UNIPROT:P01189 - FACTA Search

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

To characterize the short-term ACTH secretion pattern and to investigate factors regulating it, pituitary venous (PV) blood was collected using our nonsurgical method from 8 unperturbed horses every 20 or 30 s for approximately 1 h. In all but 1 horse, sampling occurred during the broad circadian maximum in plasma cortisol concentrations. Concentrations of corticotropin-releasing hormone (CRH; n = 7 horses), arginine vasopressin (AVP), ACTH and cortisol were measured by radioimmunoassay. In all horses, CRH, AVP and ACTH secretion patterns appeared irregular in time and amplitude. The mean (+/- SEM) numbers of peaks per hour detected by the cluster program were 2.8 +/- 1.2, 10.1 +/- 1.9 and 10.2 +/- 1.4 for CRH, AVP and ACTH, respectively. However, when 2- and 5-min sampling frequencies were simulated by meaning consecutive values, significantly fewer peaks were detected in each hormone. There was no correlation between the prevailing cortisol concentration and peak frequencies of CRH, AVP or ACTH. Secretion patterns of ACTH and AVP were closely related in all horses as assessed by cross correlation analysis and coincidence of peaks, although the ratio between PV ACTH and AVP concentrations fluctuated markedly within each horse. In contrast, the relationship between CRH and ACTH secretion was variable. Bivariate spectral analysis showed only a modest degree of underlying periodicity in CRH, AVP and ACTH secretion during the very short term studied. Nevertheless, distinct peaks exceeding the 95% confidence limits of white noise were observed at periods between 2 and 30 min in 5 of 7 CRH, 6 of 8 AVP and 5 of 8 ACTH spectra. Furthermore, the slope of the regression line through each spectrum did not become indistinguishable from zero, i.e. the flat white noise continuum, until mean (+/- SEM) periods of 2.6 +/- 0.8, 1.6 +/- 0.2, and 2.0 +/- 0.2 min, for CRH, AVP and ACTH spectra, respectively. At the ACTH spectral maximum, the coherence coefficient, which is analogous to the squared correlation coefficient, exceeded 0.5 in comparisons of all ACTH and AVP spectra and of 5 of 7 ACTH and CRH spectra.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Short-term secretion patterns of corticotropin-releasing hormone, arginine vasopressin and ACTH as shown by intensive sampling of pituitary venous blood from horses. 796 80

Previous studies have reported dissociations between plasma cortisol and immunoactive adrenocorticotropic hormone (ACTH) concentrations in both normal controls and in patients with major depression. In order to investigate this issue further, placebo and dexamethasone (DEX) were administered to normal controls and depressed patients at 11 PM, and plasma cortisol and ACTH were measured the following morning at 7 AM. Plasma ACTH concentrations were quantitated by both immunoassay (I-ACTH) and by bioassay (B-ACTH). In 10 normal controls, DEX (0.25, 0.5, and 1.0 mg, PO, elixir) produced a dose-related suppression of cortisol, I-ACTH and B-ACTH, with all three hormones significantly suppressed by DEX (0.5 and 1.0 mg) (p < or = 0.01). In 20 depressed patients, 7 AM plasma ACTH and cortisol concentrations were assessed following a single dose of DEX (0.5 mg). Fifteen patients were classified as suppressors and five as escapers, as reflected by mean (+/- SEM) cortisol concentration of 19.9 +/- 3.0 ng/ml and 81.2 +/- 7.0 ng/ml, respectively. Mean I-ACTH concentrations were comparable in both the escapers (8.6 +/- 1.6 pg/ml) and in the suppressors (7.0 +/- 1.0 pg/ml). In contrast, the mean B-ACTH concentration was more than two-fold higher in the escapers (4.5 +/- 0.5 pg/ml) than in the suppressors (2.2 +/- 0.3 pg/ml) (p < or = 0.001). Eleven of the 20 patients received both placebo and DEX (0.5 mg) on two separate occasions. Although DEX significantly suppressed both cortisol (p < or = 0.0001) and B-ACTH (p < or = 0.01) concentrations, I-ACTH was not significantly reduced.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dissociation between plasma bioactive and immunoactive ACTH concentrations in depressed patients. 801 99

An increase in plasma beta-endorphin concentrations during exercise has been reported in adult men and women by several investigators. However, very little is known about this physiological hormonal response to exercise in children. In this study, we investigated plasma beta-endorphin, ACTH and GH responses to exercise in 40 prepubertal and pubertal children. Subjects were recruited as part of a population of children and adolescents presenting growth retardation and were selected on the basis of the absence of any clinical or biological signs of endocrine or metabolic disease. There were 16 girls and 24 boys with 24 prepubertal and 16 pubertal individuals. A standardised 15 min workload on cycloergometer was used to progressively increase the heart rate of the children up to 90% of the theoretical maximal value. Exercise resulted in a significant increase (p < 0.01) in plasma beta-endorphin (mean +/- SEM) (4.26 +/- 0.47 vs 5.74 +/- 0.56 fmol/ml), ACTH (3.71 +/- 0.41 vs 6.2 +/- 0.62 fmol/ml) and GH (147 +/- 29 vs 364 +/- 67 fmol/ml). The percentage of children with significant hormonal response to exercise was about 75% for each of the 3 hormones but only 3 of the 40 children studied did not show any hormonal response to exercise. Exercise-induced increases in plasma beta-endorphin and ACTH were significantly correlated (p < 0.01). By contrast, there was no significant relationship between GH and beta-endorphin or ACTH values. Furthermore, whereas exercise-induced plasma GH increase was significantly higher in pubertal than in prepubertal children (p < 0.001), corresponding beta-endorphin and ACTH levels were quite similar in the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma beta-endorphin, corticotrophin and growth hormone responses to exercise in pubertal and prepubertal children. 808 74

It has been hypothesized that the corticotropin-releasing hormone (CRH) neurons of the hypothalamic paraventricular nucleus (PVN) become hyperactive with age, and even more so in Alzheimer's disease. This hyperactivity could be due to an increased production of CRH per neuron, or an increased number of PVN neurons producing CRH, or both. As a first step in elucidating which of these biological mechanisms might be operative, we have estimated the absolute number of CRH immunoreactive neurons in the PVN of 10 human control subjects between 36 and 91 years of age and 10 Alzheimer patients between 40 and 97 years of age. CRH neurons were immunocytochemically detected in 6 microns paraffin sections with the aid of a highly specific monoclonal antibody to CRH. The antibody signal was amplified by the biotin-streptavidin and alkaline phosphatase methods. The absolute number of CRH neurons in the PVN was obtained by multiplying the number of CRH neurons in a unit volume (NV) by the total volume of the PVN. Two different methods were used to estimate the NV: an unfolding method and a disector method (about three times more time-consuming). Compared to the disector, the unfolding method consistently yielded a lower cell number for all patients by 38% (+/- 2.8%; mean +/- SEM). However, both methods yielded an increase in the absolute number of CRH neurons in control and Alzheimer patients with age. No statistically significant difference in the absolute number of CRH neurons was found between control and Alzheimer patients with both methods. The age-dependent increase in the absolute number of CRH neurons within the PVN of both control and Alzheimer patients is interpreted as a sign of activation of the CRH neurons with age.
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PMID:Age-related increase in the total number of corticotropin-releasing hormone neurons in the human paraventricular nucleus in controls and Alzheimer's disease: comparison of the disector with an unfolding method. 813 71

Inflammation normally results in enhanced synthesis and secretion of hypothalamic corticotropin-releasing hormone (CRH) which, in turn, exerts antiinflammatory effects by virtue of increased adrenal glucocorticoid production. CRH and CRH binding sites are also expressed in the peripheral nervous and immune systems. Our groups have recently shown that CRH is secreted locally in acute carrageenin-induced inflammation in rats and has predominantly proinflammatory effects. We have also shown that CRH is expressed in the joints of Lewis rats with experimental arthritis. To determine if CRH is present in human inflammatory arthritis, we examined synovial fluids and tissues from patients with rheumatoid arthritis (RA) or osteoarthritis (OA) and normal individuals. We found markedly enhanced expression of immunoreactive CRH in situ in synovium from patients, which was significantly greater in RA than in OA (p < 0.01). CRH concentrations were also significantly higher in RA (140 +/- 33 pg/ml, mean +/- SEM; n = 10) than OA (25 +/- 4 pg/ml; n = 6) synovial fluids (p < 0.005). HPLC showed immunoreactive CRH extracted from RA and OA synovial tissues and fluids coeluted with CRH 1-41. CRH mRNA was present in low levels in synovial tissue from patients with RA and, to a lesser extent, OA. In summary, immunoreactive CRH is locally secreted in the synovium of patients with RA and, at lower levels, OA. These data support the view that CRH functions as an autocrine and/or paracrine mediator of inflammation in humans.
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PMID:Corticotropin-releasing hormone in synovial fluids and tissues of patients with rheumatoid arthritis and osteoarthritis. 833 47

In 6 cats, mean +/- SEM baseline plasma concentrations of cortisol, corticotropin, and alpha-melanocyte-stimulating hormone (alpha-MSH) were 87 +/- 16 nmol/L, 73 +/- 14 ng/L, and 129 +/- 12 ng/L, respectively. The cats were subjected to: handling and subsequent skin testing without anesthesia; anesthesia with 50 mg of ketamine HCl and 2.5 mg of diazepam given IV, immediately followed by handling and skin testing; and anesthesia and handling as previously described, but without skin testing. Significant (P < 0.05; multivariate analysis for repeated measures) increase in plasma cortisol, corticotropin, and alpha-MSH concentrations was observed until 20 minutes after the start of the experiments in cats undergoing physical restraint and subsequent skin testing with or without preceding anesthesia. These responses were largely abolished when anesthesia with ketamine and diazepam was only followed by handling. We conclude that, during stress in cats (in contrast to dogs), the pituitary intermediate lobe is activated to secrete alpha-MSH. In addition, the cortisol response after skin testing of cats under anesthesia may be a reasonable explanation for the reported weak skin test reactivity in cats.
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PMID:Changes in plasma cortisol, corticotropin, and alpha-melanocyte-stimulating hormone concentrations in cats before and after physical restraint and intradermal testing. 838 Dec 60

We studied the responses of plasma epinephrine, norepinephrine, adrenocorticotropic hormone (ACTH), cortisol, and antidiuretic hormone (ADH) during and immediately after sevoflurane-nitrous oxide anaesthesia supplemented with vecuronium in seven elderly patients (mean 76.6 +/- 1.7 SEM) who underwent major intra-abdominal surgery. The plasma concentrations of norepinephrine, ACTH, cortisol, and ADH increased in response to surgical procedures (P < 0.05). The plasma concentration of ADH increased to a peak concentration of 189.1 +/- 20.7 pg.ml-1 30 min after skin incision (P < 0.05). The plasma concentrations of epinephrine, norepinephrine, ACTH, and cortisol increased to peak concentrations of 408.6 +/- 135.5 pg.ml-1, 635.7 +/- 167.8 pg.ml-1, 222.6 +/- 48.0 pg.ml-1, and 113.6 +/- 67.5 micrograms.dl-1, respectively immediately after tracheal extubation (P < 0.05). We conclude that, in the elderly patients, the responses of stress hormones to major intra-abdominal surgery were preserved during sevoflurane-nitrous oxide anaesthesia sufficient to prevent increases in arterial pressure and heart rate. The strongest responses of epinephrine, norepinephrine, ACTH, and cortisol were elicited immediately after tracheal extubation.
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PMID:Stress hormone responses to major intra-abdominal surgery during and immediately after sevoflurane-nitrous oxide anaesthesia in elderly patients. 839 Mar 30

Vasodepressor (vasovagal) syncope, the most common cause of acute loss of consciousness, can occur in otherwise vigorously healthy people during exposure to stimuli decreasing cardiac filling. Antecedent physiological or neuroendocrine conditions for this dramatic syndrome are poorly understood. This study compared neurocirculatory responses to non-hypotensive lower body negative pressure (LBNP) in subjects who subsequently developed vasodepressor reactions during hypotensive LBNP with responses in subjects who did not. In 26 healthy subjects, LBNP at -15 and -40 mmHg was applied to inhibit cardiopulmonary and arterial baroreceptors. All the subjects tolerated 30 min of LBNP at -15 mmHg, but during subsequent LBNP at -40 mmHg 11 subjects had vasodepressor reactions, with sudden hypotension, nausea, and dizziness. In these subjects, arterial plasma adrenaline responses to LBNP both at -15 and at -40 mmHg exceeded those in subjects who did not experience these reactions. In 16 of the 26 subjects, forearm noradrenaline spillover was measured; in the eight subjects with a vasodepressor reaction, mean forearm noradrenaline spillover failed to increase during LBNP at -15 mmHg (delta = -0.06 +/- (SEM) 0.04 pmol min-1 100mL-1), whereas in the eight subjects without a vasodepressor reaction, mean forearm noradrenaline spillover increased significantly (delta = 0.31 +/- 0.13 pmol min-1 100mL-1). Plasma levels of beta-endorphin during LBNP at -15 mmHg increased in some subjects who subsequently had a vasodepressor reaction during LBNP at -40mmHg. The findings suggest that a neuroendocrine pattern including adrenomedullary stimulation, skeletal sympathoinhibition, and release of endogenous opioids can precede vasodepressor syncope.
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PMID:Neurohumoral antecedents of vasodepressor reactions. 855 62

We have examined whether the lack of clinical response to corticosteroids seen in corticosteroid resistant (CR) bronchial asthma is reflected in abnormalities of endogenous cortisol secretion and in the sensitivity of the hypothalamic-pituitary-adrenal (HPA) axis in CR subjects by using a modification of the standard dexamethasone suppression test (DST) in response to 0.25 and 1 mg oral dexamethasone. Five corticosteroid-sensitive (CS) and five CR asthmatic subjects were studied on two occasions 1 mo apart. In the first limb of the study subjects received 0.25 mg of oral dexamethasone, and in the second limb they received 1 mg. Urinary cortisol was measured by fluorimetry after extraction, and plasma cortisol and adrenocorticotropic hormone (ACTH) concentrations were estimated by enzyme-linked immunosorbent assay (ELISA) and immunoradiometric assays, respectively. On Day 1, a 24-h urine sample was collected for estimation of urinary free cortisol. On Day 2, a fasting blood sample was taken at 9:00 A.M. for estimation of plasma cortisol and ACTH. At 11:00 P.M., 0.25 mg (1 mg) of dexamethasone was taken orally by each subject. On Day 3, blood was taken at 9:00 A.M. and 3:00 P.M. for similar estimations. The levels of urinary free cortisol (nmol/24 h) and predose plasma ACTH (ng/L) and cortisol (nmol/L) were 199 +/- 42, 27.4 +/- 5.7, and 300 +/- 48 (mean +/- SEM), respectively, in the CS group, and 210 +/- 74, 23.4 +/- 6.7, and 263 +/- 32 (mean +/- SEM), respectively, in the CR group (p > 0.05 for all comparisons). Plasma ACTH and cortisol concentrations were not significantly suppressed in either group after 0.25 mg dexamethasone, but were equally suppressed in both groups to undetectable levels by 1 mg dexamethasone. We conclude that CR asthma is not reflected in an altered secretory rate of endogenous cortisol or in an altered sensitivity of the HPA axis to dexamethasone suppression.
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PMID:Hypothalamic-pituitary-adrenal axis in corticosteroid-resistant bronchial asthma. 856 97

Arginine vasopressin (AVP) acts synergistically with corticotropin-releasing hormone (CRH) to stimulate ACTH release from the anterior pituitary. In a previous study of bilateral simultaneous inferior petrosal sinus (IPS) sampling in healthy human subjects, we observed lateralized ACTH secretion, suggesting lateralized secretion of an ACTH-regulating hypothalamic factor. To investigate this possibility, we measured ACTH, CRH, AVP, and oxytocin (OT) levels in the IPS and the peripheral circulation in nine normal volunteers, before and after 1 microgram/kg i.v. bolus ovine CRH (oCRH). At baseline, ACTH, AVP, and OT exhibited a significant (P < 0.05) two to threefold intersinus gradient (ISG), indicating the existence of a dominant petrosal sinus. Endogenous CRH was undetectable in all samples. Despite similar exogenous oCRH levels in both petrosal sinuses, oCRH caused a significant increase (P < 0.001) in the ACTH ISG (15.8 +/- 5.6, mean +/- SEM), suggesting increased responsiveness of one dominant side of the anterior pituitary. This was associated with an ipsilateral CRH-induced AVP release and a significant increase (P < 0.01) in the AVP ISG (8.6 +/- 2.3), suggesting lateralized AVP secretion by the hypothalamus. Furthermore, the increased AVP ISG after oCRH correlated strongly with the ACTH ISG (r = 0.92, P < 0.01). oCRH administration did not affect OT. These findings suggest that there is a dominant petrosal sinus in healthy volunteers that appears to reflect a dominant side of the adenohypophysis, characterized by increased functional activity and/or responsiveness of the pituitary corticotrophs. This may reflect lateralized hypothalamic and/or suprahypothalamic function resulting in CRH-responsive lateralized secretion of AVP from parvocellular and/or magnocellular axons in the median eminence and the posterior pituitary. Although the functional and teleologic significance of these findings remains to be investigated, our data suggest a novel mechanism for CRH-mediated ACTH release, namely CRH-induced release of AVP which then enhances CRH action on the corticotrophs. Furthermore, our data represent the first direct evidence for the concept of brain lateralization with respect to neuroendocrine secretion.
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PMID:Inferior petrosal sinus sampling in healthy subjects reveals a unilateral corticotropin-releasing hormone-induced arginine vasopressin release associated with ipsilateral adrenocorticotropin secretion. 862 93

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