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PubMedDate not supplied

The substitutive role of ACTH in supporting aldosterone response to head-up tilt during acute renin suppression in patients with essential hypertension.

The relative contribution of the renin-angiotensin system, adenocorticotrophic hormone (ACTH) and plasma electrolytes in the response of plasma aldosterone to 30 minutes of 65 degrees head-up tilt was assessed in 10 essential hypertensive patients. Studies were carried out before and during acute blockade of renin release by propranolol, ACTH suppression by dexamethasone and combined renin and ACTH blockade. In control studies orthostasis induced significant increases only in plasma renin activity and aldosterone. In contrast, when the renin response to tilt was acutely suppressed by propranolol administration, the aldosterone response was nonetheless maintained but now appeared to be under ACTH control, since concurrent increases in cortisol were observed. During ACTH suppression aldosterone increased during tilt and so did renin. However, during combined ACTH and renin blockade aldosterone failed to increase during tilt. These studies suggest that the aldosterone secretory response to head-up tilt is normally mediated by the renin-angiotensin system but, when the renin response is suppressed, an ACTH response is elicited which assumes a backup role. However, when these two systems are blocked other factors appear unable to respond during tilt to support a normal aldosterone response.

Adrenergic beta-Antagonists↗
PubMed1980

Aldosterone response to prolonged ACTH infusion in juvenile hypertension.

The effects of a continuous 5-day ACTH infusion (40 units/24 hr) on plasma aldosterone (aldo) concentration and urinary excretion of aldosterone pH 1 conjugate, tetrahydroaldosterone and free aldo were investigated in 6 normotensive children, and 7 children with hypertension of unknown origin. In both groups, an initial rise of plasma aldo and all urinary aldo metabolites and a subsequent fall were observed during the ACTH test. The decline in plasma aldo correlated significantly with a decrease in plasma renin activity and serum K+. There was, however, evidence for another regulatory factor of aldo secretion during ACTH infusion because on a low salt diet. ACTH produced a similar aldo pattern which could not be attributed to the changes in plasma renin activity or serum K+. Urinary excretion of both free aldo and tetrahydroaldosterone, a metabolite formed in the liver, showed a slower decrease during ACTH infusion than aldosterone pH 1 conjugate, which is of renal origin. The change in pattern of urinary aldo metabolites may be caused by a relative increase of the free, nonprotein bound plasma fraction of aldo and an enhanced metabolism of aldo in the liver during ACTH infusion. Neither in the baseline state nor during the ACTH test was there a difference between the normotensive and the hypertensive group in any of the aldo parameters.

Adolescent↗
PubMed1998

Adrenal function in preterm infants: ACTH may not be the sole regulator of the fetal zone.

The fetal zone of the adrenal gland is known to persist after preterm birth, but there is uncertainty as to how long adrenal fetal zone steroid production continues and how it is regulated. The purpose of this study was to test two hypotheses. First, that the urinary excretion of 3beta-OH-5-ene steroids persists until term, and then declines, as it does in full-term infants. Second, that the persistence of the fetal zone is due to continuing ACTH stimulation. A longitudinal observational study was undertaken in 22 preterm infants of 24-31-wk gestation. Sequential measurements were made of urinary 3beta-OH-5-ene steroids (fetal zone steroid metabolites), plasma dehydroepiandrosterone sulfate (DHEAS), and ACTH. Excretion of urinary 3beta-OH-5-ene steroids was 1500-2000 microg kg(-1) d(-1), persisting until term, and declining abruptly at approximately 42 wk postconceptional age (PCA), to levels comparable to term infants at the same PCA. Median plasma ACTH levels rose from <7.6 pg mL(-1) at 25-wk PCA to 34.5 pg mL(-1) at 46-wk PCA. Urinary 3beta-OH-5-ene steroids were highest when ACTH levels were lowest, and were declining when ACTH was rising. In four infants given dexamethasone, urinary excretion of 3beta-OH-5-ene steroids and plasma DHEAS were not suppressed fully, when plasma ACTH and cortisol, and urinary cortisol metabolites were. These data suggest that ACTH is not the sole regulator of the adrenal fetal zone steroid synthesis and that involution of the fetal zone is related to gestation rather than birth.

Adrenal Glands↗
PubMed1999

Timing of peak serum cortisol values in preterm infants in low-dose and the standard ACTH tests.

The low-dose ACTH test seems to reveal mild cases of adrenal insufficiency and is beginning to be preferred over the standard ACTH test in the evaluation of adrenal suppression both in infants and in adults. The concentration-time profile of plasma cortisol in infants after a low ACTH dose is obscure. In this crossover study, we compared timing of the peak values in the low-dose and the standard ACTH stimulation tests in preterm and full-term infants. We performed the standard ACTH tests (250 microg/1.73 m2) and the low-dose ACTH tests (1 microg/1.73 m2) on 10 infants (26-40 wk gestational age) and measured serum cortisol concentration at 0, 30, 40, 60, and 120 min by RIA. Nine of the infants had received postnatal glucocorticoid treatment, and most of them had also been treated with dexamethasone antenatally. In the low-dose test, the peak values occurred at 30 or 40 min in 9/10 patients. In the standard-dose test, the peak values occurred at 60 or 120 min in 8/10 patients. These results are comparable with those from adults. According to this study, blood samples for the low-dose ACTH test in infants should be taken before dosing and between 30 and 40 min after dosing.

Adult↗
PubMed1990

Suramin prevents ACTH-stimulated corticosterone release by dispersed adrenocortical cells.

Suramin, a polyanionic compound which has been used in the treatment of trypanosomiasis and oncocerciasis, has recently been used in treatment of AIDS, while preliminary success has been reported in the treatment of cancer. However, suramin also causes adrenal insufficiency. The present study was undertaken in order to investigate the effect of suramin on ACTH-stimulated steroid production by dispersed rat adrenal cells. It was shown that suramin at concentrations of 10(-4)-10(-3) M inhibits ACTH-stimulated corticosterone release in a dose-dependent manner IC50 (2.10(-4) M). In addition, suramin caused a parallel decrease in ACTH-stimulated pregnenolone, progesterone and corticosterone release, suggesting that suramin does not affect corticosteroidogenesis via an inhibition of its regulatory enzymes. Suramin at 10(-4) M did not inhibit cholera toxin (10 mg/l)-, forskolin (5 microM)- and dbcAMP (5 mM)-stimulated corticosterone release, while cholera toxin completely overcame the inhibitory effects of very high concentrations of suramin (up till 10(-3) M), on ACTH-stimulated corticosterone release. Finally, chromatographic studies with a matrex gel showed that suramin directly interacted with the ACTH molecule. In conclusion, suramin at "therapeutic" concentrations (10(-4) M and higher) prevents ACTH-stimulated corticosterone release probably via a direct interaction with the ACTH molecule.

Adrenal Cortex↗
PubMed1976

Strain-dependent gonadal effects upon the response of adrenal cholesterol esters to ACTH in C57BL/10J and DBA/2J mice.

The response of adrenal cholesterol esters to ACTH administered in vivo was studied in males, females and male castrates of the C57BL)10J and DBA/21 strains of mice. The cholesterol ester fatty acids were transmethylated and analyzed by gas-liquid chromatography. There are sex and strain differences in the response of the adrenal cholesterol esters to ACTH. Neither the male nor the female C57 mouse shows a significant depletion of total cholesterol esters upon ACTH treatment. This result argues against the utilization of adrenal cholesterol esters for corticosteroid synthesis in this strain. In the female DBA mouse cholesterol ester depletion in response to ACTH is maximal. Neither the total cholesterol ester concentration nor the concentration of any individual ester is correlated with the pattern of response of the cholesterol esters to ACTH. Among the individual cholesterol esters, cholesteryl arachidonate (C20:4) is preferentially utilized after ACTH treatment in all groups except the C57 males. In contrast, cholesteryl adrenate (C22:4), which is generally the most abundant cholesterol ester, is conserved during ACTH stimulation in all groups except the DBA females. A cyclic interconversion between adrenate and arachidonate may be physiologically important in the control of adrenal function.

Adrenal Glands↗
PubMed1975

Relationships among the secretion of ACTH, GH, and cortisol during the insulin-induced hypoglycemia test in the normal and obese child.

The behavior of the secretion of ACTH, GH, and plasma cortisol during the insulin-induced hypoglycemia test on normal and obese children was studied. The secretion of the above-mentioned hormones was determined by calculating the integrals of the curves. The mean values of the integrals of the plasma cortisol and ACTH curves do not show any significant differences between the two groups of children. The mean values of the ratios between the integrals of the plasma cortisol and ACTH curves show a significant difference between the two groups (P smaller than 0.01). Since the mean values of the integrals of the plasma cortisol curves are practically the same in both groups, the difference in the above-mentioned ratios refers to the lower values of the integrals of the ACTH curves found in the obese children. This enables us to make the hypothesis that in the obese child the function of the pituitary-adrenal axis, at least during the insulin test, does not differ from the norm thanks to the adaptation of the ACTH secretion to the greater sensitivity of the adrenal glands to this hormone. In both the groups examined there was no correlation between the secretion of ACTH and plasma cortisol, between ACTH and GH, and between plasma cortisol and GH.

Adrenocorticotropic Hormone↗
PubMed1977

Adenylate cyclase of GH and ACTH producing tumors of human: activation by non-specific hormones and other bioactive substances.

The adenylate cyclase responses of the human GH or ACTH producing pituitary adenomas and ectopic ACTH producing tumors to TRH, LH-RH, biogenic amines, peptides hormones, PGE1 and rat median eminence extract (MEE) have been examined. Out of 4 GH producing pituitary adenomas obtained from patients with active acromegaly at hypophysectomy two were stimulated by TRH, two by LH-RH, three by norepinephrine, one by dopamine, four by PGE1 and none by serotonin. Glucagon stimulated the adenylate cyclase in one of three and MEE in both of two tested. The positive responses of paradoxical GH release after TRH and/or LH-RH before surgery in these patients coincidentally related to the response of adenylate cyclase of each pituitary adenoma. There seems, however, to be no consistent correlation between the adenylate cyclase responses to biogenic amines and the GH release after L-Dopa or 5-hydroxytroptophan tested. The adenylate cyclase of a pituitary adenoma from case of Cushing's disease was stimulated by LH-RH, norepinephrine glucagon and MEE but not by TRH. Plasma levels of ACTH, beta-MSH and cortisol increased after LH-RH but not after TRH in this patient before hypophysectomy. The adenylate cyclase of two ectopic ACTH producing tumors (gastric carcinoid and malignant thymoma) was activated by TRH, LH-RH, norepinephrine, epinephrine, serotonin, PGE1 and MEE. These results indicate the presence of multiple hormone receptors in GH or ACTH producing pituitary adenomas and ectopic ACTH producing tumors, and suggest that the paradoxical GH or ACTH release after TRH and/or LH-RH injection in acromegaly and Cushing's syndrome might be caused by an alteration of the cellular membrane receptors of the pituitary adenomas.

Acromegaly↗
PubMed1977

Corticotropin-releasing factor-like activity in ACTH producing tumors.

Corticotropin-releasing factor (CRF)-like activity in two different kinds of ACTH-producing tumors (human ectopic ACTH-producing colonic cancer and rat MtT/F4 tumor) was determined by an in vitro method using isolated normal rat pituitary cells. The ACTH content of the post mortem colonic cancer was 5.5 ng/g w.wt. The ACTH content of the medium of MtT/F4 tumor cells was 153+/-32 pg/10(5) cells. The ACTH content of MtT/F4 tumor cell suspensions was elevated with increasing doses of hypothalamic median eminence extract (HME). The response of MtT/F4 tumor cells to HME was suppressed by 1 mug/ml of dexamethasone. Extracts of colonic cancer, MtT/F4 tumor and HME produced elevation of the ACTH content of the medium of isolated rat pituitary cells. The CRF-like activities of two kinds of tumor extracts in multiple dilutions ran parallel to that of HME. The CRF-like activities were 0.037 HME equiv/mg w.wt in MtT/F4 tumor and 0.052 HME equiv/mg w.wt. in colonic cancer. These results demonstrated that CRF-like activity existed in these two kinds of ACTH-producing tumors.

Adrenocorticotropic Hormone↗
PubMed1978

ACTH-secreting medullary carcinoma of the thyroid presenting a severe idiopathic osteoporosis and senile purpura: report of a case and review of the literature.

A 64-yr-old female presented with severe osteoporosis and easy bruisability of over 2-yr duration. Biopsy of a neck mass revealed medullary carcinoma of the thyroid. Subsequently, lymphangitic pulmonary metastases were demonstrated which had been present radiographically for at least 4 yr. Basal serum calcitonin was markedly elevated and increased during calcium infusion. The diagnosis of ectopic ACTH syndrome was first entertained when hypokalemic alkalosis was observed during evaluation of her carcinoma. Elevated urinary 17-hydroxycorticosteroids, 17-ketosteroids, plasma cortisol, and immunoreactive plasma ACTH levels were documented. Adrenal steroidogenesis seemed to suppress on high dose dexamethasone. The primary tumor and its metastases contained high concentrations of immunoreactive ACTH and beta-melanocyte-stimulating hormone. Hepatic metastases contained extremely high concentrations of calcitonin. In contrast to the usual presentation of the ectopic ACTH syndrome as primarily hypokalemic alkalosis and glucose intolerance, patients with relatively benign and indolent ACTH-secreting tumors, such as certain cases of medullary carcinoma of the thyroid, may present with more typical signs and symptoms of Cushing's syndrome. The more pronounced cushingoid features in this latter group presumably reflects a more prolonged period of exposure to elevated glucocorticoid levels. Ten cases of ACTH-secreting medullary carcinoma of the thyroid from the literature are discussed. Extopic ACTH production by such tumors should be considered in the evaluation of patients with Cushing's syndrome or unexplained severe osteopenia.

Adrenocorticotropic Hormone↗
PubMed1979

Histamine-induced ACTH secretion and inhibitory effect of antihistaminic drugs.

Concentration of adrenocorticotropic hormone (ACTH) in the serum increased and reached the maximum level 10 min after the injection of histamine (dihydrochloride, 0.5 or 1 mg/100 g) i.p. into rats. The maximum concentration of ACTH in the serum was dependent on the dose of histamine. The ACTH concentration then decreased and was close to the normal level 30 to 60 min after the injection. The ACTH secretion induced by histamine (0.5 mg/100 g) was inhibited completely by the pretreatment with the antagonists of H1-receptor, diphenyhydramine (hydrochloride, 0.2--0.5 mg/100 g), promethazine (hydrochloride, 0.1--0.2 mg/100 g) and d-chlorpheniramine (maleate, 0.02--0.05 mg/100 g). The antagonist of H2-receptor, metiamide (2--4 mg/100 g) inhibited the ACTH secretion significantly but not completely. These results suggest that H1-receptor plays a major role in the histamine-induced ACTH secretion, although H2-receptor is also involved in this ACTH secretion.

Adrenocorticotropic Hormone↗
PubMed2005

Control of ACTH secretion by excitatory amino acids: functional significance and clinical implications.

The involvement of excitatory amino acids in the control of ACTH release is well established. Activation of ionotropic glutamate receptors has a stimulatory effect on ACTH release, while the role of metabotropic receptors is not yet understood in detail. Glutamatergic regulation of ACTH release has a clear significance for the stress response and neuroendocrine functions during development. A dysregulation of the hypothalamic-pituitary-adrenocortical (HPA) axis has been reported in several psychiatric and neurological disorders. So far, only fractional indices on the clinical importance of the interaction between glutamate and ACTH secretion have been obtained in both preclinical and clinical studies. Some antidepressant drugs, such as tianeptine, which were found to modulate ACTH release, appear to interfere with brain glutamatergic system. Changes in ACTH and cortisol release may be of importance for mood stabilizing effects of antiepileptic drugs modulating glutamate release, such as lamotrigine. Brain glutamate and HPA axis interaction seems to be of importance in alcohol and drug abuse. Little information is available on ACTH release in response to glutamate-modulating drugs used in the treatment of schizophrenia and Alzheimer disease. Nevertheless, pharmacological interventions influencing interaction between glutamate and the HPA axis are promising treatment possibilities in psychiatry and neurology.

Adaptation, Physiological↗
PubMed1998

Elevated proenkephalin-derived peptide levels in ACTH-producing adenomas: nucleus and cytoplasm localization.

The biosynthesis of met-enkephalin in human pituitary and human pituitary adenomas is still not well known. In this work, we studied the processing of proenkephalin-derived peptides in postmortem human pituitary (PMHP), ACTH-producing adenomas (ACTH-PA), nonfunctioning adenomas (NFA), and GH-producing adenomas (GH-PA). ACTH-PA contained at least 10 times more proenkephalin-derived peptides than PMHP, NFA,and GH-PA. Proenkephalin processing was different in the four tested tissues. In ACTH-PA, proenkephalin was processed to high-, intermediate-, and low-mol-wt products. The highest met-enkephalin-containing peptides levels corresponded to intermediate and low-mol-wt materials, although met-enkephalinArg-Phe and synenkephalin immunoreactivity appeared only in high-mol-wt peptides. In PMHP and NFA, met-enkephalin-Arg-Phe immunoreactivity was detected in intermediate- and low-mol-wt materials, and it was absent in GH-PA. Immunoblotting of ACTH-PA showed that met-enkephalin-Arg-Phe immunoreactivity corresponded to peptides of 44, 32-30, 27, and 17 kDa. The 32-30 and 17-kDa molecules were localized in the nuclear fraction where they were extracted after enzymatic digestion with DNase I. Plasmatic met-enkephalin levels did not increase in patients with Cushing's disease, suggesting that the pentapeptide stored in ACTH-PA was not released to the general circulation. In conclusion, we demonstrated that only ACTH-PA contained high levels of proenkephalin peptides, which were stored in cytoplasm organelles and in the nucleus, probably bound to chromatin. These results suggest an adenoma-specific physiological role of proenkephalin products.

Adenoma↗
PubMed2001

Increased ACTH levels do not alter renal 11beta-hydroxysteroid dehydrogenase type 2 gene expression in the sheep.

The regulation of renal 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2) gene expression is poorly understood. Inhibition of expression can result in hypertension. An example of this is in ectopic adrenocorticotropin (ACTH) syndrome (EAS). Inhibition of 11betaHSD2 activity is suggested by the observed increased ratio of cortisol to cortisone in both plasma and urine. To investigate whether ACTH or ACTH-dependent steroids can modulate renal 11betaHSD2 gene expression we analysed renal 11betaHSD2 mRNA levels after treatment with ACTH of 1 H and 24 H and demonstrated no change in the levels of gene expression. We have demonstrated in this study that the expression of 11betaHSD2 in the kidney is unaltered by ACTH. The reduced inactivation of cortisol by 11betaHSD2 observed in EAS is likely to be in part due to end product inhibition or substrate overload of the enzyme by endogenous substrates (cortisol, corticosterone, etc) rather than inhibition of 11betaHSD2 at the transcriptional level by either ACTH or ACTH regulated steroids.

11-beta-Hydroxysteroid Dehydrogenase Type 2↗
PubMed1991

A case of pituitary adenoma producing both growth hormone (GH) and adrenocorticotropic hormone (ACTH).

The authors report a very rare case of pituitary adenoma producing both GH and ACTH. A 29-year-old female was admitted with obesity, amenorrhea, acromegaly, hirsutism, excessive pigmentation, acne, and diabetes mellitus. Computed tomography revealed an intrasellar tumor 16 mm in height, with a destroyed sellar floor. The blood concentrations of GH, ACTH and cortisol were increased (GH: 92 ng/ml, ACTH: 94 pg/ml, cortisol: 18.3 micrograms/dl). No diurnal variation in the amount of cortisol was observed. The urinary 17-OHCS was suppressed by 8 mg but not by 2 mg of dexamethasone. A subtotal adenomectomy was then performed through the transsphenoidal approach, which led to a sufficient reduction of both blood GH and ACTH (cortisol). Histologically the tumor was an acidophilic pituitary adenoma. Immunoperoxidase staining showed diffuse GH and sporadic ACTH producing cells, but failed to show any cells producing both hormones. The electron micrograms of neoplastic cells showed the ultrastructural characteristics of respective GH and ACTH cells. Another increase in both GH and cortisol, which occurred 19 months after the operation, has been controlled by bromocriptine administration. This case may be the first reported case of a pituitary adenoma producing both GH and ACTH, not accompanied by prolactin (PRL) hypersecretion, which has been fully confirmed endocrinologically and histopathologically.

Adenoma↗
PubMedDate not supplied

Non-corticotropic ACTH peptides modulate nerve development and regeneration.

Short peptide sequences of ACTH 1-39 (the ACTH 4-9 analog Org 2766, ACTH 4-10 and its analog BIM 22015, and ACTH 1-13 [alpha-MSH]), which do not stimulate the adrenal cortex, have profound effects on the developing and regenerating neuromuscular system, in neonatal and in adult rats. Both development and regeneration are accelerated, as indicated by improved morphological, electrophysiological, behavioral and biochemical parameters. Regeneration in the central nervous system is problematic but the ACTH peptides may provide protection for CNS neurons, enhance denervation sensitivity or permit compensatory processes which facilitate functional recovery. Neuronal cells in culture respond to ACTH peptides by greater neurite outgrowth, and in some cell types, by increased B-50 expression. In all cases, susceptibility to ACTH peptide treatment varies with cell type, age, the specific peptide administered, its dosage and pattern of administration. External stress and the gender of the animal are additional factors that interact with the neurotrophic actions of the melanocortins.

Adrenocorticotropic Hormone↗
PubMed1982

A case of ectopic ACTH syndrome: diagnostic difficulties caused by intermittent hormone secretion.

A patient with a thymic carcinoid tumour causing ectopic ACTH syndrome is presented. The case illustrates the rapid development of the clinical and laboratory findings often associated with ectopic secretion of ACTH, including severe proximal myopathy, emotional lability, and hypokalaemic alkalosis. Interpretation of conventional tests of pituitary-adrenal function was complicated by intermittent secretion of ACTH by the tumour. The results of selective venous sampling for ACTH ruled out pituitary ACTH hypersecretion and were suggestive of a thymic source; computerized tomography of the chest localized the tumour. In vivo and in vitro investigations confirmed excessive ACTH production by the tumour, and surgical resection plus radiotherapy has resulted in resolution of the syndrome. The diagnostic problems created by intermittent secretion of ACTH by these tumours and the pre-operative and post-operative medical management of these patients are discussed.

17-Hydroxycorticosteroids↗
PubMed1982

ACTH suppression after oral administration of cortisone in Addisonian and adrenalectomized patients.

Plasma cortisol and the corresponding ACTH concentrations were determined before, and for 6 h following a single oral dose of 25 mg cortisone acetate in 7 patients with Addison's disease, 6 patients adrenalectomized for Cushing's disease and 1 patient adrenalectomized for congenital adrenal hyperplasia. The basal plasma cortisol concentrations 12 h after an evening dose of cortisone acetate 12.5 mg were below 100 nmol/l, and the corresponding ACTH concentrations were markedly elevated in all patients. Great interindividual variations were found in cortisol peak concentrations (Cmax) and the time to peak values, but without significant differences between the two patient groups. The maximal ACTH suppression occurred within 60-330 min after the cortisol Cmax, and was not significantly different in the two groups. The suppressed plasma ACTH concentrations were considerably above normal in 3 of the patients with Addison's disease and in 4 of the 6 patients adrenalectomized for Cushing's disease, including 2 patients with Nelson's syndrome. A similar degree of impaired ACTH suppression in patients with Addison's disease as in adrenalectomized patients suggests the occurrence of a secondary hypothalamic-pituitary dysfunction with ACTH hypersecretion in Addison's disease. The adequacy of the commonly used adrenocortical replacement therapy and its possible relation to the impaired ACTH suppression is discussed.

Addison Disease↗