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 effect of psychological and psychophysical stress on pentobarbital (PbNa)-induced sleeping time was examined in rats to clarify the influence of psychological stress on arousal. Psychological stress and electric footshock of 5-60 min duration significantly shortened PbNa-induced sleeping time, and the shortening was reversed by intracerebroventricular administration of a corticotropin-releasing hormone (CRH)-receptor antagonist. Electrical footshock and restraint significantly raised plasma adrenocorticotropin (ACTH) and catecholamine levels, whereas psychological stress did not significantly affect the plasma hormones levels. These results suggest that both psychological and psychophysical stress increase arousal through brain CRH. It is also concluded that expression of the central nervous system action of CRH, such as increasing arousal, is not necessarily accompanied by a significant increase in the secretion of ACTH and catecholamine in psychological stress.
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PMID:Psychological stress increases arousal through brain corticotropin-releasing hormone without significant increase in adrenocorticotropin and catecholamine secretion. 840 79

Salivary cortisol and heart rate responses to a) psychological stress (public speaking and mental arithmetic), b) human corticotropin-releasing hormone (hCRH), and c) bicycle ergometry until exhaustion were investigated in 10 smokers and 10 nonsmokers. Compared to d), an injection of physiological saline, psychological stress as well as hCRH resulted in significant elevations of salivary cortisol levels in the total group. Ergometry workload induced only moderately enhanced cortisol concentrations. Profound changes in heart rates were observed following bicycle ergometry [+83 beats per minure (bpm)] and after the psychological stress (+29 bpm). hCRH injection increased heart rate by 5 bpm while heart rates dropped after saline administration (-2 bpm). Smokers showed an attenuated cortisol response to the psychological stressor. Mean cortisol increases reached only one third in smokers compared to nonsmokers. Similarly, cortisol levels in smokers tended to be lower after hCRH injection; however, this difference was not statistically significant. Cortisol responses to ergometry did not differ between the two groups. Likewise, heart rates did not reveal different profiles in any of the three stimulations in smokers compared to nonsmokers.
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PMID:Attenuated cortisol response to psychological stress but not to CRH or ergometry in young habitual smokers. 845 Dec 56

Among the various factors thought to be associated with the reactivation of latent herpesviruses is psychological stress. An increase in levels of 'stress hormones' such as glucocorticoids occurs in individuals who are stressed and previous studies have shown that glucocorticoid hormones can reactivate latent Epstein-Barr virus (EBV) in vitro. In this study, we confirm that the EBV genome in latently infected lymphoblastoid cells can be reactivated with two glucocorticoid hormones, hydrocortisone and dexamethasone. In addition to hydrocortisone and dexamethasone, we also found that other hormones of the hypothalamic-pituitary-axis (corticotropin-releasing factor and adrenocorticotropin hormone but not epinephrine and norepinephrine) as well as somatostatin can enhance the lytic replication of the HR-1 strain of EBV in superinfected cells. These results suggest that multiple endocrine interactions may be involved in stress-induced reactivation/replication of latent EBV.
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PMID:Hormonal modulation of Epstein-Barr virus replication. 854 49

In a previous study, we demonstrated that premenopausal women with visceral obesity have hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis, characterized by an exaggerated hormone response to corticotropin-releasing factor (CRF) and corticotropin (ACTH) stimulation. The hypothalamic peptide flow that stimulates the pituitary, particularly after a physiological stress challenge, involves not only CRF, but also arginine-vasopressin (AVP), which synergizes the CRF capacity to stimulate pituitary hormone secretion. Previous studies in humans have demonstrated that combining AVP with CRF permits maximal stimulation of the pituitary, providing a more appropriate method of assessing pituitary hormone reserve. We therefore investigated the response of the HPA axis to combined CRF and AVP stimuli in obese women with different obesity phenotypes. Moreover, we examined hormonal and cardiovascular responses to several mental stress tasks, according to previously standardized procedures. Two groups of age-matched premenopausal eumenorrheic obese women with visceral (V-BFD) or subcutaneous (S-BFD) body fat distribution and a group of normal-weight healthy controls were investigated. All women randomly underwent the following protocol: (1) a combined CRF/AVP test (100 micrograms plus 0.3 IU intravenously [IV], respectively); (2) a standardized stress test, which consisted of completing two puzzles and a mental arithmetic test; and (3) a control saline test. Blood samples for ACTH and cortisol determinations were obtained before and during each test, and measurements of arterial blood pressure and pulse rate were made at regular intervals during the stress test. After combined CRF/AVP administration, ACTH and cortisol were significantly higher in V-BFD than in the other two groups. In contrast, no significant hormonal variation was found in either group during stress tasks. During the stress test, pulse rate (but not arterial blood pressure) significantly increased after 8 and 15 minutes in the V-BFD group, whereas no significant variation was found in S-BFD and control women. A significant correlation was present between the pulse rate and change in cortisol level during the stress test at minutes 8 (r=.54, P<.05) and 15 (r=.57, p<.01) in all women considered together. Subjective emotional involvement during stressful tasks was measured by a two-dimensional short verbal scale, which revealed that the stress section had a more significant impact in obese V-BFD than in S-BFD and control women. These data therefore confirm that women with visceral obesity have hyperactivity of the HPA axis, and that the combined CRF/AVP stimulation may offer a good tool for investigating pituitary reserve in this obesity phenotype. Moreover, the results indicate that these women probably have a hyperreactive sympathetic response to acute stress that seems interrelated to that of the HPA axis.
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PMID:Hypothalamic-pituitary-adrenal axis activity and its relationship to the autonomic nervous system in women with visceral and subcutaneous obesity: effects of the corticotropin-releasing factor/arginine-vasopressin test and of stress. 860 43

Intracerebroventricular injection of neuropeptide Y (NPY) prolonged sodium pentobarbital (PhNa)-induced sleep in rats. The prolongation of PbNa-induced sleep by NPY was blocked by naloxone. Both corticotropin-releasing hormone and psychological stress caused shortening of PbNa-induced sleep, and the shortening was reversed by NPY. These results suggest that NPY has a sedative action and that an opioid system in the brain mediates at least in part the action of NPY.
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PMID:Neuropeptide Y reverses corticotropin-releasing hormone- and psychological stress-caused shortening of sodium pentobarbital-induced sleep in rats. 883 36

It is unknown whether plasma catecholamines have direct physiologic effects on pituitary-adrenocortical secretion in man. Therefore we investigated the effects of epinephrine and norepinephrine on plasma concentrations of adrenocorticotropin (ACTH), beta-endorphin and cortisol. Nineteen healthy male volunteers received infusions of either NaCl, epinephrine (0.10 micrograms/kg/min) or norepinephrine (0.15 micrograms/kg/min) for 20 minutes. 30 min before to 120 min after the infusion blood was continuously drawn to determine plasma levels of epinephrine, norepinephrine, and cortisol. In addition, ACTH and beta-endorphin plasma concentrations were analyzed at 6 time points before, during and after infusion. Infusion of catecholamines increased epinephrine and norepinephrine concentrations in physiological ranges as observed during intense psychological stress or exhausting physical exercise. However, these increases in catecholamine plasma levels neither affected concentrations of POMC-derived hormones nor plasma levels of cortisol. We conclude that in man, physiologic increases in circulating catecholamines have no influence on pituitary-adrenal hormone concentrations.
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PMID:Epinephrine or norepinephrine fail to influence pituitary-adrenal secretion in man. 892 14

We have studied, on blood samples, the level of immunocompetence (concentration of immune cells, phagocytic process of polymorphonuclear neutrophils, proliferative response of lymphocytes to mitogens), the ascorbic acid content of such immunocompetent cells and the "stress hormone" status (cortisol, ACTH and beta-endorphin) of 10 cyclists, members of the Spanish Indoor Olympic Team and participants in the Olympic Games of Barcelona '92. The study was performed twice during their training for such an event: during the third year of the program (February, 1991) and immediately before the Games (June, 1992). As regards the phagocytic process of neutrophils, we studied the different steps of this process: adherence to endothelium, directed mobility or chemotaxis, ingestion of latex beads and superoxide anion production measured by the nitroblue tetrazolium (NBT) reduction test. We observed a statistically significant increase in chemotaxis and NBT reduction activity just before the Games as compared to the third year of the program, whereas variations were not found in the other parameters. The values of the proliferative capacity of lymphocytes were slightly higher in June '92 than in February '91, but no statistically significant differences were found. The ascorbic acid content decreased strikingly (especially in lymphocytes) immediately before the Games. Regarding the stress hormones and neuropeptides (cortisol, ACTH and beta-endorphin), we observed an increase in serum ACTH and beta-endorphin levels in the last determination (June '92) in comparison to the first one (February '91). These results suggest that, at the end of a long-term training program. no immunosuppression occurs, although an important increase in the concentration of stress hormones (ACTH and beta-endorphin) is found. This is probably caused by the psychological stress associated to the participation in such an important event as the Olympic Games.
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PMID:Effects of a long-term training program of increasing intensity on the immune function of indoor Olympic cyclists. 897 80

When red deer (Cervus elaphus) were hunted by humans with hounds the average distance travelled was at least 19 km. This study of 64 hunted red deer provides the first empirical evidence on their state at the time of death. Blood and muscle samples obtained from hunted deer after death were compared with samples from 50 non-hunted red deer that had been cleanly shot with rifles. The effects on deer of long hunts were (i) depletion of carbohydrate resources for powering muscles, (ii) disruption of muscle tissue, and (iii) elevated secretion of beta-endorphin. High concentrations of cortisol, typically associated with extreme physiological and psychological stress, were found. Damage to red blood cells occurred early in the hunts; possible mechanisms are discussed. Taken together, the evidence suggests that red deer are not well-adapted by their evolutionary or individual history to cope with the level of activity imposed on them when hunted with hounds.
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PMID:Physiological effects of hunting red deer (Cervus elaphus). 944 28

Interstitial cystitis (IC) is a sterile bladder condition occurring primarily in females. It is characterized by frequency, nocturia, and suprapubic pain. IC symptoms are exacerbated during ovulation and under stress, thus implicating neurohormonal processes. The most prevalent theories to explain the pathophysiology of IC appear to be altered bladder lining and increased number of activated bladder mast cells. A defective bladder glycosaminoglycan (GAG) layer could allow penetration of allergic triggers, as well as chemicals, food preservatives, drugs, toxins, and adherent bacteria, all of which can activate bladder mast cells. Vasoactive, nociceptive, and proinflammatory molecules released can lead to immune cell infiltration and can sensitize neurons to secrete neurotransmitters or neuropeptides that can further activate mast cells. Mast cell-derived proteases can directly cause tissue damage, and it is noteworthy that urine tryptase is elevated in IC. Bladder mast cells are located close to neuronal processes, which are increased in IC, and they can be activated in situ by acetylcholine (ACh) and substance P (SP). Such activation is augmented by estradiol, which acquires significance in view of the fact that human bladder mast cells express estrogen receptors, but few progesterone receptors, which may explain the worsening of IC symptoms during ovulation. Finally, acute psychological stress in rats leads to mast cell activation that can be reduced by depletion of SP or neutralization of peripheral immune corticotropin-releasing hormone (CRH). These findings suggest that IC could be a syndrome with neural, immune, and endocrine components, in which activated mast cells play a central role.
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PMID:Interstitial cystitis: a neuroimmunoendocrine disorder. 962 89

Stress worsens certain disorders such as migraines or asthma, and has also been implicated in sudden myocardial arrest. It was previously shown that acute psychological stress by immobilization results in dura mast cell degranulation, an effect blocked by pretreatment with antiserum against corticotropin-releasing hormone (CRH). Moreover, CRH was recently shown to induce skin mast cell degranulation. The effect of psychological stress was investigated on rat cardiac mast cells, because their release of coronary constrictive and proinflammatory molecules contributes to myocardial ischemia and possibly arrhythmias. Immobilization of rats for 30 min induced maximal cardiac mast cell degranulation as evidenced by light and electron microscopy. This effect was inhibited by pretreatment with the "antiallergic" drug sodium cromoglycate (cromolyn), which is thought to act primarily through mast cell stabilization. Mast cell degranulation was also blocked by preincubation with antiserum against CRH and was partially inhibited by a CRH type-1 receptor selective antagonist. Sensory neuropeptides did not appear to influence this effect, but a nonpeptide neurotensin receptor antagonist blocked stress-induced cardiac mast cell degranulation. This finding supports the involvement of neuropeptide neurotensin which is present in the heart and is known to trigger mast cell degranulation. These results indicate acute stress could result in local CRH and nonpeptide neurotensin release which could contribute to myocardial pathophysiology through direct or indirect release of cardiac mast cell mediators.
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PMID:A neurotensin receptor antagonist inhibits acute immobilization stress-induced cardiac mast cell degranulation, a corticotropin-releasing hormone-dependent process. 976 51


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