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  • 1
    Electronic Resource
    Electronic Resource
    Metal peptide complexes: preparations and proton and carbon-13 NMR spectra of cobalt(III) tripeptide complexes (1980)
    s.l. : American Chemical Society
    Inorganic chemistry 19 (1980), S. 3496-3502 
    Details
    ISSN: 1520-510X
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1021/ic50213a057
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  • 2
    Electronic Resource
    Electronic Resource
    L-TYPE CALCIUM CHANNELS AND CRH-MEDIATED ACTH AND CORTISOL RELEASE IN HUMANS (1991)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 18 (1991), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The effect of pretreatment with nifedipine on naloxone-stimulated corticotrophin-releasing hormone (CRH)-induced adrenocorticotrophin (ACTH) release in humans was investigated. The mean peak plasma ACTH and cortisol levels and the mean peak change in cortisol levels from basal were significantly lower in the nifedipine/naloxone test than in the naloxone alone test. The integrated areas under the ACTH-time and cortisol-time curves were reduced by 33 and 49%, respectively, in the nifedipine/naloxone test compared with the naloxone alone test. These results correlate well with published in vitro studies.2. Acute administration of oral nifedipine partially inhibited naloxone-stimulated ACTH and cortisol release, probably by blockade of plasma membrane voltage-dependent L-type calcium channels normally activated following binding of CRH to pituitary corticotroph receptors.3. Naloxone-induced CRH release may replace insulin hypoglycaemia testing of pituitary ACTH reserve in humans.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1991.tb01451.x
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  • 3
    Electronic Resource
    Electronic Resource
    EFFECT OF FLUMAZENIL ON BASAL AND NALOXONE-STIMULATED ACTH AND CORTISOL RELEASE IN HUMANS (1994)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 21 (1994), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Endogenous benzodiazepine receptor ligands are thought to influence the human hypo-thalamic-pituitary-adrenal (HPA) axis and naloxone, a known stimulator of adrenocorticotropic hormone (ACTH) release, is thought to act via release of hypothalamic corticotropin-releasing hormone.2. The aim of the present study was to assess the influence of endogenous benzodiazepine-receptor ligands by administering flumazenil (Ro 15–1788), a benzodiazepine antagonist, and measuring ACTH and cortisol release, both basal and during naloxone-stimulation.3. Nine normal volunteers in a placebo-controlled double-blind design were studied. Flumazenil (0.5 mg, i.v. bolus) was given 2 min before naloxone (125 μg/kg bodyweight, i.v. bolus) immunoreactive-adrenocorticotropic hormone (IR-ACTH) and cortisol levels were measured at frequent intervals from 60 min before to 120 min after naloxone injection.4. Flumazenil had no effect on ACTH and cortisol release when given alone; flumazenil area under the ACTH/time curve (pmol/L.min) = -36.5 ± 63.5 compared with placebo = - 53.5± 31.8, flumazenil area under the cortisol/time curve (nmol/L.min x 10−3) = - 2.4 ± 2.4 compared with placebo - 0.56 ± 1.4. Flumazenil did not change the ACTH and cortisol release achieved with naloxone; naloxone area under the ACTH/time curve (pmol/L. min) = 327.8 ± 61.7 compared with flumazenil/naloxone = 366.3 ± 88.1, naloxone area under the cortisol/time curve (nmol/L.minX 10−3) = 12.2 ± 3.4 compared with naloxone/flumazenil = 10.5±2.1.5. The authors conclude that flumazenil does not modify basal or stimulated ACTH and cortisol release in healthy humans. This would suggest that endogenous benzodiazepine-like ligands and the benzodiazepine/gamma-aminobutyric acid receptor complex do not tonically influence the hypothalamic-pituitary-adrenal axis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1994.tb02487.x
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  • 4
    Electronic Resource
    Electronic Resource
    POTENTIATION OF FENFLURAMINE-INDUCED ACTH RELEASE IN MAN BY NALOXONE (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 16 (1989), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. This study set out to compare the effect of the combination of fenfluramine (Fen) and naloxone (Nal) on ACTH and cortisol release with each of these agents alone in six normal volunteers. Three protocols were used: 1.5 mg/kg bodyweight oral Fen; 125 μg/kg bodyweight i.v. Nal; oral Fen plus i.v. Nal 135 min later. Plasma ACTH and cortisol were measured at intervals of 285 min over each test.2. The mean peak levels and mean peak changes from basal in plasma ACTH and cortisol were significantly greater in the combination test (Fen/Nal) than in either the Fen alone or the Nal alone tests. Fen and Nal given together cause a synergistic release of ACTH and cortisol as determined by the areas under the ACTH-time and cortisol-time curves for Fen/Nal compared to the sums of Fen alone plus Nal alone curves for ACTH and cortisol.3. We conclude that Fen and Nal acting synergistically work through different and potentiating mechanisms at the hypothalamic, central nervous system and/or pituitary levels to cause ACTH release.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1989.tb01555.x
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  • 5
    Electronic Resource
    Electronic Resource
    NIFEDIPINE BLOCKS ACTH AND CORTISOL RELEASE IN MAN (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 16 (1989), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The present study investigated the effect of prior administration of nifedipine on AVP-induced ACTH release in seven normal volunteers. Three protocols were used: 20 mg oral nifedipine; 0.14 pressor units intramuscular (i.m.) per kg bodyweight aqueous AVP; oral nifedipine plus i.m. AVP 90 min later. Plasma ACTH and cortisol were measured at intervals for 2.5 h during each test.2. The mean peak plasma ACTH and cortisol levels and the mean peak changes from basal in these levels were significantly lower in the nifedipine/AVP test than in the AVP alone test. The integrated area under the cortisol time curve was significantly lower for the nifedipine/AVP test than that for the AVP test alone. Nifedipine alone caused no changes in ACTH or cortisol.3. Acute administration of oral nifedipine caused an inhibition of AVP-stimulated ACTH and cortisol release in normal humans. This effect may be due to blockade of plasma membrane calcium channels normally activated during AVP stimulation of pituitary corticotrophs.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1989.tb01554.x
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  • 6
    Electronic Resource
    Electronic Resource
    NALOXONE-INDUCED ACTH RELEASE IN MAN IS INHIBITED BY CLONIDINE (1990)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 17 (1990), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Adrenergic mechanisms play an important role in regulation of ACTH release. We used the α2-adrenergic agonist, clonidine, as a central nervous system inhibitor of ACTH release to see if it would alter naloxone-induced ACTH secretion in normal human volunteers.2. There was a significant blunting of the mean peak level of ACTH and the mean peak change of ACTH from basal as well as the area under the ACTH-time curve when clonidine was given prior to naloxone.3. We conclude that clonidine, by blocking central noradrenergic pathways, which stimulate corticotropin-releasing hormone secretion, inhibits naloxone-induced ACTH secretion. This suggests that naloxone causes ACTH release through these same central noradrenergic pathways.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1990.tb01302.x
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  • 7
    Electronic Resource
    Electronic Resource
    PITUITARY-ADRENAL RESPONSES TO COMBINED ORAL D-FENFLURAMINE AND INTRAVENOUS NALOXONE IN HUMANS (1998)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 25 (1998), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Fenfluramine is an optically active 5-hydroxytryptamine (5-HT) releaser and re-uptake inhibitor. Increased brain 5-HT mediates appetite suppression, the d enantiomer being more active than l- or dl-fenfluramine. Fenfluramine also stimulates the hypothalamic-pituitary-adrenal (HPA) axis, leading to suggestions that this could act as a marker for its biological actions. However, the d enantiomer appears less active than a comparable dl racemate dose in animals, while effects of D-fenfluramine on the human HPA axis remain unproven. The aim of the present study was to clarify this.2. Seven healthy human volunteers (three male, four female; 18-58 years) received 30 mg oral D -fenfluramine or placebo, followed by 125 p-g/kg, i.v. naloxone or placebo, in randomized, double-blinded, placebo-controlled afternoon studies. We measured plasma adrenocorticotropic hormone (ACTH) and Cortisol levels in samples taken at intervals throughout the study period.3. In contrast to previous results with dl-fenfluramine, we found no dynamic responses to d -fenfluramine alone and no augmentation of responses to naloxone.4. Central pathways to HPA axis activation are apparently not stimulated by d -fenfluramine at this dose in humans, in contrast with dl-fenfluramine, where the l enantiomer may be more selective for proposed corticotropin-releasing hormone-mediated, post-synaptic 5-HT2 or noradrenergic mechanisms. As previously reported, d-fenfluramine significantly blunted the circadian fall in basal plasma Cortisol, providing in vivo evidence for serotonergic involvement in circadian regulation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1998.tb02263.x
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  • 8
    Electronic Resource
    Electronic Resource
    NALOXONE STIMULATION OF ACTH SECRETION DURING PETROSAL SINUS SAMPLING IN CUSHING'S SYNDROME (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 20 (1993), S. 0 
    Details
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Petrosal sinus sampling has been used to establish the source of adrenocorticotropin (ACTH) in ACTH-dependent Cushing's syndrome. Naloxone, an opioid antagonist, stimulates ACTH secretion, probably via release of endogenous hypothalamic corticotropin releasing hormone (CRH).2. Three patients with hypercortisolism were studied. Two showed suppressed (〉50%) urinary-free cortisol excretion with high-dose dexamethasone treatment (2 mg every 6h for 2 days), one did not suppress. The patients were subjected to bilateral simultaneous inferior petrosal sinus sampling (BSIPSS) with simultaneous peripheral venous (forearm) samples. Basal (unstimulated) samples were taken and naloxone (125 pg/kg bodyweight) was given intravenously with subsequent simultaneous sampling. Plasma ACTH was measured by radio-immunoassay (RIA).3. All cases exhibited a marked rise in immunoreactive (IR)-ACTH levels (pmol/L) after naloxone injection, basal to peak: case 1, left 11.5–22.1, right 9.8 with no rise, peripheral 9.1–9.5; case 2, left 456–863, right 125–501, peripheral 59–82; case 3, left 12.7–13.0, right 277–431, peripheral 12.1–11.7. All results indicate pituitary Cushing's syndrome, with a central to peripheral ratio 〉2.3:1. Pituitary Cushing's syndrome was confirmed on the results of trans-sphenoidal pituitary surgery in cases 1 and 3.4. It is suggested that naloxone injection during petrosal sinus sampling in Cushing's syndrome may assist in the diagnosis of ACTH source, by enhancing ACTH release from a pituitary micro-adenoma.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1681.1993.tb01688.x
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  • 9
    Electronic Resource
    Electronic Resource
    Adrenocorticotropin Hyperresponsiveness in Myotonic Dystrophy Following Oral Fenfluramine Administration (1991)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neuroendocrinology 3 (1991), S. 0 
    Details
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The plasma immunoreactive adrenocorticotropin and cortisol responses to oral fenfluramine hydrochloride (1.5mg/kg body wt) or placebo were examined in 11 patients with myotonic dystrophy, 4 controls with facioscapulohumeral dystrophy, a similarly debilitating muscle wasting disease, and 14 normal controls in single-blind studies performed in mid-afternoon.Mean areas under the adrenocorticotropin response versus time curve were significantly greater in myotonics (2573 + 429 pmol.min/L) than in facioscapulohumeral dystrophy controls (696 + 279 pmol.min/L, P〈0.02) and normals (560±61 pmol.min/L, P〈0.0001). Corresponding cortisol responses were significantly greater in myotonics (35757 + 3949 nmol.min/L) than in normals (21828±1669 nmol.min/L, P 〈 0.001), but not significantly greater than those in facioscapulohumeral dystrophy controls (22830 + 6140 nmol.min/L, P = 0.055). No stressful side-effects which could affect hormone responses, and no significant changes in blood pressure or heart rate were noted.Fenfluramine activates central serotonergic and/or noradrenergic pathways initiating secretion of corticotropin-releasing hormone and possibly arginine vasopressin. We postulate that these fenfluramine-activated pathways are hyperstimulated in myotonics, leading to adrenocorticotropin and cortisol hypersecretion. This may be a manifestation of a general cell membrane defect in myotonic dystrophy. We found a lack of correlation of age (and severity of disease) with adrenocorticotropin response in myotonics, and therefore, the hyperresponse may serve as a useful marker for the disease before development of other overt signs.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2826.1991.tb00241.x
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  • 10
    Electronic Resource
    Electronic Resource
    Effect of Exogenous Arginine Vasopressin on Adrenocorticotropin and Cortisol Release in Myotonie Dystrophy Patients: Delayed Responses of Normal Magnitude (1991)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neuroendocrinology 3 (1991), S. 0 
    Details
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We administered intramuscular arginine vasopressin (AVP) to ten normal controls and eight myotonic dystrophy patients. By measuring plasma AVP levels in five of the myotonics and all the normals, we showed that absorption and distribution of AVP was not delayed or significantly reduced in myotonics. The magnitude of the mean plasma adrenocorticotropin (ACTH) response to AVP in the myotonics was not different from that of normals, although it was significantly delayed (mean peak time, 37.5±4.9 versus 17.0 ± 3.2 min). We propose that this delay was caused by a significantly reduced ACTH secretion rate in myotonics, because the maximum rate of detection of ACTH in plasma is reduced in myotonics (0.6 ± 0.2 versus 1.7 ± 0.5 pmol/L/min), whose corticotropes, while having the same capacity to respond to the AVP stimulus, are slower to attain that capacity. The mean integrated cortisol response (AUC) was significantly smaller for myotonics (8072 ± 2017 versus 13049±1630 nmol.min/L). This may be due to the slower rate of ACTH delivery to the adrenal in myotonics. The timing of the adrenal response does not appear to be impaired in myotonic dystrophy, with the cortisol peak following the ACTH peak by approximately 15 min in both groups. The normal magnitude ACTH response to AVP in myotonics is in contrast to that seen to ACTH secretagogues acting via corticotropin- releasing hormone-initiated pathways, where a rapid hypersecretion is seen. We propose a mechanism of defective calcium transport to account for these observations.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-2826.1991.tb00240.x
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