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)

Changes in the blood and the behaviour of 14 growing pigs from 4 different litters were evaluated under different experimental conditions of blood sampling, grouping and adrenal stimulation. The results showed that the different techniques of blood sampling influenced lactic dehydrogenase (LDH) and creatine kinase (CK) activities. Cortisol, proteins and CK levels were negatively correlated with social hierarchy after regrouping. Cortisol was also correlated with total activity levels. Adrenal stimulation by adrenocorticotropic hormone (ACTH) administration caused a sharp increase in plasma cortisol levels. However, plasma glucose, plasma proteins and total leukocyte counts were not affected by the ACTH treatment.
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PMID:Effects of blood sampling procedures, grouping and adrenal stimulation on stress responses in the growing pig. 253 97

Aldosterone is a major regulator of fluid and electrolyte balance after hemorrhage and is released from the adrenal cortex by the action of adrenocorticotropin (ACTH) and angiotensin II (AII). Past work has shown that the hemorrhage-induced release of ACTH and cortisol is potentiated by prior hemorrhage. We therefore studied the response of adrenal aldosterone secretion to repeated hemorrhage and its control by ACTH and AII. Six awake dogs with chronic lumboadrenal vein catheters were bled 10% of measured blood volume (H1) with reinfusion at 30 minutes. The hemorrhage was repeated 5 hours later (H2). Adrenal presentation rates for AII (AII-PR) and ACTH (ACTH-PR) were calculated for each sample. Control hormonal and hemodynamic parameters before each hemorrhage were not different; hemodynamic responses to H1 and H2 did not differ. Aldosterone secretion increased significantly after each hemorrhage. The increase in aldosterone secretion after H1 was associated with an early increase in AII-PR and late increase in ACTH-PR. Aldosterone secretion following H2 was greater than that following H1 and was associated with early and larger responses of AII-PR and ACTH-PR. Aldosterone secretion following H1 correlated with the AII-PR (r = 0.75; p less than 0.001), but not with the ACTH-PR. In contrast, aldosterone secretion following H2 correlated with both the AII-PR (r = 0.54; p less than 0.01) and ACTH-PR (r = 0.71; p less than 0.001) and multiple regression analysis showed a highly significant relation with both AII and ACTH (r = 0.81; p less than 0.001). The data suggest that aldosterone secretion after initial small hemorrhage occurs as a result of increased AII, whereas both AII and ACTH may contribute to the larger aldosterone secretory response to H2. Since major trauma commonly involves at least two insults separated in time (e.g., injury followed by surgery), potentiated responses of aldosterone and other pituitary-adrenal hormones (ACTH, vasopressin, and cortisol) may have important implications for the control of fluid and electrolyte balance and metabolism in injured patients.
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PMID:Aldosterone secretion following non-hypotensive hemorrhage is potentiated by prior blood loss. 254 67

Rats bearing kidney grafts of the pituitary pars intermedia were divided into three groups: unstressed, acutely stressed, and chronically stressed. Corresponding sham-operated rats were used for comparisons. Twenty days after grafting, the rats were sacrificed and alpha-melanocyte-stimulating hormone (alpha-MSH), adrenocorticotropin (ACTH), and corticosterone were estimated in plasma. The adrenal/body weight ratio and DNA content of the glands were also investigated. The following results were obtained: MSH was found not to be increased in unstressed rats, but it was in grafted animals subjected to acute and chronic swimming stress. ACTH and corticosterone rose in all three groups. Adrenal/body weight ratio and DNA content increased only in grafted chronically stressed rats. Moreover, plasma corticosterone was found higher in grafted hypophysectomized rats than in non-grafted hypophysectomized animals. Administration of ergocryptine to nonstressed grafted rats induced a decrease in the blood content of ACTH and MSH, indicating that the grafts were the source of a part of the circulating ACTH. On the other hand, the fall in MSH levels could show the effect of the drug upon the pars intermedia. Comparison of the ratios of both hormones released in incubations showed that grafts secreted more ACTH than MSH; on the other hand, when intact neurointermediate lobes were incubated, MSH predominated over ACTH. For the first time it is demonstrated that the pars intermedia can secrete ACTH in vivo. Nevertheless, the ability to secrete this hormone is not a property of normal intact pars intermedia, but it manifests in the transplantations probably due to the overactivity of light cells induced by chronic stoppage of dopaminergic inhibition.
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PMID:Secretion of melanocyte-stimulating hormone and adrenocorticotropin from transplanted pituitary pars intermedia in stressed and nonstressed rats. 254 38

Gonadectomy and gonadectomy plus chronic estradiol administration decrease the content of hypothalamic corticotropin-releasing factor-like immunoreactivity (CRF-ir). This investigation was conducted to determine whether this was a result of chronic inhibition of CRF synthesis or stimulation of release. Administration of the protein synthesis inhibitor anisomycin one hour prior to sacrifice in otherwise untreated controls resulted in a 21% decrease in median eminence CRF-ir (p less than 0.01). Rats were ovariectomized and then administered either estradiol or vehicle daily for 3 weeks. Compared to vehicle-treated controls, estradiol treatment decreased CRF-ir in median eminence (p less than 0.01). In contrast to controls, administration of anisomycin to these ovariectomized rats did not significantly decrease median eminence CRF-ir in either the vehicle or estradiol-treated groups, implying that CRF synthesis was already depressed. Plasma adrenocorticotropin (ACTH) was increased by anisomycin treatment in all groups whether intact, ovariectomized or estradiol-treated (p less than 0.0005). Adrenal weights did not differ between these groups, or in comparison to sham-ovariectomized rats, indirectly implying lack of chronically elevated plasma ACTH. These data suggest that the mechanism for both the ovariectomy and chronic estradiol-induced decrease in CRF-ir content is an inhibition of CRF synthesis as opposed to a stimulation of CRF release.
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PMID:Estradiol or ovariectomy decreases CRF synthesis in hypothalamus. 255 31

Positive emotional activities have been suggested as modifiers of neuroendocrine hormones involved in the classical stress response. To detect changes in these components during a mirthful laughter experience, the authors studied 10 healthy male subjects. Five experimental subjects viewed a 60 minute humor video and five control subjects did not. Serial blood samples were measured for corticotropin (ACTH), cortisol, beta-endorphin, 3,4-dihydrophenylacetic acid (dopac)--the major serum neuronal catabolite of dopamine, epinephrine, norepinephrine, growth hormone, and prolactin. Repeated measures analysis of variance showed that cortisol and dopac in the experimental group decreased more rapidly from baseline than the control group (p = 0.011, p = 0.025, respectively). Epinephrine levels in the experimental group were significantly lower than the control at all time points (p = 0.017). Growth hormone levels in the experimental group significantly increased during baseline (p = 0.027) and then decreased with laughter intervention (p less than 0.0005), whereas, the controls did not change over time (p = 0.787). ACTH, beta-endorphin, prolactin, and norepinephrine levels did not significantly increase. The mirthful laughter experience appears to reduce serum levels of cortisol, dopac, epinephrine, and growth hormone. These biochemical changes have implications for the reversal of the neuroendocrine and classical stress hormone response.
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PMID:Neuroendocrine and stress hormone changes during mirthful laughter. 255 17

Eight healthy young men were studied during three periods of heat exposure in a Finnish sauna bath: at 80 degrees C dry bulb (80 D) and 100 degrees C dry bulb (100 D) temperatures until subjective discomfort, and in 80 degrees C dry heat, becoming humid (80 DH) until subjective exhaustion. Oral temperature increased 1.1 degrees C at 80 D, 1.9 degrees C at 100 D and 3.2 degrees C at 80 DH. Heart rate increased about 60% at 80 D, 90% at 100 D and 130% at 80 DH. Plasma noradrenaline increased about 100% at 80 D, 160% at 100 D and 310% at 80 DH. Adrenaline did not change. Plasma prolactin increased 2-fold at 80 D, 7-fold at 100 D and 10-fold at 80 DH. Blood concentrations of the beta-endorphin immunoreactivity at 100 D, adrenocorticotropic hormone (ACTH) at 100 D and 80 DH, growth hormone at 100 D and testosterone at 80 DH also increased, but cortisol at 80 D and 100 D decreased. The plasma prostaglandin E2 and serum thromboxane B2 levels did not change. Patterns related to heat exposure were observed for heart rate, plasma noradrenaline, ACTH and prolactin in the three study periods.
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PMID:Haemodynamic and hormonal responses to heat exposure in a Finnish sauna bath. 275 81

Post-training treatment alters memory by different mechanisms. Naloxone enhances memory by antagonism of endogenous beta-endorphin-induced state dependency. Epinephrine facilitates consolidation at low doses and generates state dependency at high doses. Exposure to a session of tones causes retroactive interference through a cognitive effect. The present data show that chronic ethanol ingestion, in rats, inhibited the post-training effect of naloxone and of a high dose of epinephrine on the retention of an inhibitory avoidance task but did not inhibit retrograde interference by a session of tones or retrograde facilitation by a low dose of epinephrine. Therefore, ethanol appears to selectively affect post-training influences related to state dependency.
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PMID:Chronic ethanol ingestion selectively affects memory modulation in rats. 280 74

In Zucker obese rats (fa/fa) there are disturbances in the regulation of ACTH and corticosterone. In addition, beta-endorphin concentrations are higher in the pituitary and hypothalamus in obese than in lean rats. Since ACTH and beta-endorphin are thought to be controlled by corticotropin releasing factor (CRF), these effects may be due to abnormalities in CRF regulation. This possibility was investigated by immunizing rats against CRF. Obese rats immunized against CRF developed higher titer antibodies than lean rats. Hypothalamic CRF concentrations were higher in CRF-immunized obese but not lean rats compared with those of control rats, suggesting that compensation for sequestration of peripheral CRF developed in obese rats. In obese, but not lean rats, immunization against CRF decreased weight gains during weeks 1-4 and increased gains during weeks 9-12 and food intakes were decreased during weeks 5-8 compared with those for obese rats immunized against bovine serum albumin (BSA). Adrenal glands weighed 30% less in both obese and lean rats immunized against CRF compared with those immunized against BSA. These responses to immunization against CRF occurred even though plasma, hypothalamic and pituitary concentrations of ACTH and beta-endorphin were unaffected at the end of the study.
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PMID:Weight gain and food intake in corticotropin releasing factor immunized Zucker rats. 282 27

Pyrimethamine, sodium salicylate or ethanol were administered to adrenalectomized rats 3 and 21 days after the operation. It is shown that cytogenetic effect in the operated rats is less pronounced, particularly 3 weeks after the operation. Adrenaline (0.2 mg/kg) increases the effect of chemicals on the chromosome apparatus, while hydrocortisone (50 mg/kg) and corticotropin (10 U/kg) decrease it.
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PMID:[Cytogenetic activity of chemical compounds in adrenalectomized animals]. 282 97

The stimulatory effect of ethanol on the hypothalamo-pituitary-adrenal (HPA) axis was investigated in the long-sleep (LS) and short-sleep (SS) lines of mice. Plasma corticosterone concentrations peaked 30 min after IP administration of ethanol in both lines of mice. Ethanol produced dose-dependent elevations in plasma corticosterone in both LS and SS mice; however, at low doses of ethanol (0.25 to 1 g/kg) the adrenocortical response observed in LS mice was markedly greater than in SS mice. Passive immunoneutralization of circulating corticotropin releasing factor (CRF) completely abolished ethanol-induced elevation in plasma corticosterone in LS mice. CRF or ACTH (adrenocorticotropin) produced dose-dependent elevations in plasma corticosterone in the two lines of mice. Epinephrine co-administered with CRF did not potentiate the adrenocortical response obtained with CRF in either line of mice, and hexamethonium only slightly attenuated ethanol-induced elevations in plasma corticosterone in both lines of mice, suggesting that differentially elevated plasma catecholamines are not responsible for differences in ethanol-induced adrenocortical response. The results suggest that differential adrenocortical response to ethanol exhibited by LS and SS mice is due primarily to differential ethanol-induced CRF release.
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PMID:Ethanol differentially enhances adrenocortical response in LS and SS mice. 285 96


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