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 effects of acute stress on growth hormone (GH) secretion and the mechanisms involved in its changes have been investigated in sheep. An acute isolation-restraint stress induced a rapid and significant increase in jugular GH levels in 12 out of 14 rams. GH-releasing hormone (GHRH) and somatostatin secretion during the same stress were studied in 5 animals prepared for hypophysial portal blood collection. A 3.5-fold increase in portal GHRH levels was observed concomitantly with a slight elevation in portal somatostatin. Portal corticotropin-releasing hormone (CRH) and jugular cortisol plasma levels increased during the same stress. Our data suggest that an isolation-restraint stress stimulates GH secretion in the sheep and that GHRH may be responsible for GH response.
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PMID:Acute stress stimulates secretion of GHRH and somatostatin into hypophysial portal blood of conscious sheep. 781 15

Acute stress results in activation of the hypothalamic-pituitary-adrenal (HPA) axis. ACTH and cortisol secretion is stimulated by corticotropin-releasing hormone (CRH). It has also been shown that activation of the HPA axis during stress is accompanied by changes in the immune response. However, little is known about the influence of acute stress on the release of cytokines such as interleukin-1 (IL-1) or interleukin-2 (IL-2). In this study, we determined serum IL-1 alpha and IL-2 levels in 19 patients undergoing the acute stress of angioplasty for coronary artery disease. A second protocol was devised to determine serum IL-1 alpha and IL-2 concentrations as well as lymphocyte subpopulations in 10 normal volunteers receiving 1 microgram kg-1 human CRH intravenously. Finally, IL-1 alpha concentrations were measured in CRH-incubated mononuclear cell (MNC) and monocyte cultures. In response to the stress of angioplasty, ACTH and cortisol as well as IL-1 alpha and IL-2 concentrations were clearly above baseline levels (IL-1 alpha, mean +/- SEM, baseline: 1.39 +/- 0.34 ng ml-1, after angioplasty: 2.64 +/- 0.73 ng ml-1, P < 0.05; IL-2, baseline: 1.2 +/- 0.13 ng ml-1, after angioplasty: 2.8 +/- 1.14 ng ml, P < 0.05). A similar pattern was obtained in normal subjects in response to CRH (Il-1 alpha, baseline: 0.8 +/- 0.2 ng ml-1, after angioplasty: 3.7 +/- 1.4 ng ml-1, P < 0.05; IL-2, baseline: 1.9 +/- 0.4 ng ml-1, after angioplasty: 5.4 +/- 2.2 ng ml-1, P < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Systemic interleukin-1 alpha and interleukin-2 secretion in response to acute stress and to corticotropin-releasing hormone in humans. 789 16

The levels of beta-endorphin, insulin, cortisol, GH, glucagon, prolactin and TSH were measured in serum samples of 9 hyperglycaemic patients (3 female, 6 male) with a mean age of 4.1 years admitted to the pediatric emergency unit. All patients were in acute stress due to severe diseases (acute gastroenteritis, bronchopneumonia, septicaemia, etc.). Initial and repeat blood samples for hormone determination were taken at admission and in the recovery phase (after 4-6 weeks of treatment). OGTT was also performed in the recovery phase. The hyperglycaemia, monitored hourly following the initial determination, returned to normal in all patients in 1-5 h without specific treatment. Mean serum glucose values at admission and in the recovery phase were 287.0 and 84.1 mg/dl. Concomitant to the hyperglycaemia encountered in these patients in the acute phase of stress, an increase was noted in all hormone levels excluding glucagon and cortisol. All elevated hormone levels fell to normal in 4-6 weeks with significant differences from initial levels for beta-endorphin (P < 0.05) and insulin (P < 0.01). OGTT gave a normal curve. These results indicate that stress hyperglycaemia, despite high insulin levels, is associated with an increase in beta-endorphin levels. The results also show that hyperglycaemia in acute disease does not alter OGTT in short-term follow up.
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PMID:beta-Endorphin and some hormonal levels in children with acute stress hyperglycaemia. 795 15

In addition to the release of adenohypophysial hormones adrenocorticotropin and beta-endorphin, most types of acute stress induce rapid release of prolactin (PRL) from the anterior pituitary lobe. Endogenous opioid peptides are believed to participate in the stress-induced PRL secretion via an action within the central nervous system. In the present study, we have investigated the effect of acute stress on anterior pituitary PRL secretion and the hypothalamic expression of messenger ribonucleic acids (mRNAs) encoding precursors of the endogenous opioids Met-enkephalin and beta-endorphin. Adult male rats were subjected to 1 h of restraint and the stress-induced rise in plasma PRL was measured both during and after termination of the stress paradigm. Using quantitative in situ hybridization histochemistry, it was observed that levels of proenkephalin A mRNA increased significantly within the medial parvocellular subset of the hypothalamic paraventricular nucleus, and within the arcuate nucleus levels of proopiomelanocortin (POMC) mRNA were slightly, but significantly, increased. The employed stress paradigm also induced an elevation of anterior pituitary levels of PRL and POMC mRNAs. The present data suggest that restraint stress activates gene expression of endogenous opioid systems in the hypothalamus and that the employed stress paradigm is of sufficient magnitude to stimulate both mRNA expression and release of PRL in the anterior pituitary lobe.
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PMID:Effect of acute stress on the expression of hypothalamic messenger ribonucleic acids encoding the endogenous opioid precursors preproenkephalin A and proopiomelanocortin. 798 95

We evaluated the adrenocortical response to acute stress in free-living Gambel's white-crowned sparrows (Zonotrichia leucophrys gambelii) using a standardized capture stress protocol in which five serial blood samples (70 microliters) were taken for measurement of plasma corticosterone (B) over the course of an hour of captivity (at 1, 5, 10, 30, and 60 min). In field-captured birds, male plasma B levels rose two to four times higher than those of females under capture stress during the breeding season, but were no different during winter (nonbreeding). We investigated the basis of this pattern by conducting dexamethasone (DEX) suppression tests on breeding and nonbreeding sparrows of both genders. This test involves pretreatment with subcutaneous DEX implants (a potent synthetic glucocorticoid) and challenge with intrajugular injections of either corticotropin (ACTH) or saline, followed by collection of a series of blood samples for evaluation of plasma B levels over a 2-hr period. ACTH injections in DEX-treated birds resulted in elevated B in both genders, with nonbreeding B profiles consistently lower than those of breeding birds. All DEX-treated, saline-injected birds, except breeding males, maintained low B levels for the entire 2-hr post-challenge period. This result indicates effective negative feedback by DEX on the hypothalamic-pituitary-adrenal axis, thus inhibiting endogenous B secretion. The apparent reduction in glucocorticoid feedback inhibition in breeding males may be related to an uncoupling of adrenal effects on reproductive behavior.
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PMID:Gender and seasonal differences in the adrenocortical response to ACTH challenge in an arctic passerine, Zonotrichia leucophrys gambelii. 804 66

Chronic stress affects the reproductive function by modifying the neuroendocrine homeostasis. The aim of the present study was to clarify the neuroendocrine and the gonadal changes following chronic intermittent stress in male rats and the action of a neuroactive drug, acetyl-l-carnitine (ALC). The effect of two different stressors, cold water swimming or ether, on central beta-endorphin (beta-EP) and GnRH contents, and on plasma testosterone levels was investigated. In addition, the response to an acute stress in chronically stressed rats, treated or untreated with ALC (10 mg/day/rat p.o.), was evaluated. The stressors were applied twice a day for 10 days, and rats were killed before, during and after the last stress session. Mediobasal hypothalamus (MBH) beta-EP and GnRH contents, and plasma testosterone levels were evaluated by radioimmunoassay. The following results were obtained: (1) both chronic swimming and ether stress caused a decrease in hypothalamic beta-EP contents; (2) MBH GnRH contents increased after chronic swimming stress but not after ether stress; (3) chronic swimming stress induced a twofold decrease in plasma testosterone levels, while no changes were observed after ether stress; (4) the treatment with ALC prevented the decrease in plasma testosterone levels after chronic swimming stress, and (5) acute stress in chronically stressed animals caused an increase in MBH-beta-EP. The present data showed that chronic swimming stress reduces the reproductive capacity and impairs the capacity to respond to the acute stress and that ALC modulates the hormonal changes to physical stress and prevents the antireproductive effect of chronic cold swimming.
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PMID:Effect of different chronic intermittent stressors and acetyl-l-carnitine on hypothalamic beta-endorphin and GnRH and on plasma testosterone levels in male rats. 823 73

In conclusion, we have demonstrated that in the primate increased activity of the immune system and the consequent IL-1 release result in the activation of neuropeptides of the adrenal axis, mainly CRF and AVP. These neuropeptides, through a direct effect on the GnRH pulse generator or indirectly through the hypothalamic endogenous opioid peptides, inhibit the GnRH pulse generator. Some of the POMC derivatives, such as alpha-MSH, may antagonize these effects. The consequential decrease in GnRH pulse frequency results in an acute decrease in LH and FSH secretion. This decrease in gonadotropin release may explain the deleterious effects of stress on the menstrual cycle. However, an acute decrease in gonadotropins following activation of the adrenal axis is not observed in the presence of estradiol. Thus, during the menstrual cycle, a relative protection against the deleterious effects of acute stress may exist. How potent this protective mechanism is against repetitive stress is not known.
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PMID:Neuropeptides, the stress response, and the hypothalamo-pituitary-gonadal axis in the female rhesus monkey. 825 5

Corticotropin-Releasing-Hormone (CRH) is the principal secretagogue for plasma ACTH and corticosterone secretion and plays an important role in coordinating a variety of physiological and behavioral responses to stress. To explore whether there is a rapid change in the secretory response of the hypothalamic CRH neuron during acute stress, we report here a study of the effects of KCl and norepinephrine (NE) on CRH release in vitro from rat hypothalami explanted after 5, 30, 60, and 120 minutes of immobilization. We also measured the plasma levels of ACTH, beta-endorphin, corticosterone, prolactin, GH, and TSH at these intervals. As the duration of immobilization increased, KCl and NE-induced CRH release in vitro progressively fell. After reaching a maximal rise after 30 minutes of immobilization, plasma ACTH, beta-endorphin, and prolactin progressively fell in plasma, whereas corticosterone remained elevated up to 120 minutes; TSH and GH secretion rapidly declined and remained suppressed. Taken together, these data suggest that during immobilization stress, the responsiveness of the hypothalamic CRH neuron rapidly falls, owing either to CRH depletion and/or desensitization to NE, and this is paralleled by a concomitant decrease in pituitary-adrenal responsiveness.
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PMID:Immobilization stress rapidly decreases hypothalamic corticotropin-releasing hormone secretion in vitro in the male 344/N Fischer rat. 839 19

Previous studies have demonstrated that acute stress or ovine corticotropin-releasing hormone (oCRH) in vivo, or oCRH in vitro, stimulates release of beta-endorphin over beta-lipotropin from anterior pituitary corticotropes. This occurs despite the predominance of beta-lipotropin in corticotrope peptide stores. In vitro studies with primary anterior pituitary cultures suggested that chronic exposure to oCRH results in a shift towards more beta-lipotropin secretion into the media than with short-term exposure. The current studies explored whether increased secretory drive in vivo results in a similar shift towards more beta-lipotropin. We used removal of glucocorticoids by adrenalectomy or metyrapone blockade of corticosterone synthesis, to stimulate endogenous secretion of CRH and vasopressin. Both treatments resulted in shifts of the ratio of beta-endorphin: beta-lipotropin in plasma of experimental animals in comparison to the sham-treated control rats. In vitro testing with oCRH of anterior lobe cultures from adrenalectomized or metyrapone-treated rats demonstrated similar effects of these treatments on the ratio of beta-endorphin:beta-lipotropin. These changes occurred despite similar ratios of beta-endorphin:beta-lipotropin in anterior pituitary peptide stores.
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PMID:Altered ratios of beta-endorphin: beta-lipotropin released from anterior lobe corticotropes with increased secretory drive. I. Effects of diminished glucocorticoid secretion. 848 40

The aims of the present study were: 1) to compare the effect of two different chronic intermittent stressors i.e. cold-swimming versus ether, on the pituitary opioidergic system; 2) to evaluate the response of pituitary and plasma beta-endorphin (beta-EP) to an acute stress in chronically stressed rats; and 3) to evaluate the effect of acetyl-l-carnitine treatment (10 mg/day/rat per os at night) on pituitary and plasma beta-EP changes induced by two different types of chronic stress. The stressors were applied twice a day for 10 days. Rats were killed either before, during or after the last swimming or ether stress session. beta-EP was measured by radioimmunoassay in anterior pituitary and in neurointermediate lobe extracts and in plasma. The following observations were made: 1) Chronic intermittent cold-swimming stress increased anterior pituitary contents and plasma beta-EP levels; 2) both chronic intermittent cold-swimming stress and ether stress caused an increase of neurointermediate lobe beta-EP contents; 3) as in control animals, rats exposed to chronic intermittent swimming stress reduced pituitary beta-EP contents and raised plasma beta-EP levels in response to the last acute swimming stress; 4) in contrast to control animals, rats exposed to chronic intermittent ether stress did not show any significant response of the pituitary-plasma opioidergic system to the last acute ether session; 5) the acetyl-l-carnitine treatment counteracted the changes evoked by chronic intermittent cold-swimming stress on the pituitary and plasma beta-EP levels.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acetyl-L-carnitine effect on pituitary and plasma beta-endorphin responsiveness to different chronic intermittent stressors. 848 49


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