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)

Systemic administration of yohimbine augments sympathetic outflow and blocks presynaptic alpha 2-adrenergic receptors, releasing the sympathetic neurotransmitter norepinephrine (NE) into the bloodstream. The present study examined sympathoadrenal and hemodynamic responses to yohimbine in 19 patients with essential hypertension and 19 normotensive control subjects. Baseline mean values for arterial NE, epinephrine, dihydroxyphenylglycol (the main intraneuronal metabolite of NE), spillover of NE into arterial plasma, and corticotropin did not differ between the hypertensive and normotensive groups. Yohimbine (0.125 mg/kg i.v. bolus followed by 0.001 mg/kg/min infusion for a total of 15 minutes) increased mean arterial pressure in all but one subject (by 13 +/- 2% [SEM] in the normotensive and 17 +/- 2% in the hypertensive group) and increased arterial NE levels in all subjects (by 253 +/- 50 pg/ml in the normotensive and 312 +/- 51 pg/ml in the hypertensive group). Among hypertensive patients, pressor, cardiac, output, and arterial NE responses were distributed bimodally. Patients with large hemodynamic and NE responses to yohimbine typically reported a history of anxiety, depression, or other psychopathology and of marked pressor or tachycardic episodes during emotional stress. In the hypertensive and normotensive groups, baseline arterial NE concentrations predicted the magnitude of pressor responses to yohimbine (r = 0.59, r = 0.54,p less than 0.01), whereas baseline mean arterial pressure was unrelated to the pressor response. A yohimbine challenge test can identify patients with pressor hyperresponsiveness and can distinguish patients with pressor hyperresponsiveness due to excessive sympathoadrenal reactivity from patients with enhanced postsynaptic responsiveness to endogenous NE.
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PMID:Sympathetic reactivity during a yohimbine challenge test in essential hypertension. 165 75

Hormones of the hypothalamo-pituitary-adrenocortical (HPA-) axis are considered to be of physiological and clinical relevance in regulating spontaneous growth hormone (GH) secretion. To further investigate interdependencies between both systems, we studied the effects of adrenocorticotropin [ACTH(1-24)] and human corticotropin-releasing hormone (h-CRH) upon spontaneous GH secretion in 10 male volunteers. Administration of 1 microgram ACTH (1-24), 10 micrograms h-CRH or saline (control: CTL) every hour from 9.00 to 6.00 p.m. resulted in significant differences of cortisol secretion during the entire observation period (8.00 a.m.-3.00 a.m.) between the three groups (p less than 0.001, Friedman two-way ANOVA). Mean area under the time course curve (AUC) values (+/- SEM) for cortisol expressed as ng x 1,000 x min/ml showed also significant differences between the three treatments from 8.00 a.m. to 3.00 a.m.: CTL 64.0 +/- 6.4, ACTH(1-24) 178.5 +/- 9.4 (p less than 0.01, Wilcoxon test), h-CRH 88.5 +/- 5.6 (p less than 0.01). The main portion of cortisol was released during daytime from 8.00 a.m. to 11.00 p.m., where the most significant differences in the AUC values emerged: CTL 59.6 +/- 5.8, ACTH(1-24) 171.5 +/- 8.8 (p less than 0.01, Wilcoxon test), h-CRH 80.2 +/- 5.1 (p less than 0.01). With regard to GH secretion, significant differences became obvious between the three treatments during daytime from 8.00 a.m. to 11.00 p.m. and the sleep-related period from 11.00 p.m. to 3.00 a.m. (p less than 0.01 and p less than 0.02, Friedman two-way ANOVA).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of human corticotropin-releasing hormone and adrenocorticotropin upon spontaneous growth hormone secretion. 174 61

To determine whether the adrenal androgen 11 beta-hydroxyandrostenedione is a more sensitive and specific marker than dehydroepiandrosterone sulfate, we compared these serum androgens in 81 women with anovulatory hyperandrogenism before treatment, after corticotropin and corticotropin-releasing-factor stimulation, and after short- and long-term dexamethasone suppression. Of all subjects, 65% and 57% had elevated levels of 11 beta-hydroxyandrostenedione (greater than 2.0 ng/ml) and dehydroepiandrosterone sulfate (greater than 2.8 micrograms/ml), respectively. However, 11 beta-hydroxyandrostenedione and dehydroepiandrosterone sulfate levels did not correlate in either the women with hyperandrogenism (r = 0.12) or the 26 normal women (r = 0.29). After 0.25 mg corticotropin was administered intravenously (n = 16), 11 beta-hydroxyandrostenedione increased by 157% +/- 53% (mean +/- SEM), whereas dehydroepiandrosterone sulfate, androstenedione, dehydroepiandrosterone, and cortisol increased by 6% +/- 2%, 46% +/- 10%, 416% +/- 80%, and 2326% +/- 371%, respectively. After intravenous administration of 100 micrograms corticotropin-releasing factor to eight patients, the percent change from baseline level to peak was 148% +/- 26%, 24% +/- 5%, 61% +/- 15%, 117% +/- 15%, and 116% +/- 18% for 11 beta-hydroxyandrostenedione, dehydroepiandrosterone sulfate, androstenedione, dehydroepiandrosterone, and cortisol, respectively. After 2 mg dexamethasone for 3 days (n = 10), 11 beta-hydroxyandrostenedione, dehydroepiandrosterone sulfate, androstenedione, and testosterone were suppressed by 95% +/- 2%, 74% +/- 3%, 51% +/- 9%, and 32% +/- 9%, respectively. Suppression with 0.5 mg dexamethasone for 3 months lowered 11 beta-hydroxyandrostenedione and dehydroepiandrosterone sulfate levels equally by 50% +/- 14% and 62% +/- 12%, respectively. 11 beta-Hydroxyandrostenedione is a useful marker of adrenal androgen secretion with a calculated sensitivity and specificity greater than that of dehydroepiandrosterone sulfate. The greater sensitivity of 11 beta-hydroxyandrostenedione over dehydroepiandrosterone sulfate to adrenal stimulation and suppression suggests its unique diagnostic use.
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PMID:Is 11 beta-hydroxyandrostenedione a better marker of adrenal androgen excess than dehydroepiandrosterone sulfate? 183 6

Plasma corticotropin-releasing hormone immunoreactivity (CRH IR) rises with gestational age in women. In order to investigate the physiological changes of the hormone in pregnant women's urine, CRH IR was measured by radioimmunoassay in urine collected over a 24-hour period, a blood sample and a subsequent single collection of urine after the 24-hour collection (spot urine). Plasma CRH IR in pregnant subjects, 8682.8 +/- 2063.0 pg CRH IR/ml plasma (mean +/- SEM, n = 25), was significantly higher than that in the non-pregnant controls (7.2 +/- 1.6 pg/ml, n = 5; separate t = 4.21, p = 0.0003, d.f. = 24). Similarly, pregnant women had higher spot urine CRH IR - 54.6 +/- 15.5 pg/mumol creatinine (Cr) versus 5.0 +/- 0.5 pg/mumol Cr (separate t = 3.20, p = 0.0038, d.f. = 24.0) - and 24-hour urine CRH IR - 13.7 +/- 1.2 pg/mumol Cr compared with 7.7 +/- 0.8 pg/mumol Cr (separate t = 4.28, p = 0.003, d.f. = 24.4) than the non-pregnant cohort. The difference between urinary excretion of CRH IR as estimated by 24-hour urine (13.7 +/- 1.2 pg/mumol Cr) and spot urine (54.6 +/- 15.5 pg/mumol Cr) indicated that CRH IR in 24-hour urine may be degraded during storage. The weak associations between plasma and 24-hour urine CRH IR of pregnant women (correlation coefficient r = 0.34, p greater than 0.1), and total 24-hour urine and spot urine CRH IR (r = 0.25, p less than 0.1) further indicate CRH degradation. Plasma and spot urinary CRH IR, however, were strongly correlated (r = 0.80, p = 0.001). The total CRH IR excreted as estimated from the spot urine value (0.5 +/- 0.1 micrograms/day) compared with the total filtered load of CRH IR in the pregnant group (1306.9 +/- 324.6 micrograms/day) showed that 99.97% of the filtered CRH IR was reabsorbed or metabolized by the kidneys. Acidic gel chromatography of spot and 24-hour urine samples showed a CRH IR peak at CRH41 standard elution position (Kd = 0.5), indicating that the molecular form in urine is similar to the 41-residue standard. Pregnancy-induced hypertension correlated positively with plasma CRH IR (r = 0.62, p less than 0.001) and spot urine CRH IR (r = 0.46, p less than 0.01), and negatively with parity (r = -0.60, p less than 0.001). Plasma CRH IR and parity also negatively correlated (r = -0.41, p less than 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Urinary corticotropin-releasing hormone immunoreactivity is elevated during human pregnancy. 208 19

The role of a high CRH level in normal pregnancy remains unknown. Therefore we evaluated the concentrations of CRH and the related hormones in patients with pregnancy-induced hypertension. Fourteen women with pregnancy-induced hypertension, aged 20-39, at 30-39 gestational week, were investigated. The control group consisted of 20 healthy pregnant women matched according to gestational age. Plasma CRH beta-endorphin-like immunoreactivity, cortisol, and human placental lactogen were measured by radioimmunoassay, ACTH by an immunoradiometric method. It was found that in hypertensive patients the mean CRH concentration was significantly higher (4257 +/- 840 (SEM) ng/l) than that in healthy pregnant women (1083 +/- 227 ng/l, p less than 0.001). The concentration of ACTH, however, was only slightly higher 65.0 +/- 6.0 vs 50.7 +/- 2.5 ng/l p less than 0.025, whereas the differences in beta-endorphin, cortisol and human placental lactogen were not significant. In both groups there was no correlation between the CRH level and those of the related hormones. In healthy pregnant women the CRH level closely correlated with gestational age (r = 0.76, p less than 0.001), whereas in patients with hypertension no such correlation was present (r = 0.29). We assume that the marked enhancement of plasma CRH in pregnancy-induced hypertension is probably caused by its decreased breakdown in ischemic placental tissue, but its increased synthesis in the placenta and its indirect counterregulatory hypotensive role must also be considered.
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PMID:Enhancement of plasma corticotropin-releasing hormone in pregnancy-induced hypertension. 214 45

The hormonal responses to exercise of 10 asthmatic patients and 12 normal subjects were compared by studying the changes in the plasma levels of growth hormone, prolactin, adrenocorticotropic hormone (ACTH) and cortisol induced by treadmill running. The asthmatic patients demonstrated absence of the plasma cortisol response to exercise (peak increment -15 +/- 21 (SEM) vs 108 +/- 34 nmol.l-1 p less than 0.02). None of these patients were being treated with systemic corticosteroids and there was no difference between the responses of users and non-users of beclomethasone dipropionate. The results suggest the presence of an impaired adrenocortical response to the stress of physical exercise in asthma and indicate the need for detailed evaluation of hypothalamic-pituitary-adrenal function in patients with the disease.
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PMID:The hormonal response to exercise in asthma. 215 17

We evaluated the role of the hypothalamic paraventricular nucleus (PVN) in control of ACTH secretion in fetal sheep. Dexamethasone (DEX, 700 micrograms) (n = 6) or cholesterol (CHOL, 700 micrograms) (n = 5) implants were placed bilaterally 2 mm lateral to PVN of fetal sheep at 108 to 111 days of gestation (dga). After 5 days recovery, fetuses were challenged with: 1) hypotension (50% drop of blood pressure), 2) hypoxemia (fall of greater than 5 mm Hg in fetal PaO2), and 3) corticotropin-releasing hormone (CRH) (10 micrograms iv, single injection to fetus). Hypotension and hypoxemia were repeated after 125 dga. Compared with CHOL, DEX fetuses had lower average concentrations of ACTH in plasma after hypotension [23 +/- 0.5 vs. 149 +/- 83.8 and 31 +/- 13.1 vs. 101 +/- 31.3 pg ml-1 at less than 125 and more than 125 dga, respectively (mean +/- SEM, P less than 0.05)] and during hypoxemia [11 +/- 1.6 vs. 292 +/- 152.8 and 33 +/- 9.4 vs. 304 +/- 91.3 pg ml-1 at less than 125 and more than 125 dga, respectively (P less than 0.05)]. DEX and CHOL responses to CRH at 122 to 127 dga (10 micrograms iv) were not different (38 +/- 23.9 vs. 92 +/- 26.7 pg ml-1, respectively). Immunocytochemistry demonstrated that CRH was decreased in PVN and eliminated from median eminence in DEX, but not in CHOL fetuses. Arginine vasopressin (AVP) immunostaining of PVN of DEX and CHOL fetuses was similar; however, unlike CHOL, DEX fetuses showed no AVP immunostaining of the external zone of median eminence. These results show that, in fetal sheep, high concentrations of glucocorticoid near the fetal PVN prevent increases in plasma ACTH secretion seen in controls in response to hypotension and hypoxemia, and exert at least part of their effect at the level of the CRH- and AVP-producing neurons located in the PVN.
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PMID:Hypothalamic glucocorticoid implants prevent fetal ovine adrenocorticotropin secretion in response to stress. 217 38

The purpose of this study was to investigate the effects of physical training on the responses of serum adrenocorticotropic hormone (ACTH) and cortisol concentration during low-intensity prolonged exercise. Five subjects who had fasted for 12 h cycled at the same absolute intensity that elicited 50% of pre-training maximal oxygen uptake (VO2max), either until exhaustion or for up to 3 h, before and after 7 weeks of vigorous physical training [mean daily energy consumption during training exercise, 531 kcal (2230 kJ)]. In the pretraining test, serum ACTH and cortisol concentrations did not increase during the early part of the exercise. Increases in concentrations of both hormones occurred in all subjects when blood glucose concentration decreased during the later phase of the exercise. The mean values and SEM of serum ACTH and cortisol concentrations at the end of the exercise were 356 ng.l-1, SEM 79 and 438 micrograms.l-1, SEM 36, respectively. After the physical training, VO2max of the subjects improved significantly from the mean value of 50.2 ml.kg-1.min-1, SEM 2.5 to 57.3 ml.kg-1.min-1, SEM 2.0 (P less than 0.05). In the post-training test, exercise time to exhaustion was prolonged in three subjects. Comparing the pre- and post training values observed after the same length of time that the subjects had exercised in the pre-training test, the post-training values of serum ACTH (44 ng.l-1, SEM 3) and cortisol (167 micrograms.l-1, SEM 30) concentration were less than the pre-training value (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of physical training on the responses of serum adrenocorticotropic hormone during prolonged exhausting exercise. 217 89

Cerebrospinal fluid (CSF) samples from 18 female patients with fibromyalgia (fibrositis syndrome) were analyzed for beta-endorphin. The mean CSF level of beta-endorphin was 20.7 +/- 0.7 fmol/ml in the patients compared to 20.5 +/- 2.0 fmol/ml (mean +/- SEM) in healthy controls (p greater than 0.05). Thus, patients with fibromyalgia (fibrositis syndrome) seem to have normal CSF levels of the pain modulatory neuropeptide beta-endorphin.
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PMID:Cerebrospinal fluid levels of beta-endorphin in patients with fibromyalgia (fibrositis syndrome). 246 20

The equilibrium dissociation constants and maximal binding capacities of 3H-dihydromorphine (DHM), 3H-D-Ala2-D-leu3-enkephalin (DADL), and 3H-dynorphin A(1-8) for their respective mu, delta, and kappa opiate binding sites were studied in brain membrane preparations from lean and genetically obese-hyperglycaemic (Aston ob/ob) mice. The concentration of kappa binding sites was 2.7 fold higher in obese compared with lean mouse brain (231 +/- 44.6 versus 83.8 +/- 10.3 fmoles 3H-dynorphin/mg protein respectively, mean +/- SEM). The concentration of delta binding sites in obese was 1.6 fold that in lean mouse brain (94.5 +/- 8.6 versus 59.5 +/- 6.5 fmoles 3H-DADL/mg protein). In contrast, the concentration of brain mu receptors was 40% lower in obese compared with lean mice (20.8 +/- 2.19 and 34.8 +/- 3.1 fmoles 3H-DHM/mg protein respectively). Binding affinities of delta and kappa sites for their respective ligands were not significantly different in lean v. obese mice. However, for mu sites, lean mouse binding data showed two affinities, one was not significantly different from obese (0.35 nM) the second was lower (1.18 nM) for DHM. Increases of approximately 5 fold and 3 fold in the brain content of beta-endorphin and met-enkephalin respectively, and no differences in brain dynorphin levels, were demonstrated in obese mice compared with lean controls. In obese mice, pituitary beta-endorphin content was 9 fold higher, met-enkephalin 4 fold higher and dynorphin 12 fold higher than in lean mice. The striking differences in opioid binding-site characteristics and in endogenous opioid peptide levels in obese compared with lean mice may contribute to the hyperphagia and, directly or indirectly, to the development of hyperglycaemia and hyperinsulinaemia in obese mice.
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PMID:Central mu, delta, and kappa opioid binding sites, and brain and pituitary beta-endorphin and met-enkephalin in genetically obese (ob/ob) and lean mice. 252 15

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