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)

Female Wistar rats of different ages (1-45 days) were used. Extracts were made of the mediobasal hypothalamus (MBH) and beta-endorphin immunoreactivity (beta-ENDi) was quantitated by radioimmunoassay. Low but significant amounts of beta-ENDi (6.5 ng/MBH) were present on the first postnatal day. Hypothalamic beta-ENDi content did not change during the first week but decreased during the second week to a minimum (4.5 ng/MBH) on day 14. Thereafter, beta-ENDi increased rapidly to 13 ng/MBH on day 28 and remained at this level. Gel filtration showed that beta-ENDi substances with chromatographic characteristics identical to those of beta-END and beta-LPH were present in MBHs of 14-, 20- and 45-day-old rats. A beta-ENDi substance, possibly representing beta-END1-27, was nearly absent on day 14, but represented a major component of the MBH of the 45-day-old rat. In vitro incubation of MBH resulted in spontaneous release of beta-ENDi. Depolarization of neuronal membranes by incubation in medium containing 45 mMK+ stimulated beta-ENDi release. Both the spontaneous and K+-stimulated release of beta-ENDi were low on day 10 but reached postpubertal levels on day 20. These observations lead us to propose that the beta-ENDi-containing neurons in the hypothalamus of developing female rats rapidly mature between 14 and 20 days after birth. This may be causally related to the rapid decrease in circulating FSH levels that occurs during this period.
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PMID:Immunoreactive beta-endorphin in the hypothalamus of female rats: changes in content and release during prepubertal development. 629 64

The effects of several anesthetic drugs and artificial respiration on the release of pituitary beta-endorphin-like immunoreactivity (beta-END-LI) were examined in rats. Plasma beta-END-LI responses to halothane and pentobarbital were similar in magnitude and duration, being maximal (2- to 3-fold) by 10 min and returning to control values by 30 min after induction. Urethane anesthesia was associated with an 8-fold increase in plasma beta-END-LI throughout the 30-min treatment period. In comparison to anesthesia alone, anesthesia plus intubation with artificial respiration (standard parameters) was associated with considerably greater elevations in plasma beta-END-LI (up to 30-fold). Further, intubation and artificial respiration appear to have contributed separately, and in an additive fashion, to the overall beta-END-LI responses observed. As compared to halothane anesthesia alone, intubation evoked a 4-fold increase in circulating beta-END-LI, whereas intubation plus ventilation was associated with a 12-fold increase. Treatment with morphine (1 or 5 mg/kg), but not pancuronium (0.3 mg/kg), attenuated the plasma beta-END-LI response to mechanical ventilation, suggesting that a subconscious phenomenon, perhaps related to pain, was partially responsible for the profound release of pituitary beta-END-LI associated with artificial respiration. Chromatographic analysis of the molecular forms of beta-END-LI released into plasma revealed that both beta-END- and beta-lipotropin (beta-LPH)-sized peptides were secreted under the present experimental conditions. Since the analgesic form of beta-END (beta- END1 -31) is cosecreted with beta-LPH from the pars distalis, increases in the fraction of plasma beta-END-LI corresponding to beta-END in size were probably due to the release of opiate active beta- END1 -31.
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PMID:Anesthesia and stimulation of pituitary beta-endorphin release in rats. 632 33