[Adrenal cortex function test using a synthetic ACTH -- a comparison between 1-18 ACTH and 1-24 ACTH].
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11-Hydroxycorticosteroids↗
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[Adrenal cortex stimulating effects of synthetic ACTH in adrenal cortex hyperfunction. Comparison between 1-18 ACTH and 1-24 ACTH].
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Adrenocortical Hyperfunction↗
[Pulmonary neoplasms and adrenal gland insufficiency: study of a case and hypothesis on an ACTH-inhibiting factor (ACTH-IF) or an abnormal ACTH secreted by the tumor].
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Adenocarcinoma, Papillary↗
Glucocorticoid incubation of human ACTH-producing pituitary tumours in vitro. A study on ACTH secretion and cell morphology.
ACTH-producing pituitary adenomas obtained from two patients with Cushing's disease were maintained in organ culture for 2 weeks. After 4-6 days of incubation, hydrocortisone (0.1, 1, and 5 mg/ml) was added to the culture medium. Addition of cortisol to the media in concentrations which generally inhibit the ACTH secretion in vivo in patients with Cushing's disease (1 mg/ml) failed to affect the ACTH secretion in vitro. A decrease of ACTH secretion occurred only with 5 mg/ml after 5 days of incubation. A similar effect on growth hormone (GH) release was seen when cortisol (10 mg/ml) was added to cultures from GH-producing pituitary adenoma. No ultrastructural changes were found in cultured cells that could be attributed to the addition of 0.1 mg/ml cortisol in the culture medium. With higher concentrations, (1 mg/ml and 5 mg/ml) minor ultrastructural changes were suspected. Our present findings implicate the hypothalamus as the target area for the feedback control of ACTH in Cushing's disease but could not reveal whether or not the primary lesion (i.e. the tumor) was of pituitary or hypothalamic origin. Our organ culture system appears to be a suitable model for investigating possible ACTH-regulating factors.
Adenoma↗
Differential behavioral effects of ACTH 4-10 and [D-Phe7] ACTH 4-10.
Intraventricular administration of an access of ACTH 4-10 does not interfere with the excessive grooming behavior of rats, elicited by intraventricular administration of [D-Phe7] ACTH 4-10. In an avoidance extinction paradigm, the two ACTH analogs have opposite effects. ACTH 4-10 counteracts the facilitation of extinction seen after [D-Phe7] ACTH 4-10, only under conditions that treatment with ACTH 4-10 alone results in retardation of that extinction. The data are discussed in terms of a multiple interaction of these peptides with brain function.
Adrenocorticotropic Hormone↗
Effects of adrenalectomy on CRH regulation of ACTH release: adenylate cyclase activity, cyclic AMP-dependent protein kinase activity and ACTH release.
Corticotropin releasing hormone (CRH) stimulation of ACTH release and cyclic AMP-mediated events involved in the control of ACTH release were compared in sham-operated and adrenalectomized rats. CRH-stimulated adenylate cyclase activity was decreased in pituitary homogenates from adrenalectomized animals. CRH-stimulated cyclic AMP accumulation was essentially abolished and CRH-stimulated cyclic AMP-dependent protein kinase (A-kinase) activity was decreased in freshly prepared anterior pituitary cells from adrenalectomized animals. Basal and CRH-stimulated ACTH release was elevated in these cells. Since ACTH release is increased in adrenalectomized rats despite the down regulation of CRH-linked pituitary mechanisms, we speculate that the site of action of disinhibition by corticosterone of ACTH release (or synthesis) following adrenalectomy is distal to the generation of cyclic AMP and/or that non-CRH mediated mechanisms assume a greater role in ACTH regulation following adrenalectomy.
Adenylyl Cyclases↗
CSF ACTH and beta-endorphin in infants with West syndrome and ACTH therapy.
Corticotrophin (adrenocorticotropic hormone, ACTH) and beta-endorphin levels of the cerebrospinal fluid (CSF) were determined in 16 infants with the West syndrome during individualized ACTH treatment. Prior to treatment, the levels of CSF ACTH were significantly higher in infants with cryptogenic spasms, normal perinatal events, or normal development than in infants with symptomatic spasms or delayed development. The CSF beta-endorphin levels did not differ among the groups. At response, the infants could be divided into three groups: (1) short-course, low-dose responders with a substantial CSF ACTH decline, (2) long-course, high-dose responders with no such effect (but with a tendency towards an upward incline), and (3) non-responders with no significant CSF ACTH changes. The changes in CSF beta-endorphin were somewhat similar to the changes in CSF ACTH, but the greater variability did not allow statistical significance.
Adrenocorticotropic Hormone↗
Effects of gender and gonadectomy on ACTH response to interleukin-1beta in the rat: comparison with the modulation of ACTH response to immobilization stress.
We examined the influence of gender and gonadectomy on the plasma adrenocorticotropin (ACTH) response to intravenous administration of human recombinant interleukin (IL)-1beta (3 microg/kg) in the rat. For comparison, we also examined whether gender and gonadectomy affect ACTH secretion after immobilization stress (a 30-min period), which is a nonimmunological stressor. IL-1beta induced a significantly higher ACTH response in females than in males, and this sexual difference was abolished by gonadectomy in both sexes. By contrast, ACTH secretion after immobilization was statistically the same in males and females, but tended to be higher in gonadectomized males than in gonadectomized females. These results may suggest a dissociative regulation by gonadal steroids of IL-1beta- and immobilization-induced ACTH responses in the rat. The sexual difference in ACTH response to IL-1beta may represent another example of the sexually dimorphic immunological activity, which is known to be higher in females than in males.
Adrenocorticotropic Hormone↗
ACTH adrenal cell bioassay: improved sensitivity (12 ng/L) achieved by immunoextraction of ACTH from human plasma by a monoclonal antibody.
We have previously reported a bioassay for human plasma ACTH based upon trypsin dispersed guinea-pig adrenal cells which was sensitive to 100 ng/L ACTH in unextracted human plasma when measured against human pituitary ACTH (1-39) standard 74/555. We now present a bioassay of increased sensitivity (12 ng/L) which incorporates three major changes. The trypsin/trypsin inhibitor step in the cell dispersion protocol has been replaced with collagenase, donor calf serum (3%) has been incorporated into the standard curve and ACTH has been extracted from human plasma and dilutions of standard hormone by a sephacryl bound monoclonal antibody (2A3) directed towards the 25-39 sequence. The extracted standard curve has a detection limit of 6 ng/L and the cells can tolerate up to 50% plasma equivalent concentration. Thus, the improved assay has a detection limit of 12 ng/L ACTH in plasma. The assay can now measure bioactive plasma ACTH levels reliably in the normal range.
Adrenal Glands↗
A23187 inhibits adrenal protein synthesis and the effects of adrenocorticotropin (ACTH) on steroidogenesis and phospholipid metabolism in rat adrenal cells in vitro: further evidence implicating phospholipids in the steroidogenic action of ACTH.
We examined the effects of ACTH and the Ca++ ionophore, A23187, on steroidogenesis and phospholipid metabolism during incubation of dispersed rat adrenal cells. Increasing doses of ACTH elicited nearly parallel increases in corticosterone production and adrenal inositide (mono- and di-) concentrations. As reported previously by other investigators in Y1 cells, A23187 inhibited ACTH- and cAMP-stimulated, but not basal or pregnenolone-stimulated, corticosterone production. A23187 also inhibited ACTH-induced increases in phosphatidic acid, phosphatidylinositol, and diphosphoinositide, and this was attended by inhibition of [3H]leucine incorporation into protein. These findings support our previous contentions that: 1) a labile protein is required for ACTH-induced increases in adrenal phospholipids in the phosphatidate-polyphosphoinositide-polyglycerophospholipid pathway; and 2) these phospholipids are involved in the steroidogenic action of ACTH.
Adrenal Cortex Hormones↗
Acute adrenocorticotropin-(1-24) (ACTH) adrenal stimulation in eumenorrheic women: reproducibility and effect of ACTH dose, subject weight, and sampling time.
Assessment of adrenal reserve and the diagnosis of adrenal insufficiency by acute adrenocortical stimulation with ACTH-(1-24) has been well established. Alternatively, estimation of adrenocortical enzymatic activities by this method for the detection of inherited or acquired biosynthetic abnormalities has been less well characterized. Some of the discrepancies between studies estimating adrenocortical enzymatic activities in different pathological conditions (e.g. hyperandrogenism) may result from the different stimulation protocols used. The objective of this prospective study was to establish the inherent variability of the adrenal response to acute ACTH-(1-24) stimulation and to determine the effect of sampling time, stimulation dose, and subject weight on the same. Forty-one normal female volunteers were recruited (mean age, 29.1 yr), 30 within 90-110% ideal body weight and 11 weighing more than 120% ideal body weight. Three protocols were designed to study 1) the effects of sampling time, ACTH-(1-24) dose, and subject weight on adrenal response; 2) the effect of time of the day on the variability of basal steroid levels and the adrenal response to stimulation; and 3) the long term reproducibility of the adrenal response to ACTH-(1-24). Androstenedione, 17-hydroxyprogesterone, 11-deoxycortisol, dehydroepiandrosterone, and cortisol were measured in serum under basal and stimulated conditions. All subjects had normal basal levels of testosterone, androstenedione, dehydroepiandrosterone sulfate, and PRL. The acute iv administration of 0.10, 0.25, and 1.0 mg ACTH-(1-24) elicited similar and maximal steroid responses, with all steroid levels reaching a plateau 60-90 min poststimulation regardless of subject weight. Sampling of basal steroid levels every 5 min in the morning (AM; beginning 0700-0900 h) or evening (PM; 1500-1700 h) did not reveal any difference in steroid variability. Only the mean basal cortisol level was higher in AM than PM testing (P less than 0.03). Although the mean levels of dehydroepiandrosterone and 17-hydroxyprogesterone 60 min after stimulation were significantly higher in AM than PM studies, these differences were minimal. Ten volunteers underwent an average of four (range, 2-6) adrenal stimulation studies using 1.0 mg ACTH-(1-24) over a 1-yr period. The long term coefficient of variation (CV) for basal steroid levels ranged from 15-28%. Calculations of net adrenal response (delta steroid O-T and area delta steroid O-T) were less reproducible (CV, 0-82%) than measures of absolute response (steroid T, area steroid T, and %steroid T; CV, 7-32%). This difference in CV between the measures of net and absolute adrenal responses was significant for all steroids except androstenedione.(ABSTRACT TRUNCATED AT 400 WORDS)
17-alpha-Hydroxyprogesterone↗
Elevated plasma adrenocorticotropin (ACTH) with adrenal hyperplasia: a new factor in ACTH regulation?
We report a patient with Cushing's syndrome in whom the etiology of the hypercortisolemia could not be definitely established despite extensive biochemical investigations. Results included raised basal serum cortisol, plasma ACTH, and urinary free cortisol; failure to suppress even a paradoxical rise in serum cortisol after dexamethasone (1 mg overnight, 2, 8, and 16 mg/day); and a definite but not exaggerated rise in 11-deoxycortisol after metyrapone. After iv CRF, plasma ACTH rose from 22 to 30 pmol/L. Abdominal computed tomographic scanning showed adrenal hyperplasia; the presence of an adrenal adenoma, although suspected, was not established. An unusual finding was the presence in the urine of large amounts of 21-deoxycortisol metabolites, including 3 alpha,11 beta,17 alpha-trihydroxy-5 beta-pregnan-20-one and 5 beta-pregnane 3 alpha,11 beta,17 alpha,20 alpha-tetrol. On the basis of preoperative biochemical/radiological findings, a provisional diagnosis of ACTH-dependent Cushing's syndrome associated with autonomous bilateral adrenal hyperplasia was made. Incomplete bilateral adrenalectomy was performed; adrenal hyperplasia was histologically confirmed, but no tumor was found. However, ACTH was measured 1) just before operation when the patient was receiving treatment with metyrapone, and 2) postoperatively when the patient was receiving steroid replacement only, and on these occasions ACTH levels were lower than during the initial investigations. Pituitary scans before and after adrenalectomy were similar, offering no evidence of pituitary infarction. We propose that abnormal production of 21-deoxycortisol contributed to the aberrant regulation of ACTH and cortisol in this case, providing an example of a previously unreported cause of hypercortisolemia.
Adrenal Glands↗
The 5-HT1A receptor full agonist, 8-OH-DPAT inhibits ACTH-induced 5-HT2A receptor hyperfunction in rats: involvement of 5-HT1A receptors in the DOI-induced wet-dog shakes in ACTH-treated rats.
We examined the influence of 8-hydroxy-2-di-n-propylamino tetralin (8-OH-DPAT), a serotonin 1A (5-HT1A) receptor full agonist, on the wet-dog shake response induced by the (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI), a 5-HT2A receptor agonist, in adrenocorticotropic hormone (ACTH)-treated rats. Chronic ACTH (100 microg/rat, s.c.) treatment for 14 d increased the wet-dog shake response induced DOI. The 8-OH-DPAT inhibited the wet-dog shake response induced by DOI in rats with ACTH for 14 d. On the other hand, the 8-OH-DPAT-induced hypothermia and flat body posture were inhibited when ACTH was administered for 14 d. These findings suggest that chronic treatment with ACTH decreased the sensitivity of the 5-HT1A receptor system; however, the inhibitory effects from the 5-HT1A receptors to the 5-HT2A receptor system is not inhibited in ACTH-treated rats.
8-Hydroxy-2-(di-n-propylamino)tetralin↗
ACTH release in pituitary cell cultures. Effect of neurogenic peptides and neurotransmitter substances on ACTH release induced by hypothalamic corticotropin releasing factor (CRF).
The effects of various neurogenic peptides and neurotransmitter substances on the release of ACTH induced by hypothalamic corticotropin releasing factor (HY-CRF) were investigated using monolayer cultured anterior pituitary cells. Test substances were given in combination with 0.05-0.1 hypothalamic extract (HE)/ml, because HE evoked a significant ACTH release and a linear dose response relationship was demonstrated sequentially between 0.0165 HE/ml and 0.5 HE/ml. Relative high doses of lysine-vasopressin showed a slight additive effect on the release of ACTH induced by 0.1 HE/ml. Leu-enkephalin, dopamine, prostaglandin E1 and E2 slightly reduced the release of ACTH induced by HY-CRF, but the inhibitory effect of these substances were not dose-related. Other tested substances including luteinizing hormone releasing hormone, thyrotropin releasing hormone, somatostatin, melanocyte stimulating hormone release inhibiting factor, beta-endorphin, neurotensin, substance P, vasoactive intestinal polypeptide, angiotensin II, norepinephrine, serotonin, acetylcholine, histamine and gamma-amino butyric acid showed neither agonistic nor antagonistic effect on the release of ACTH induced by HY-CRF. These results indicate that the release of ACTH is controlled specifically by HY-CRF and corticosterone, and modified slightly by some other substances such as vasopressin and prostaglandins, and that the effect of most other neurogenic peptides and neurotransmitter substances is negligible or non-physiological at the pituitary level.
Adrenocorticotropic Hormone↗
Effects of angiotensin II infusion on the early morning surge of ACTH and o-CRH-provoked ACTH secretion in normal man.
UNLABELLED: The question of whether elevated plasma angiotensin II (AII) levels modulate ACTH secretion in man still awaits a definite answer. We performed two sets of experiments pertinent to that problem: Seven healthy young males each received AII (5 ng/kg/min) and sham infusions on different days in a randomized sequence from 03.00 h to 06.00 h in the morning, while plasma ACTH and cortisol were measured every 20 min. Mean blood pressure rose by about 10 mmHg during AII infusion. Mean plasma ACTH levels were slightly higher with AII than with sham infusion in every single individual (P less than 0.05). Differences in a pre- and post-infusion period were significant. Plasma cortisol levels were almost identical with or without AII infusion. Nine healthy young males received AII (5 ng/kg/min) or sham infusions on different days from 16.30 h to 20.00 h in a randomized sequence and a 100 micrograms o-CRH injection at 17.00 h. Plasma ACTH and cortisol were measured every 15 or 30 min between 16.30 h and 20.00 h. Mean blood pressure rose by about 14 mmHg during AII infusion. The rapid increment and further change in plasma ACTH and cortisol was not significantly different between the AII and sham infusion studies. CONCLUSIONS: The dose of AII infused was probably just above the threshold of ACTH stimulation, although AII plasma levels obtained were probably far above the physiological range. On the adrenal level, a vasoconstrictor effect of AII may have prevented stimulation of cortisol. This may be different in states of sodium depletion with reduced vascular effects of AII.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Comparison of ACTH and ACTH precursor peptides secreted by human pituitary and lung tumour cells in vitro.
The molecular forms of ACTH secreted by established human small cell lung cancer (SCLC) cells and primary cultures derived from a bronchial carcinoid tumour, a pituitary adenoma and hyperplastic pituitary tissue have been characterized by Sephadex G-75 chromatography and quantified with two novel immunoradiometric assays for ACTH and ACTH precursor peptides. Pro-opiomelanocortin (POMC; Mr 31,000) and pro-ACTH (Mr 22,000) were secreted by all cell types. No smaller peptides were identified in the culture media from SCLC and bronchial carcinoid cells, implying a deficiency in the enzymes and/or intracellular organelles required for extensive POMC processing. A more heterogeneous profile of ACTH-containing peptides was produced by cells of pituitary origin, indicating more extensive proteolytic processing of POMC. However, the major peptide secreted by cells from a large aggressive pituitary adenoma was unprocessed POMC (Mr 31,000). These results suggest that both lung and pituitary cells in vitro retain their in-vivo pattern of POMC processing and provide valuable models in which to study the regulation of ACTH synthesis and secretion.
Adenoma↗
[Radioimmunologic determination of ACTH in the rabbit: stress-ACTH-corticosteroid relationship and diarrhea].
Plasma ACTH was measured in young and adult rabbits with a CEA-SORIN kit. The reliability of the analysis was controlled by liquid chromatography, several biochemical tests such as parallelism and reproducibility and several physiological tests such as plasma ACTH response to ethylic ether stress, to adrenalectomy, to dexamethasone and metopyrone. In young diarrhoeic rabbit plasma, ACTH (293 +/- 45 pg/ml) and corticosteroid (111 +/- 13 ng/ml) levels were significantly much higher than in young healthy rabbits (ACTH: 130 +/- 35 pg/ml; corticosteroids: 66 +/- 7 ng/ml). Furthermore, transporting young rabbits by car caused such violent stress that plasma ACTH levels increased from 52 +/- 11 to 130 +/- 35 pg/ml. A causal relationship between stress - ACTH and diarrhoea is discussed.
Adrenal Cortex Hormones↗
Increased plasma ACTH responses to stress in nonhandled compared with handled rats require basal levels of corticosterone and are associated with increased levels of ACTH secretagogues in the median eminence.
Postnatal handling of rat pups is known to alter permanently hypothalamic-pituitary-adrenal (HPA) responses to a wide variety of stressors. As adults, handled (H) and nonhandled (NH) animals also differ in sensitivity to the delayed negative-feedback effects of glucocorticoids on stress-induced HPA activity. However, it is not understood how handling alters neuroendocrine responses to stressful stimuli, and how differences in feedback sensitivity might account for changes in HPA activity both during and following stress. In the present studies, plasma ACTH responses to both restraint and ether stress were significantly greater in NH compared with H animals. Administration of 100 micrograms/kg corticosterone (B) immediately prior to restraint stress significantly decreased subsequent plasma ACTH responses to restraint to the same extent in H and NH animals, suggesting that H and NH animals do not differ in glucocorticoid fast feedback. H and NH animals adrenalectomized (ADX) 5 d prior to testing did not differ in plasma ACTH responses to restraint stress, demonstrating that the differences between the groups are dependent upon the presence of circulating B. However, the handling effect was apparent in ADX animals provided with a low level of B replacement (approximately 5-6 micrograms/dl). B replacement significantly decreased plasma ACTH levels under both basal conditions and in response to restraint stress in H/ADX rats. In contrast, although B replacement also decreased basal ACTH levels in ADX/NH rats, there were no differences in plasma ACTH responses to restraint between NH/ADX and NH/ADX+B animals.(ABSTRACT TRUNCATED AT 250 WORDS)
Adrenalectomy↗