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PubMed2005

Evaluation of serum 17-hydroxyprogesterone concentration after administration of ACTH in dogs with hyperadrenocorticism.

OBJECTIVE: To evaluate serum 17-hydroxyprogesterone (17-OHP) concentration measurement after administration of ACTH for use in the diagnosis of hyperadrenocorticism in dogs. DESIGN: Prospective study. ANIMALS: 110 dogs. PROCEDURE: Serum 17-OHP concentrations were measured before and after ACTH stimulation in 53 healthy dogs to establish reference values for this study. Affected dogs had pituitary-dependent (n = 40) or adrenal tumor-associated (12) hyperadrenocorticism or potentially had atypical hyperadrenocorticism (5; diagnosis confirmed in 1 dog). In affected dogs, frequency interval and borderline and abnormal serum 17-OHP concentrations after ACTH stimulation were determined. Serum cortisol concentrations were assessed via low-dose dexamethasone suppression and ACTH stimulation tests. RESULTS: In healthy dogs, serum 17-OHP concentration frequency intervals were grouped by sex and reproductive status (defined as < 95th percentile). Frequency intervals of serum 17-OHP concentrations after ACTH stimulation were < 77, < 2.0, < 3.2, and < 3.4 ng/mL (< 23.3, < 6.1, < 9.7, and < 10.3 nmol/L) for sexually intact and neutered females and sexually intact and neutered males, respectively. In 53 dogs with confirmed hyperadrenocorticism, serum cortisol concentrations after ACTH stimulation and 8 hours after administration of dexamethasone and serum 17-OHP concentrations after ACTH stimulation were considered borderline or abnormal in 79%, 93%, and 69% of dogs, respectively. Two of 5 dogs considered to have atypical hyperadrenocorticism had abnormal serum 17-OHP concentrations after ACTH stimulation. CONCLUSIONS AND CLINICAL RELEVANCE: Serum 17-OHP concentration measurement after ACTH stimulation may be useful in the diagnosis of hyperadrenocorticism in dogs when other test results are equivocal.

17-alpha-Hydroxyprogesterone↗

PubMedDate not supplied

Phosphotyrosine protein phosphatases activation by ACTH in rat adrenal gland.

The steady state level of most cellular phosphoproteins is dependent on the relative catalytic activities of intracellular protein kinases and phosphatases. In adrenal cortex, ACTH acts through PKA activation and Ser/Tre phosphorylation. Phosphatases involved in this pathway are not completely described, particularly the role of phosphotyrosine protein phosphatase (PTP) activity on ACTH action. We investigated potential changes in PTPs activity in adrenal gland upon in vivo and in vitro PKA activation. In vivo ACTH stimulates cytosolic PTP activity (2-fold). Similar effect is detected by in vitro stimulation. In accordance with the effects of ACTH on PTP activity, cell permeable PTP inhibitors block ACTH stimulation on adrenal zona fasciculata (ZF) cells: ACTH (1 nM) = 108.2 +/- 3.5 ng corticosterone/10(5) cells vs. ACTH + phenylarsine oxide (2 nM) = 60 +/- 4 (P < 0.001) and ACTH + pervanadate (10 mM) = 68 +/- 2 (P < 0.01). These results are reproduced when cells are stimulated with cAMP. The inhibition is not observed when steroidogenesis is supported by 22(R)OH cholesterol. We describe, for the first time, a hormonal regulation of PTP activity. According to the effect of PTP inhibitors on steroid production activated by ACTH we propose that PTP activation is a crucial event in hormone action in the steroidogenic pathway. We also propose that PTP activity is located after PKA activation and prior to cholesterol transport to the inner mitochondrial membrane.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1993

Reactivity and intracellular location of the ACTH cell autoantigen in human fetal and adult anterior pituitary tissue.

Autoantibodies to anterior pituitary ACTH cells have been described in the sera from patients with Cushing's disease. We were here able to show that true ACTH cell autoantibodies do not react with the hormone itself or with Fc receptors in ACTH cells. They rather recognize a distinct pituitary cell-specific cytoplasmatic autoantigen located in a juxtanuclear position. ACTH cells from human adult pituitaries express Fc receptors producing a non-specific broad and diffuse cytoplasmic binding of normal immunoglobulins. After preparation of Fc-free F(ab)2 fractions from human immunoglobulins it could be demonstrated by immunohistochemical methods that human adult pituitary ACTH cells also contain the fetal ACTH cell autoantigen. However, Fc receptors, ACTH hormone or other proopiomelanocortin- (POMC-) derived fragments and the ACTH cell autoantigen are all located at distinct intracellular sites. ACTH cells in human fetal pituitaries were shown to lack Fc receptors. Thus, with this source of antigen the characteristic autoantibody pattern can be detected with undigested sera.

Adrenocorticotropic Hormone↗

PubMed1998

Adrenal androgenic response to 2-hour ACTH stimulation test in women with PCOS.

Adrenal function may be abnormal in women with polycystic ovary syndrome (PCOS). This study aims to evaluate adrenal steroid response to the adrenocorticotropic hormone (ACTH) stimulation test and to find out the effect of high serum testosterone levels on adrenal response. We have also investigated any subtle enzyme deficiency by extending blood sampling to 2 h with 30 min intervals following ACTH administration. Twenty-eight women with PCOS and 18 healthy controls without hirsutism and oligomenorrhea were included in the study. After determining their serum basal levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, dehydroepiandrosterone sulfate (DHEAS), 17-hydroxyprogesterone (17-OHP), and progesterone, ACTH stimulation test was performed. The change in serum 17-OHP and the summed rate of change in serum 17-OHP and progesterone levels were estimated and 95th percentile for each value was computed. Women with PCOS were heavier and more hirsute than controls (p < 0.01, p < 0.001, respectively). Serum basal LH, LH:FSH ratio, testosterone (p < 0.001, for all), DHEAS (p < 0.01), and 17-OHP (p < 0.05) were higher in women with PCOS. All of the 17-OHP measurements, including basal and each 30 min interval after the administration of ACTH, were higher in women with PCOS than those of healthy controls (p < 0.05, p < 0.002, p < 0.001, p < 0.015, p < 0.018, respectively). However, the incremental changes in serum 17-OHP30-0, 17-OHP60-0, 17-OHP90-0, 17-OHP120-0, and the summed rate of change in serum 17-OHP and progesterone in women with PCOS were not different from those in healthy controls. The incremental response in terms of serum progesterone, DHEAS, and testosterone levels to the ACTH stimulation test for each 30 min interval was not different in women with PCOS than in healthy controls. We were not able to show any critical value for serum basal testosterone and DHEAS levels that would effect response to ACTH stimulation in terms of 17-OHP levels. We have concluded that extending the duration of blood sampling up to 2 h has no advantage in evaluating adrenal steroid response to ACTH stimulation. Since serum 17-OHP levels remain within normal limits in response to ACTH stimulation, the origin of elevated serum basal 17-OHP levels may be polycystic ovaries. Elevated serum testosterone level does not have any adverse effect on adrenal function. Serum progesterone measurement seems to have no place in the diagnosis of 21-hydroxylase deficiency. Adrenal androgenic response to ACTH stimulation is normal in women with PCOS.

17-alpha-Hydroxyprogesterone↗

PubMed1998

Effect of L-NAME, a specific nitric oxide synthase inhibitor, on corticotropin-releasing hormone-elicited ACTH and corticosterone secretion.

This study was designed to determine the role of endogenous nitric oxide (NO) in the corticotropin-releasing hormone (CRH)-induced ACTH and corticosterone secretion, as well as possible involvement of hypothalamic dopamine and noradrenaline in that secretion in conscious rats. CRH given i.p. stimulated dose-dependently the pituitary-adrenocortical activity measured 1 h later. Dexamethasone (0.2 mg/kg i.p.) injected 1 h before CRH (1 microg/kg i.p.) totally abolished the CRH-elicited ACTH and corticosterone secretion, indicating a predominantly pituitary site of CRH-evoked stimulation. L-arginine (120 mg/kg i.p.) and N(omega)-nitro-L-arginine methyl ester (L-NAME 5-10 mg/kg i.p.) did not markedly affect the basal plasma ACTH and corticosterone levels. L-NAME given 15 min before CRH markedly, but not significantly, augmented the CRH-induced ACTH response, and enhanced more potently and significantly the corticosterone response. Pretreatment with L-arginine, a substrate for NOS, slightly diminished the CRH-induced ACTH response and considerably reduced the corticosterone response. L-arginine also significantly reversed the L-NAME-evoked increase in the CRH-induced ACTH and corticosterone secretion. L-NAME did not markedly alter the CRH-induced hypothalamic dopamine and noradrenaline levels, while L-arginine significantly increased noradrenaline level. However, those alterations were not directly correlated with the observed changes in ACTH and corticosterone secretion. These results indicate that in conscious rats NO plays a marked inhibitory role in the CRH-induced ACTH secretion and inhibits more potently corticosterone secretion. Hypothalamic dopamine and noradrenaline do not seem to be directly involved in the observed alterations in ACTH and corticosterone secretion.

Adrenocorticotropic Hormone↗

PubMedDate not supplied

Evaluation of low dose ACTH stimulation test in suspected secondary adrenocortical insufficiency.

BACKGROUND: Several studies in the last few years have shown that the standard 250 micro g dose used in ACTH stimulation test may be very high and have suggested that a dose of 1 micro g may be sufficient for evaluating hypothalamo-pituitary adrenal (HPA) axis. AIMS: To evaluate the role of low dose ACTH stimulation test in patients with suspected Secondary Adrenal Insufficiency (SAI). SUBJECTS AND METHODS: Thirty-one patients of suspected SAI with a documented pituitary lesion and seven normal healthy controls were included in the study. All the subjects underwent ACTH stimulation test with standard high dose (HD= 250 microg) and low dose (LD= 1 microg) ACTH. Insulin Induced Hypoglycaemia (IIH) test was done in 7 out of 9 patients in whom the results of the two tests were discordant. The cut off for normal HD stimulation test was taken as peak cortisol response > 18 microg/dl and for LD test, either a cortisol response of > 18 microg/dl or an increment of more than 7 micro g/dl over the basal value at any time during the test, on the basis of response observed in controls. RESULTS: 22/31 patients (74%) in SAI group showed concordant results with both tests, whereas nine patients had discordant results. These nine patients showed AI with LD ACTH, but HD ACTH test showed a normal response. In 7 of these 9 patients who underwent IIH, AI was confirmed in 6. CONCLUSION: The LD ACTH stimulation test seems to be better than HD ACTH stimulation test for evaluating HPA axis in patients with suspected SAI. When basal cortisol is normal, LD ACTH stimulation test detects subtle SAI.

Adrenal Cortex Function Tests↗

PubMed2005

ACTH responses to somatostatin, valproic acid and dexamethasone in Nelson's syndrome.

OBJECTIVE: Pituitary tumours occurring in patients bilaterally adrenalectomized because of Cushing's disease (Nelson's syndrome) are frequently invasive and a complete their resection is not possible in most of them. Administration of the drugs decreasing ACTH secretion could be helpful in such unresectable tumours. We tried to evaluate the influence of somatostatin and valproic acid, compared to dexamethasone, in short-term studies, on plasma ACTH levels in Nelson's syndrome (NS). MATERIAL AND METHODS: Basal ACTH levels were determined within 18 h after last dose of hydrocortisone and next, 1 and 2 hours following oral administration of 20 mg of hydrocortisone. Somatostatin was injected s.c. in two patients with NS while sodium valproate and dexamethasone were administered orally for three days in three patients with NS (two with an invasive pituitary tumour and one with a localized, intrasellar adenoma). The blood for ACTH and cortisol determination was drawn before the tests (two hours after 20 mg of hydrocortisone ingestion) as well as 1 and 2 hours following somatostatin injection and after 3 days of valproic acid or dexamethasone administration. RESULTS: High plasma ACTH levels were found before the tests. Somatostatin lowered ACTH levels in both patients, more effectively in the patient with non-invasive pituitary adenoma. Valproic acid decreased moderately ACTH concentration in two patients, while following dexamethasone administration a fall in ACTH levels was observed in all three patients, the most evident in the patient with a non-invasive Nelson's adenoma. CONCLUSION: Somatostatin seemed to be more effective in its inhibitory action on ACTH secretion than valproic acid, thus its administration in invasive cases of NS could be tried as a supplementary method to neurosurgery. The response to dexamethasone administration indicates that a feed-back regulation, although impaired, exists in these cases.

Adrenocorticotropic Hormone↗

PubMed1989

[ACTH receptors].

Corticotropin (ACTH) has two main actions in mammalian adrenal cortex: acute stimulation of glucocorticoids secretion and trophic effect which allow the expression of genes encoding for the steroidogenic enzymes. The ACTH membrane bound receptor was one of the first to be demonstrated by direct binding of labeled hormone to subcellular preparations of the adrenal cortex. However, detection and characterization of physiological relevance to ACTH receptors has been difficult, because of the low biological activity of the labeled ACTH. Introduction of a bulky iodine atom into Tyr2 and the oxidation of Met4 appear to contribute most to the loss of activity. These difficulties were overcome recently by using an [125I]-ACTH labeled only in Tyr23, which retains full biological activity. Using this labeled hormone, physiologically relevant ACTH receptors, with high affinity (KD congruent to 10-10M) and low capacity (congruent to 2000 sites/cell) have been characterized in several mammals. A second site of low affinity (KD congruent to 10(-7M) and high capacity, has been found in some studies but the significance of this second site is unknown since it cannot be related to any physiological response of adrenal cells to ACTH. In contrast with the loss of receptors and desensitization of target cells caused by most polypeptide hormones, ACTH seems to regulate positively its own receptors and the cAMP response. The molecular weight of the ACTH receptor appears to be between 83 and 100 KD.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗

PubMed1989

[Blood levels of ACTH and endogenous digitalis-like substances in in man].

Simultaneous determination of immunoreactive ACTH and immunoreactive digitalis like substances (DLS) in 71 plasma specimens of 44 persons proved that in spite of a great range of ACTH concentrations in the followed individuals (1.7-271 nmol/l) there is not a major correlation between DLS and ACTH or a significant difference in plasma DLS concentrations in the groups of persons with suppressed, normal or increased ACTH concentrations. Acute increase of ACTH plasma concentrations after synthetic ACTH application or a suppression of plasma ACTH by dexamethasone were not accompanied by corresponding changes of immunoreactive DLS. Thus it follows from this investigation that in spite of its biological digitalis like activity and interference of synthetic ACTH 1-24 high concentrations with digoxin enzymoimmunoassay in vitro, ACTH in concentrations found in human plasma is not responsible for endogenous immunoreactive DLS levels in plasma.

Adrenocorticotropic Hormone↗

PubMed1989

Thymopentin induces release of ACTH-like immunoreactivity by human lymphocytes.

Peripheral mononuclear (PMN) cells are known to produce ACTH-like immunoreactivity (ACTH-LIR) in vitro. Based on these findings the aim of this study was to find out whether thymopentin (the active pentapeptide of the native hormone thymopoietin) may stimulate ACTH-LIR production and release by cultured normal human lymphocytes. Thymopentin at concentration of 1 microgram/ml was capable of inducing ACTH-LIR release by normal human PMN cells (median 22 pg/ml) whereas ACTH-LIR inside cells was lower (median 11 pg/10(7) cells). The chromatographic characterization of the eluted material identified the presence of ACTH immunoreactive peptides with the elution characteristics of the precursors 31 K proopiomelanocortin, 22 K ACTH and 4.5 K ACTH, together with higher molecular weight material (greater than 43 K). These data demonstrate that thymopentin induces ACTH-LIR release by human lymphocytes, thus adding a novel factor to those already reported (corticotrophin releasing factor, lipopolysaccharide, viruses) capable of such function.

Adrenocorticotropic Hormone↗

PubMed1989

[Levels of ACTH and endogenous-digitalis-like substances in human blood].

Adrenocorticotropic Hormone↗

PubMed1989

[Changes in anterior pituitary function during ACTH therapy of patients with infantile spasms].

Serum cortisol, prolactin (PRL), TSH, GH, LH and FSH levels were measured before and immediately after daily ACTH-Z therapy (0.01 mg/kg/day, 1-2 weeks) for 5 patients with infantile spasms and one patient with myoclonus epilepsy. Total number of ACTH-Z therapy were 8 times, and all patients became seizure free after ACTH-Z therapy. In 6 occasions, TRH, LH-RH and insulin tolerance tests were performed before and after daily ACTH-Z therapy. Serum cortisol levels were significantly increased after daily ACTH-Z therapy but all other hormone levels were significantly decreased. In TRH and LH-RH tolerance tests, peak levels and increments of PRL, LH and FSH were significantly decreased after daily ACTH-Z therapy and those of TSH were mildly decreased. In one case insulin tolerance test revealed an adequate decrease of blood glucose before and after ACTH-Z therapy, and there was a poor GH response after ACTH-Z therapy. Daily ACTH-Z therapy was thought to suppress secretion of anterior pituitary hormones.

Child, Preschool↗

PubMed1987

Corticotropin-releasing hormone: stimulation of ACTH secretion in normal man.

Synthetic ovine corticotropin-releasing hormone (oCRH) is a potent and specific ACTH secretagogue in man. Threshold and maximal i.v. doses are 0.01-0.03 and 3-10 micrograms/kg or less, but increase in frequency, severity, and duration at higher doses. oCRH produces a biphasic plasma immunoreactive (IR)-ACTH response and has a prolonged duration of action that is probably due to its long circulating half-life. Other pro-opiomelanocortin IR-peptide are secreted concomitantly in equimolar amounts. Plasma IR-cortisol concentration tends to follow that of ACTH, but also reflects cortisol's longer circulating half-life and the fact that acutely the maximally-stimulating plasma IR-ACTH level is about 45 pg/ml. oCRH is as effective given s.c. as i.v., but intranasal administration is only 1% as effective. Sex and age have no effect on the plasma IR-ACTH and IR-cortisol responses to oCRH. The time of day of oCRH administration has little influence on the plasma IR-ACTH response, but the plasma IR-cortisol response is much greater to oCRH given later in the day than early in the morning. Plasma IR-ACTH response to oCRH is more dependent on the basal plasma IR-cortisol level than the time of day. Arginine vasopressin given at the same time as oCRH potentiates 4-fold the plasma IR-ACTH response to oCRH alone, almost to levels obtained with insulin-induced hypoglycemia. However, oCRH administered at the onset of insulin-induced hypoglycemia does not cause higher plasma IR-ACTH levels, indicating that endogenous CRH levels are maximally-stimulating during the hypoglycemic response.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗

PubMed1988

Consistent capacity for adrenocortical response to ACTH administration in pigs.

The effect of ACTH administration on plasma cortisol concentrations in purebred and crossbred pigs was investigated. Pigs were given either 25 IU of ACTH or physiologic saline solution IM. Blood samples were collected immediately before and 1 hour after ACTH or saline solution administration. Administration of ACTH resulted in a significant (P less than 0.01) increase in plasma cortisol concentration compared with that resulting from administration of saline solution; mean values after ACTH administration were similar in both breed groups. In contrast, a fivefold range of differences was observed among individual pigs of the same age, sex, and body weight, irrespective of breed group. The type and magnitude of the adrenocortical response was consistent and repeatable in pigs over a 3-month period, suggesting that pigs have a consistent capacity for adrenocortical response to ACTH administration. Development of a dynamic test allowed the high and low responding extremes in a population to be detected. The most suitable dose of synthetic ACTH was established to be 50 IU, and the best time for blood sample collection was 60 minutes after ACTH administration. The classification of individual pigs as high or low responders was repeatable and was not affected by prior short-term exposure to ACTH.

Adrenocorticotropic Hormone↗

PubMed1984

Adrenal function in the cat: comparison of the effects of cosyntropin (synthetic ACTH) and corticotropin gel stimulation.

The serum cortisol responses of 10 normal cats to natural adrenocorticotrophic hormone (ACTH) gel and synthetic ACTH (cosyntropin) were evaluated and compared. Following administration of either ACTH gel or cosyntropin, mean serum cortisol concentrations increased significantly (P less than 0.05) within 30 minutes and reached a maximal response (2.5 to 10 times basal values) at 90 minutes. The time to reach peak serum cortisol concentrations was variable, however, and occurred sooner after cosyntropin (30 to 60 minutes) than after ACTH gel administration (90 to 180 minutes). While ACTH gel tended to produce a prolonged cortisol response, the effects of cosyntropin were more transient, with serum cortisol concentrations returning to normal range within three hours after injection. Results of this study indicate that the administration of either ACTH gel or cosyntropin consistently produces an adequate adrenocortical response in the cat. Based on the time response studies, post ACTH cortisol samples should be collected 60 to 90 minutes after cosyntropin or 90 to 120 minutes after ACTH gel injection to ensure detection of peak adrenocortical response with either ACTH preparation.

Adrenal Cortex↗

PubMed1980

Influences of heparin on ACTH distribution and immunoreactivity in plasma of the rat. In vivo and in vitro studies.

1. Blood samples from non-pregnant female rats were incubated in vitro with porcine 125I-ACTH, and the corresponding plasmas were chromatographed on fine Sephadex G 50. When heparin was added in vivo or in vitro, almost all the radioactivity appeared in the void volume of the columns; the same was observed when labelled ACTH was added to heparin-containing saline. In contrast, when NaCl instead of heparin was added to the blood in vivo as well as in vitro, almost all the plasma radioactivity was eluted later, with 125I-ACTH. 2. When labelled ACTH was i.v. administered to pregnant females, it was eluted in the void volume in the presence of heparin, and further down in its absence. 3. The same plasma samples from non-stressed or ether-stressed females were radioimmunoassayed for ACTH, with and without heparin. The degradation of ACTH was greater in the presence of heparin, and plasma ACTH concentration was understimated for low blood levels of heparin (5 UI/ml or less) and in contrast overestimated for high ones (25 or 50 UI/ml). 4. In conclusion, the reported data clearly demonstrated firstly that heparin added to rat blood traps ACTH molecules, promoting the formation of aggregates with apparent height molecular weight; secondly that heparin interferes with the direct radioimmunoassay of ACTH in the plasma.

Adrenocorticotropic Hormone↗

PubMed1982

[ACTH in the dexamethasone suppression test].

Despite the great clinical importance of the low-dose dexamethasone suppression test (determination of cortisol after dexamethasone 2 mg p.o. at 11.00 p.m. in the evening before) and of the determination of ACTH in plasma, so far only little is known about the ACTH response to dexamethasone in normal subjects. In the present study cortisol and ACTH were determined by radioimmunoassay in normal subjects at 8.00 a.m., 10.00 a.m. and noon before and after dexamethasone. Additionally the cortisol response to ACTH was tested under both conditions. The ACTH concentrations in the morning show a periodicity quite similar to the well-known circadian rhythm of cortisol secretion. Dexamethasone blocks this periodicity without decreasing ACTH significantly. The cortisol response to ACTH after dexamethasone is normal. In the morning only a basal and presumably biologically inactive ACTH is secreted which can not further be suppressed by dexamethasone. Therefore it is advisable for the diagnosis of hypercortisolism to measure ACTH only in stimulation tests, e.g. insulin-induced hypoglycemia.

Adrenocorticotropic Hormone↗

PubMed1982

[ACTH response in the dexamethasone suppression test].

Adrenocorticotropic Hormone↗