiratory stimulant in normal people, and that it does not reverse the fall in CO2 response that follows sleep loss.
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PMID:Effect of sleep loss on beta-endorphin activity, epinephrine levels, and ventilatory responsiveness. 294 80

To investigate whether endogenous opioid peptides mediate time-dependent changes in ventilatory control during prolonged hypoxia, we studied four adult goats at rest during 14 days at simulated high altitude in a hypobaric chamber (PB approximately 450 Torr). Arterial PCO2 fell during the first several hours of hypoxia, remained stable over the next 7 days, and then rose slightly (but without statistical significance) by day 14. Ventilatory responsiveness to CO2 increased during the first week of hypoxia. By day 14, while still greater than control, the ventilatory response to CO2 was less than that observed on day 7. Immunoactive beta-endorphin levels in plasma and CSF did not change during the 14-day period. Administration of naloxone on day 14 did not restore the ventilatory response to CO2 to the level observed during the first week of acclimatization. We conclude that in adult goats, time-dependent changes in ventilatory response to CO2 during acclimatization to prolonged hypoxia are not primarily attributable to alterations in endogenous opioid peptide activity.
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PMID:Endogenous opioids and ventilatory adaptation to prolonged hypoxia in goats. 294 30

The respiratory stimulant properties of iv injections of 33, 67, and 100 micrograms synthetic human corticotropin-releasing hormone (hCRH) were studied in 12 normal men in a single blind, placebo-controlled trial. All doses of hCRH induced a respiratory stimulation in every subject, and the stimulation was dose dependent. The onset of respiratory stimulation occurred within 15-30 sec after hCRH infusion was started. Initially, there was an increase in tidal volume (VT), followed by an increase in respiratory rate. The maximum minute ventilation (VE) occurred 60-120 sec after starting the injection. The 33-micrograms hCRH dose induced a 35% increase in VE from 6.3 +/- 0.6 (+/- SD) to 9.7 +/- 1.3 liters/min (P less than 0.001) due to a marked increase in VT from 531 +/- 105 to 688 +/- 142 ml (P less than 0.001) and only a slight increase in the respiratory rate from 12.4 +/- 3.0 to 14.3 +/- 3.1 breaths/min (P less than 0.001); heart rate was not altered at this dose. The 100-micrograms hCRH dose increased the VE by 81% to 11.5 +/- 1.5 liters/min, mainly due to an increase in VT. VE was elevated for 5.8, 7.2, or 8.3 min after the end of injection of the three hCRH doses. Increases in VE markedly lowered the end-tidal partial pressure of carbon dioxide (P(ET)CO2; nearly identical with the arterial PCO2 in normal subjects). hCRH (33 micrograms) lowered P(ET)CO2 from 40.3 +/- 1.2 to 37.2 +/- 1.9 mm Hg (P less than 0.001), and 100 micrograms hCRH lowered P(ET)CO2 to 33.4 +/- 1.2 mm Hg. End-tidal partial pressure of oxygen, i.e. the most sensitive parameter for the duration of action of respiratory stimulation, was elevated for 8.5, 10.2, and 14 min after injection of 33, 67, or 100 micrograms hCRH. Sixty-seven micrograms of hCRH was the lowest effective dose for an increase in the heart rate (from 66.4 to 79.0 beats/min; P less than 0.001), and 100 micrograms hCRH markedly increased the heart rate by 20% to a peak value of 83.5 beats/min. Heart rate increased within 90 sec and returned to the control value after 5-10 min. These data suggest that hCRH is a rapidly acting, dose-dependent, and potent respiratory stimulant. Since this hyperventilatory effect of hCRH occurred in every subject after all doses tested, respiratory stimulation may represent specific biological activity of CRH rather than a side-effect.
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PMID:Human corticotropin-releasing hormone in man: dose-response of minute ventilation and end-tidal partial pressures of carbon dioxide and oxygen. 309 72

Though administration of opioid peptides depresses ventilation and ventilatory responsiveness, the role of endogenous opioid peptides in modulating ventilatory responsiveness is not clear. We studied the interaction of endogenous opioids and ventilatory responses in 12 adult male volunteers by relating hypercapnic responsiveness to plasma levels of immunoactive beta-endorphin and by administering the opiate antagonist naloxone. Ventilatory responsiveness to hypercapnia was not altered by pretreatment with naloxone, and this by itself suggests that endogenous opioids have no role in modulating this response. However, there was an inverse relationship between basal levels of immunoactive beta-endorphin in plasma and ventilatory responsiveness to CO2. Furthermore, plasma beta-endorphin levels rose after short-term hypercapnia but only when subjects had been pretreated with naloxone. We conclude that measurement of plasma endorphin levels suggests relationships between endogenous opioid peptides and ventilatory responses to CO2 that are not apparent in studies limited to assessing the effect of naloxone.
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PMID:Endogenous opioids and ventilatory responses to hypercapnia in normal humans. 315 33

After 30 min rest in the lying position, 12 healthy male volunteers (average age 22 years) received, in a randomized double-blind cross-over protocol, either saline or naloxone (10 mg iv followed by a continuous infusion of 10 mg/hr). Thereafter they rested for a further 30 min in the recumbent position and for 15 min sitting on a bicycle ergometer; they then exercised to exhaustion. At rest plasma levels of adrenocorticotropin (ACTH), cortisol, and aldosterone increased during infusion of naloxone, while body temperature decreased. During exercise the difference in plasma ACTH between naloxone and saline periods was abolished, while the differences in plasma cortisol and aldosterone lost statistical significance. Intra-arterial pressure, heart rate, ventilation, O2 uptake, and CO2 output were continuously monitored throughout the experiment and were not affected by naloxone. This was also the case for several hormonal and biochemical measurements, including those of plasma renin, angiotensin II, norepinephrine, 13,14-dihydro-15-keto-prostaglandin F2 alpha, glucose and lactate, and serum insulin and growth hormone. Exercise performance was not changed by naloxone. In conclusion (1) during exhaustive graded exercise of short duration opioidergic inhibition of the pituitary-adrenocortical axis is probably not sustained, (2) apart from the latter mechanism, the present study does not support the hypothesis that endogenous opioids are involved in various hemodynamic, respiratory, and hormonal responses to this type of exercise.
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PMID:The nature of opioid involvement in the hemodynamic respiratory and humoral responses to exercise. 404 6

We studied the effect of chronic carotid body denervation on renin (plasma renin activity, PRA), adrenocorticotropin (ACTH), blood pressure, and hematocrit responses to acute normocapnic (arterial CO2 partial pressure, PaCO2, 35 Torr) and hypercapnic (PaCO2, 65 Torr) hypoxia (arterial O2 partial pressure, PaO2, 31 Torr) in five anesthetized, artificially ventilated dogs. Animals were studied at least 3 days before and again at least 10 days after carotid body denervation (bilateral carotid sinus nerve resection). Increases in PRA during hypercapnic normoxia [21.8 +/- 6.4 ng angiotensin I (ANG I) X ml-1 X 3 h-1] and normocapnic hypoxia (13.3 +/- 4.2 ng ANG I X ml-1 X 3 h-1) were not attenuated by carotid body denervation. Increases in ACTH during normocapnic hypoxia (117 +/- 34 pg/ml) were attenuated but not eliminated by carotid body denervation; the increase in ACTH during hypercapnic hypoxia (295 +/- 93 pg/ml) was not attenuated by carotid body denervation. Both the blood pressure and hematocrit responses to normocapnic and hypercapnic hypoxia were attenuated by carotid body denervation. We concluded that 1) the renin response to hypercapnia and hypoxia is not a carotid chemoreflex, 2) the ACTH response to hypoxia is partially a carotid chemoreflex, and 3) blood pressure and hematocrit responses to hypoxia are primarily carotid chemoreflexes.
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PMID:Renin and ACTH responses to hypercapnia and hypoxia after chronic carotid chemodenervation. 608 93

The endogenous opioids seem likely to be assigned a significant role in the integrated hormonal and metabolic response to exercise. This article reviews the present evidence on exercise and the endogenous opioids, and examines their involvement in a number of widely disparate physiological processes. In considering the role of individual opioid peptides, it is important to remember that many of the tools and techniques now used are still relatively crude. Most studies have demonstrated that serum concentrations of endogenous opioids, in particular beta-endorphin and beta-lipotrophin, increase in response to both acute exercise and training programmes. Elevated serum beta-endorphin concentrations induced by exercise have been linked to several psychological and physiological changes, including mood state changes and 'exercise-induced euphoria', altered pain perception, menstrual disturbances in female athletes, and the stress responses of numerous hormones (growth hormone, ACTH, prolactin, catecholamines and cortisol). Many reports have described a role for the endorphin response as seen during exercise and have used the opioid receptor antagonist, naloxone, to investigate and verify the degree of involvement of the opioids. However, whether the observed increases in peripheral endorphin concentrations are sufficient to cause immediate mood changes, create menstrual cycle dysfunction or alter pain perception is still not resolved. A relatively new implication for the endorphins and associated changes with exercise is in ventilatory regulation. A number of studies have suggested that endogenous opioids depress ventilation and may, therefore, play a role in ventilatory regulation by carbon dioxide, hypoxia and exercise. It may also be possible that during exercise, the perception of fatigue is modulated by an increase of endogenous opioids.
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PMID:Endorphins and exercise. 609 Dec 17

Parathyroid hormone is mainly regulated by the serum calcium concentration and not by another hormone which is usually the case for other hormones. We examined whether the parathyroid hormone could also be regulated by a hormone such as adrenocorticotropic hormone (ACTH). Experiment I: A two-hour urine sample was collected from 6 AM to 8 AM. At 8 AM one mg of synthetic ACTH was injected intramuscularly. Blood and urine was collected two hours after the injection for determination of the concentration of serum calcium, phosphate, parathyroid hormone and cortisol. Experiment II: Adenoma tissue was obtained during operation from patients with primary hyperparathyroidism. The adenoma was digested with trypsin. Eagle MEM containing 100 ml fetal calf serum per 500 ml medium was used as the culture medium. The specimens were incubated in an atmosphere of 95% air and 5% CO2. Several days later, 25 micrograms of ACTH was added to the medium which was then incubated for 2 hours. The parathyroid hormone in the medium was measured by radioimmunoassay. Experiment III:ACTH was injected intraperitoneally into control male rats and parathyroidectomized rats. Two hours later, serum calcium and parathyroid hormone levels were measured. After ACTH injection, a remarkable increase in serum calcium level was seen in the patients with primary hyperparathyroidism, but in the other groups, no increase in the serum calcium was observed. Parathyroid hormone was increased after ACTH injection in most subjects in all groups. Serum cortisol levels increased markedly after ACTH injection in all groups. The parathyroid concentration in the culture medium was slightly increased after ACTH addition.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Endocrinological characteristic of primary hyperparathyroidism]. 609 27


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