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At least 19 recordsLinked to original sources
PubMed2004

Mifepristone: effect on plasma corticotropin-releasing hormone, adrenocorticotropic hormone, and cortisol in term pregnancy.

OBJECTIVE: To compare the effects of in vivo mifepristone with placebo on plasma corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), and cortisol levels concentrations in term human pregnancies. STUDY DESIGN: In all, 24 women participating in a randomized controlled trial of mifepristone for preinduction cervical ripening were enrolled in this ancillary study. Participants with uncomplicated singleton pregnancies beyond 41 weeks gestation and undilated, uneffaced cervices were randomized to either placebo or mifepristone 200 mg orally and observed for 24 hours prior to receiving either intravaginal misoprostol and/or intravenous oxytocin. Blood samples were obtained before medication administration, 3 and 6 hours later, and then every 6 hours until delivery. Plasma hormone levels were measured by radioimmunoassay. RESULTS: Basal levels of CRH, ACTH, and cortisol were similar in the placebo (n=13) and mifepristone groups (n=11). Compared to placebo treatment, exposure to mifepristone resulted in significant elevation of plasma cortisol within 18 hours. Plasma CRH and ACTH were unaffected. Progression of labor was associated with significant increases in cortisol in both groups, while CRH and ACTH levels were not altered. Compared to basal levels within each group, plasma cortisol at delivery was significantly elevated within both the mifepristone (156.8+/-17.7 vs 332.6+/-48.5 ng/ml, p=0.008) and the placebo (166.6+/-34.3 vs 342.4+/-46.4 ng/ml, p=0.003) groups. However, plasma CRH, ACTH, and cortisol levels at delivery did not differ between the groups. CONCLUSION: Mifepristone exposure and induced labor were associated with significant increases in plasma cortisol without alterations of systemic CRH or ACTH levels.

Adrenocorticotropic Hormone↗
PubMed2006

Immunoreactivity of corticotropin-releasing hormone, adrenocorticotropic hormone and alpha-melanocyte-stimulating hormone in alopecia areata.

Psychological factors are believed to play a role in the pathogenesis of alopecia areata (AA), a frequently encountered hair disorder. In our study, statistically significant elevation of psychological stress was felt by AA patients prior hair loss compared with control, which was strongly believed contributory to hair loss (t-test, P < 0.01). The corticotropin-releasing hormone (CRH) and proopiomelanocortin (POMC) mRNA have been identified in the basal layer of the epidermis and pilosebaceous units of the normal scalp. And with the recent discovery of melanocytes and dermal fibroblasts capable of corticosterone production, the presence of a local stress response system resembling the hypothalamic-pituitary-adrenal (HPA) axis has been suggested. The local stress response system is involved in regulation of the normal hair cycle, but its precise role in AA is unknown. The influence of a local HPA axis or rather, CRH-POMC axis in AA was investigated by analysing immunohistochemically the expression levels of CRH and POMC peptides, including the adrenocorticotropic hormone (ACTH) and alpha-melanocyte-stimulating hormone (alpha-MSH), in a number of AA lesions and normal scalp (as control). The epidermis and pilosebaceous units of normal scalp stained weakly with CRH, ACTH and alpha-MSH, whereas those from the affected sites of the AA group showed intense expression of the peptides (chi-square test, P < 0.01). The meaning of this enhanced expression and their role in the pathogenesis of AA should be further evaluated in future.

Adolescent↗
PubMed1993

Induction of grooming in resting rats by intracerebroventricular oxytocin but not by adrenocorticotropic hormone-(1-24) and alpha-melanocyte-stimulating hormone.

Adrenocorticotropic hormone (ACTH) and alpha-melanocyte-stimulating hormone (alpha-MSH) injected i.c.v. induce so called 'excessive grooming'. Whether these peptides play a role in the initiation of grooming is not clear, since rats will groom even as a consequence of a particular environmental stimulation, such as handling and/or a novel environment. In most studies, therefore, the first 15 min after i.c.v. injection are not examined. Here we report on the effects of slow i.c.v. infusions of ACTH-(1-24), alpha-MSH and oxytocin in resting rats in their home cages. Interestingly, i.c.v. infusions of oxytocin did initiate grooming in a dose-related way. In contrast, i.c.v. infusions of both ACTH-(1-24) and alpha-MSH in resting rats were without effect on grooming. Oxytocin is apparently involved in the initiation of self-grooming in rats, whereas ACTH and alpha-MSH prolonged grooming initiated by other means, e.g. handling procedures and/or a novel environment. We conclude that the effects of alpha-MSH and ACTH on grooming are conditional, depending on the behavioural state (active or resting) of the animal.

Animals↗
PubMed1983

Phenotypic variation in testosterone and luteinizing hormone production among boars: differential response to gonadotropin releasing hormone and adrenocorticotropic hormone.

Variation in ability of boars to produce testosterone and luteinizing hormone (LH) in response to both gonadotropin releasing hormone (GnRH) and adrenocorticotropic hormone (ACTH) stimulation, as well as quantitative relationships between pretreatment and posttreatment responses, were assessed in a population of 38 boars of similar age and breeding. Peripheral testosterone concentrations following either GnRH or ACTH increased (P less than 0.01) to peak circulating levels of 7.16 +/- 0.62 and 8.42 +/- 0.81 ng/ml by 120 and 45 min, respectively. Post-GnRH testosterone area varied from 7.44 to 50.84 ng/ml X h (CV = 47.44%) and post-ACTH testosterone area ranged from 3.05 to 28.78 ng/ml X h (CV = 46.09%). GnRH-induced increases in testosterone were preceded by elevations (P less than 0.01) in peripheral LH concentrations but ACTH had no effect upon LH levels. Post-GnRH area varied from 7.07 to 125.45 ng/ml X h (CV = 76.61%). Significant (P less than 0.01) correlations were obtained between pre-GnRH and post-GnRH testosterone areas (r = 0.58) and between pre-ACTH and post-ACTH testosterone areas (r = 0.67). Nonsignificant (P greater than 0.10) correlations were obtained between post-GnRH and post-ACTH testosterone areas (r = 0.006) and between post-GnRH testosterone and LH areas (r = 0.09). The testosterone producing ability of boars was highly variable and their innate ability to produce testosterone influenced their response to GnRH and ACTH. Additionally, the mechanisms by which GnRH and ACTH influence testosterone production in boars appear to differ. Variation in the ability of boars to produce testosterone could not be explained on the basis of differences in circulating levels of LH.

Adrenocorticotropic Hormone↗
PubMed1981

Cortisol and luteinizing hormone after adrenocorticotropic hormone administration to postpartum beef cows.

Cortisol and luteinizing hormone (LH) were measured in serum after the administration of adrenocorticotropic hormone (ACTH) to suckled (S) and nonsuckled (NS) beef cows. Blood was sampled on 2 consecutive days every 2 weeks for four bleeding periods starting 14 days after calving. Cows were injected with 200 IU ACTH or saline in a 2-day switchback design. Serum was collected before ACTH or saline injection and at 30-min intervals thereafter for 8 hours. Average cortisol concentrations in serum were similar in S and NS cows (6.4 +/- .6 and 6.1 +/- .8 ng/ml, respectively) after saline. Average cortisol concentrations in serum collected during an 8-hr period after ACTH on days 14, 28, 42 and 56 postpartum were 24.7 +/- 2.4, 31.8 +/- 3.5, 36.4 +/- 4.2 and 40.7 +/- .5 ng/ml, respectively, for S cows, and 31.1 +/- 2.9, 44.7 +/- 5.2, 45.0 +/- 5.7 and 46.0 +/- 5.4 ng/ml, respectively, for NS cows. Cortisol response to ACTH, measured as area under the response curve, was greater (P less than .05) in NS than in S cows. Amount of cortisol released by 200 IU ACTH was maximal by days 28 to 29 postpartum in NS cows, but the response increased gradually between days 14 to 15 and days 56 to 57 in S cows. overall, LH in serum averaged .55 +/- .08 ng/ml for S cows and .92 +/- .06 ng/ml for NS cows after saline, and .49 +/- .07 ng/ml for S cows and .94 +/- .06 ng/ml for NS cows after ACth. Although mean and peak serum LH concentrations did not differ between cows given ACTH and those given saline, the number of LH peaks and the number of cows having LH after saline. Mean serum LH concentrations were lower (P less than. 05) in S than in NS cows at 28 days postpartum. The number of LH peaks was lower (P less than .05) and the magnitude of the largest LH peak tended to be lower (P less than .06) in S cows at all sampling periods.

Adrenocorticotropic Hormone↗
PubMed1977

Thyrotropin-releasing hormone does not alter the release of melanocyte-stimulating hormone or adrenocorticotropic hormone from the rat pars intermedia.

Thyrotropin-releasing hormone (TRH) has been reported to stimulate the release of melanocyte-stimulating hormone (MSH) from the pars intermedia (PI) of Rana esculenta. To test its effect on the rat PI, acutely dispersed rat PI cells, as well as whole nervosa-intermedias (NI), were incubated with synthetic TRH, from 10(--10)--10(--4)M. TRH did not alter the release of either MSH or adrenocorticotropic hormone (ACTH).

Adrenocorticotropic Hormone↗
PubMed2001

Development of growth hormone and adrenocorticotropic hormone deficiencies in patients with prenatal or perinatal-onset hypothalamic hypopituitarism having invisible or thin pituitary stalk on magnetic resonance imaging.

A gradual loss of anterior pituitary hormones is suspected in patients treated with irradiation due to brain tumors. Development of growth hormone deficiency (GHD) with age has been documented in patients with idiopathic GHD. A gradual loss of adrenocorticotropic hormone (ACTH) secretion has been also shown in a patient with severe GHD and an invisible pituitary stalk on magnetic resonance imaging (MRI). The purpose of this longitudinal and cross-sectional study was to evaluate the gradual loss of growth hormone (GH) and ACTH in a homogeneous group of patients with hypopituitarism. Twenty-eight patients (23 males, 5 females) from four hospitals were diagnosed as having prenatal or perinatal-onset hypothalamic hypopituitarism. They had an abnormal pituitary stalk on MRI (invisible in 18 patients, thin in 10 patients) without any other organic disease of the brain. Each patient had GHD upon initial evaluation. Height (n=20) was analyzed as standard deviation score (SDS). Longitudinal (n=8) and cross-sectional (n=28) GH secretion capacity was evaluated by GH peaks, in response to insulin tolerance test (ITT) and growth hormone releasing factor test (GRF test). Longitudinal (n=10) and cross-sectional (n=28) ACTH secretion capacity was evaluated by cortisol peaks in response to ITT. Height SDS decreased each year in all the untreated patients after birth. GH peaks decreased gradually with age. Longitudinal data showed decreased GH peaks with age in seven out of eight patients using ITT and in all four patients using GRF tests. Cortisol peaks also decreased gradually together with signs and symptoms for adrenal deficiency such as general fatigue. Cortisol peaks of less than 414 nmol/L (15 microg/dl) in response to ITT were seen in 24% of the tests before age 10 and 56% before age 25. In conclusion, GHD and ACTH deficiency developed gradually in patients with prenatal or perinatal-onset hypothalamic hypopituitarism who had invisible or thin pituitary stalks examined by MRI.

Adolescent↗
PubMedDate not supplied

Type I glucocorticoid receptor blockade does not affect baseline or ovine corticotropin-releasing-hormone-stimulated adrenocorticotropic hormone and cortisol secretion.

The type I glucocorticoid receptor antagonist spironolactone was administered to healthy volunteers to determine the effect of type I receptor blockade on adrenocorticotropic hormone (ACTH) and cortisol secretion in humans. On separate days and in a double-blind, randomized fashion, placebo and each of four increasing doses of spironolactone were administered orally to subjects. Doses were selected to be within the clinically used range and, following drug administration, baseline and ovine-corticotropin releasing hormone (oCRH)-stimulated ACTH and cortisol plasma levels were measured. In contrast to the clear effects of type II glucocorticoid receptor blockade on human pituitary adrenal function, no relationship between spironolactone dose or plasma levels and either basal or oCRH-stimulated pituitary-adrenal function was noted at doses comparable to those which induce type I receptor blockade and cardiovascular therapeutic effects in the kidney. These data suggest that, at physiologically relevant doses, type I glucocorticoid receptor blockade does not affect HPA axis function.

Adrenocorticotropic Hormone↗
PubMed1993

Domperidone treatment enhances corticotropin-releasing hormone stimulated adrenocorticotropic hormone release from the dog pituitary.

While dopamine (DA) is known to inhibit pituitary intermediate lobe proopiomelanocortin (POMC) peptide secretion and synthesis in most species, its influence on anterior-lobe (AL) POMC peptide synthesis and secretion is less clear. We, therefore, sought to determine the effects of daily treatment with the DA receptor antagonist, domperidone (DOM), on secretion of the POMC peptides adrenocorticotropic hormone (ACTH) and alpha-melanocyte-stimulating hormone (alpha-MSH) from the dog pituitary, and on concentrations of another pituitary hormone regulated by DA, prolactin (PRL). Dogs treated for 7 days with DOM had significantly higher peak ACTH concentrations in response to corticotropin-releasing hormone (CRH) injection (329 +/- 37 pg/ml, mean +/- SD) than did controls (164 +/- 42 pg/ml). PRL was also significantly (p < 0.05) increased in samples collected on a daily basis after DOM injections (9.5 +/- 4.6 vs. 4.3 +/- 3.3 ng/ml in controls). However, plasma alpha-MSH concentrations were unaffected by DOM. In a subsequent study, dogs were again treated daily with DOM or vehicle (controls), and additionally were given dexamethasone (DEX) to block AL ACTH release. DEX-treated controls showed low daily and CRH-stimulated ACTH and cortisol concentrations (generally below assay sensitivity). In contrast, DEX + DOM-treated dogs had daily mean ACTH concentrations ranging from 10 +/- 8.1 to 32 +/- 26 pg/ml and mean peak post-CRH ACTH concentrations of 174 +/- 16 pg/ml. Although daily cortisol concentrations were below assay sensitivity, the mean peak post-CRH cortisol concentration was 6.7 +/- 1.8 micrograms/dl, indicating that the immunoreactive ACTH was biologically active.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed2002

Inhibition of tumor necrosis factor-alpha stimulated NFkappaB/p65 in human keratinocytes by alpha-melanocyte stimulating hormone and adrenocorticotropic hormone peptides.

Alpha-melanocyte stimulating hormone (alpha-MSH) has pigmentary, anti-inflammatory, antipyretic, and general immunomodulatory roles. It can oppose several cytokines including tumor necrosis factor-alpha in a number of tissues, including skin. We have previously shown that alpha-MSH can inhibit tumor necrosis factor-alpha stimulated intercellular adhesion molecule 1 upregulation and nuclear factor kappaB (NFkappaB) transcription factor activation in melanocyte and melanoma cells. It is thought, however, that this MSH biology may also extend to other cells of the skin and in this study we extend our work to keratinocytes. We have investigated in detail the ability of three alpha-MSH peptides to inhibit tumor necrosis factor alpha stimulated NFkappaB activation in nonpigmentary HaCaT keratinocytes (alpha-MSH, L-Lys-L-Pro-L-Val, and L-Lys-L-Pro-D-Val) and two adrenocorticotropic hormone (ACTH) peptides (1-17 and 1-39), reported to be present in skin tissue. NFkappaB/p65 activation was analyzed by electrophoretic mobility shift assay and immunofluorescent microscopy. alpha-MSH, L-Lys-L-Pro-L-Val, and L-Lys-L-Pro-D-Val all significantly inhibited tumor necrosis factor alpha stimulated NFkappaB activation, whereas ACTH 1-17 and 1-39 did not, in the HaCaT keratinocytes. MSH peptides and ACTH 1-39 were effective, however, at inhibiting NFkappaB activation in normal human keratinocytes. Immunolabeling of inhibitor kappaBalpha of NFkappaB (IkappaBalpha) revealed an abnormal localization to the nucleus of HaCaT cells, which was unaffected by MSH/ACTH peptides. In contrast, normal human keratinocytes showed a normal IkappaBalpha distribution that responded to MSH/ACTH with nuclear translocation. Our data support previous work on the role of MSH/ACTH peptides as immunomodulatory/anti-inflammatory regulators, and extend this work to keratinocytes identifying a novel IkappaBalpha mechanism and extends findings to ACTH peptides, identifying an abnormal IkappaBalpha mechanism in the immortal HaCaT versus normal keratinocyte.

Adrenocorticotropic Hormone↗