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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of hypoxia on plasma met-enkephalin and catecholamine levels was studied in chronically catheterized fetal sheep. Maternal and fetal hypoxia was maintained for 20 min. We found hypoxia significantly increased the plasma levels of large mol wt met-enkephalin containing peptides from 1755 +/- 229 pg/mL during baseline to 4408 +/- 1426 pg/mL by 15 minutes of hypoxia. The levels of the met-enkephalin pentapeptide were unchanged during hypoxia from a baseline value of 168 +/- 56 pg/mL. Norepinephrine and epinephrine levels increased 5- and 10-fold, respectively, by 15 min of hypoxia. These observations suggest cosecretion of the large mol wt met-enkephalin peptides with catecholamines during stress in developing animals.
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PMID:The effects of hypoxia on (methionine) enkephalin peptide and catecholamine release in fetal sheep. 229 72

Mean beta-endorphin-like immunoreactivity in the plasma of 10 normal women in the 10th month of pregnancy was 144.3 +/- 7.5 ng/l. During labor in 7 women its immunoreactivity was increased and peaked at the time of vaginal delivery (1 162 +/- 69 ng/l). Two hours after delivery, beta-endorphin-like immunoreactivity was significantly decreased (297 +/- 39 ng/l) and after 4 to 5 days was 155 +/- 33 ng/l. Beta-endorphin-like immunoreactivity in the cord plasma (523 +/- 30 ng/l) was significantly lower than in the mother at the time of vaginal delivery and in venous blood of newborns 24 hours post partum was 156 +/- 11 ng/l. The correlation between beta-endorphin-like immunoreactivity in the mother and the cord blood plasma was not determined. At the time of the fetal hypoxia, beta-endorphin-like immunoreactivity in the cord blood plasma was increased (2 741 ng/l). We conclude that immunoreactive beta-endorphin influences a stress reaction in the mother and fetus at the time of labor. During intra-uterine life the fetus probably produces its own immunoreactive-like beta-endorphin independently of the maternal production of this peptide.
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PMID:Plasma beta-endorphin-like immunoreactivity during pregnancy, parturition, puerperium and in newborn. 294 69

Fetal beta-endorphin release has been associated with fetal hypoxia. The purpose of this study was to assess the degree of uterine blood flow reduction needed to elicit fetal beta-endorphin release in the sheep since there is a large reserve of oxygen supply to the fetus. Uterine blood flow was reduced by 26 +/- 2, 46 +/- 3 and 66 +/- 2%, producing fetal oxygen content concentrations of 5.7 +/- 0.6, 4.4 +/- 0.7 and 2.6 +/- 0.3 ml/dl, respectively. Although fetal oxygen concentrations were significantly decreased in the groups with a reduction in uterine blood flow of 46 and 66%, beta-endorphin was elevated only in the latter group. It is speculated that fetal beta-endorphin is released at a level of hypoxia which leads to a decrease in fetal oxygen consumption. A reduction in uterine blood flow of 66% appears to produce a stressful environment for the fetus as measured by fetal plasma beta-endorphin levels.
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PMID:Fetal beta-endorphin levels in response to reductions in uterine blood flow. 295 93

Antisera suitable for human beta-endorphin and beta-lipotropin radioimmunoassay were developed, and radioimmunoassays were established to measure these peptides in umbilical cord plasma, with silicic acid extraction and gel chromatography used to separate the beta-endorphin from the beta-lipotropin fraction. These two peptides were determined in umbilical venous plasma from 64 newborn infants. Umbilical vein beta-endorphin and beta-lipotropin concentrations averaged 38.5 +/- 3.2 and 50.4 +/- 4.1 (+/- SE) fmoles/ml in the 54 newborn infants without and 115 +/- 18 and 110 +/- 25 fmoles/ml in the 10 newborn infants with apparent fetal distress. Neither the presence or absence of labor nor the route or mode of delivery was found to affect umbilical vein beta-endorphin or beta-lipotropin concentrations. However, cord plasma levels of both peptides were significantly elevated in conjunction with fetal distress, as evidenced by prolonged bradycardia, late and prolonged variable fetal heart rate decelerations, or fetal acidosis. In 18 of 22 pairs of simultaneously measured umbilical venous and arterial beta-endorphin and beta-lipotropin concentrations in newborn infants without apparent intrapartum distress, the venous beta-endorphin concentrations, which averaged 40.4 +/- 3.5 fmoles/ml, were significantly higher than the arterial beta-endorphin levels, with a mean of 28.5 +/- 4.2 fmoles/ml. No significant umbilical arteriovenous concentration difference could be observed for beta-lipotropin. This suggests that at least a portion of the coad plasma beta-endorphin is derived from the placenta. The ratio of umbilical arterial to venous beta-endorphin concentrations rose as the absolute cord plasma beta-endorphin levels increased. Furthermore, both the molar umbilical venous and arterial beta-lipotropin to beta-endorphin ratios decreased significantly in association with intrapartum fetal distress. These data indicate tat the stress-related increase in umbilical plasma beta-endorphin exceeds that of beta-lipotropin and may be, at least in part, of fetal origin. Umbilical venous beta-endorphin and beta-lipotropin levels of neonates whose mothers did not receive meperidine or other narcotics agents did not differ from those of neonates whose mothers were given meperidine or other narcotics during labor. Our data, in conjunction with those of others, are consistent with the hypothesis that fetal hypoxia causes the release of neurotransmitters such as beta-endorphin, which may modulate the regulation of fetal heart rate patterns.
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PMID:beta-Endorphin and beta-lipotropin concentrations in umbilical cord blood. 629 93

To examine the role of endogenous adrenocorticotropic hormone (ACTH) in adrenal blood flow responses to hypoxia, we studied unanesthetized ovine fetuses during an intravenous infusion of cortisol or vehicle. Fetal hypoxia was induced after 5 h of cortisol or vehicle infusion. Control fetuses were not made hypoxic. Blood flows were determined before and at three time points during the infusions. At 2 and 6 h of hypoxia, in vehicle-infused fetuses, fetal plasma concentrations of immunoreactive ACTH (irACTH) had risen from 9 +/- 3 (SE) pg/ml to 68 +/- 25 and 127 +/- 37 pg/ml, respectively. No significant change in fetal plasma irACTH occurred in the other groups. Adrenal cortical blood flow rose three- to fourfold during hypoxia in vehicle-infused fetuses but did not change from prehypoxia levels in cortisol-infused fetuses (P < 0.005). Medullary flow rose with hypoxemia, and this was not affected by concurrent cortisol infusion. Adrenal blood flows did not change in the control groups. Thus prior infusion of cortisol suppressed the rise in fetal plasma ACTH during hypoxia and selectively blocked the increase in adrenal cortical blood flow.
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PMID:Inhibition of ACTH secretion blocks hypoxia-induced increase of adrenal cortical blood flow in fetal sheep. 757 39

To determine whether adrenocorticotropic hormone (ACTH) at plasma concentrations measured during mild hypoxemia and at term affects adrenal blood flow, we measured regional blood flows in five unanesthetized normoxemic fetuses (125-130 days gestation) during a 24-h intravenous infusion of ACTH-(1-24) in isotonic saline solution. Another five fetuses received an infusion of vehicle. Blood flows were determined before the infusion, at 2 and 24 h from its onset, and 24 h afterward using radionuclide-labeled microspheres. Blood flow to the adrenal medulla was fivefold greater than that to the adrenal cortex. Adrenal blood flow rose 99% at 24 h of the ACTH infusion. There was a large increase in adrenal cortical blood flow of 272% at this time but medullary blood flow did not change significantly during ACTH infusion. The rise in cortical blood flow was attributable to decreased vascular resistance. No significant alterations occurred in fetal arterial blood pressure and heart rate, or in blood flow to other lower body organs of the fetus or to the placental cotyledons. These findings are consistent with the hypothesis that the increase in adrenal blood flow observed during fetal hypoxia is associated with changes in plasma ACTH concentration. They are also indicative of selective regulation of cortical and medullary blood flows in the sheep fetus at this stage of gestation.
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PMID:Regional adrenal blood flow responses to adrenocorticotropic hormone in fetal sheep. 838 38

By combining the chick embryo model with incubation at high altitude, this study tested the hypothesis that development at high altitude is related to a fetal origin of adrenocortical but not adrenomedullary suppression and that hypoxia is the mechanism underlying the relationship. Fertilized eggs from sea-level or high altitude hens were incubated at sea level or high altitude. Fertilized eggs from sea-level hens were also incubated at altitude with oxygen supplementation. At day 20 of incubation, embryonic blood was taken for measurement of plasma corticotropin, corticosterone, and Po(2). Following biometry, the adrenal glands were collected and frozen for measurement of catecholamine content. Development of chick embryos at high altitude led to pronounced adrenocortical blunting, but an increase in adrenal catecholamine content. These effects were similar whether the fertilized eggs were laid by sea-level or high altitude hens. The effects of high altitude on the stress axes were completely prevented by incubation at high altitude with oxygen supplementation. When chick embryos from high altitude hens were incubated at sea level, plasma hormones and adrenal catecholamine content were partially restored toward levels measured in sea-level chick embryos. There was a significant correlation between adrenocortical blunting and elevated adrenal catecholamine content with both asymmetric growth restriction and fetal hypoxia. The data support the hypothesis tested and provide evidence to isolate the direct contribution of developmental hypoxia to alterations in the stress system.
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PMID:Adrenocortical suppression in highland chick embryos is restored during incubation at sea level. 2145 69