Serotoninergic regulation of corticosterone secretion in domestic fowl

1987 ◽  
Vol 113 (2) ◽  
pp. 159-165 ◽  
Author(s):  
A. Cheung ◽  
T. R. Hall ◽  
S. Harvey
Keyword(s):  
Domestic Fowl ◽  
Serotonin Receptor ◽  
Plasma Concentrations ◽  
Adrenocortical Function ◽  
Serotoninergic System ◽  
Acth Stimulation ◽  
Corticosterone Secretion ◽  
Corticosterone Release ◽  
Adrenal Corticosterone

ABSTRACT The effects of serotoninergic drugs on adrenocortical function in domestic fowl were examined. Administration of the serotonin receptor agonist 2-(1-piperazinyl)quinoline maleate (quipazine), an inhibitor of serotonin metabolism, N-methyl-N-2-propynylbenzylamine HCl (pargyline), as well as serotonin itself, all increased plasma concentrations of corticosterone. The maximum responses to serotonin and quipazine occurred 1 h after treatment. The quipazine-stimulated response was partly prevented by the serotonin antagonist cyproheptadine. Cockerels pretreated with dexamethasone, a synthetic steroid known to inhibit pituitary ACTH release, showed attenuated responses to subsequent quipazine, pargyline or serotonin injection. Serotonin, quipazine and cyproheptadine did not affect corticosterone release directly from the adrenal gland incubated in vitro, nor did they affect adrenal responsiveness to ACTH stimulation. The neurotoxin 5,6-dihydroxytryptamine injected into day-old chicks decreased plasma concentrations of corticosterone for up to 7 days after treatment, with corresponding decreases in the hypothalamic concentration of serotonin, but not dopamine or noradrenaline concentrations. These results show that adrenal corticosterone secretion is regulated by a central serotoninergic system, probably acting on the hypothalamo-pituitary-adrenal axis. J. Endocr. (1987) 113,159–165

Regulation of CRH-induced secretion of ACTH and corticosterone by SOM230 in rats

2005 ◽  
Vol 153 (3) ◽  
pp. R7-R10 ◽  
Author(s):  
A P Silva ◽  
P Schoeffter ◽  
G Weckbecker ◽  
C Bruns ◽  
H A Schmid
Keyword(s):  
Adrenocorticotropic Hormone ◽  
Plasma Concentrations ◽  
Inhibitory Effect ◽  
Corticotropin Releasing Hormone ◽  
Acth Secretion ◽  
Releasing Hormone ◽  
Corticosterone Secretion ◽  
Corticosterone Release ◽  
Acth Release

Objective: Adrenocorticotropic hormone (ACTH)-dependent Cushing’s syndrome is biochemically characterized by increased plasma concentrations of ACTH inducing hypersecretion of cortisol. Somatostatin is known to inhibit ACTH secretion, and in vitro data have shown the inhibition of ACTH secretion by agonists activating sst2 and sst5 receptors. The present study aimed to determine the inhibitory effect of the multireceptor ligand SOM230, compared with the sst2-preferring agonist octreotide, on corticotropin-releasing hormone (CRH)-stimulated secretion of ACTH and corticosterone in rats. Methods: Secretion of ACTH and corticosterone was induced by i.v. application of CRH (0.5 μg/kg) in rats pretreated 1 h before by i.v. application of SOM230 (1, 3, or 10 μg/kg), octreotide (10 μg/kg) or NaCl 0.9%. Results: SOM230 (3 and 10 μg/kg) inhibited CRH-induced ACTH release by 45±3% and 51±2%, respectively, and corticosterone release by 43±5% and 27±16%, respectively. 10 μg/kg of octreotide tended to be less potent at inhibiting ACTH release (34±6% inhibition) and did not alter the secretion of corticosterone. Conclusion: SOM230 has a stronger inhibitory effect on ACTH and corticosterone secretion than octreotide in rats. This difference can be explained by its higher affinity to sst1, sst3 and especially sst5 receptors compared with octreotide.

STUDIES ON THE MECHANISM OF SECRETION OF CORTICOSTEROIDS BY THE ISOLATED PERFUSED ADRENAL OF THE RAT

1981 ◽  
Vol 91 (2) ◽  
pp. 313-323 ◽  
Author(s):  
C. P. SIBLEY ◽  
B. J. WHITEHOUSE ◽  
G. P. VINSON ◽  
C. GODDARD ◽  
E. McCREDIE
Keyword(s):  
Culture Medium ◽  
Ion Concentration ◽  
Acth Stimulation ◽  
Steroid Production ◽  
Simple Diffusion ◽  
Corticosterone Secretion ◽  
Complex Process ◽  
Doc Production ◽  
Different Levels

A technique for the perfusion of the rat adrenal cortex is described. With tissue culture Medium 199 the preparation was responsive in terms of steroid production to both ACTH and K+ ions. Production of corticosterone and 18-hydroxydeoxycorticosterone (18-hydroxy-DOC) was stimulated by ACTH when it was administered at rates between 5 μu./min and 5 mu./min. Increasing the K+ ion concentration of the perfusate from 3·6 to 5·4 and 8·9 mmol/l stimulated the production of aldosterone, 18-hydroxycorticosterone and deoxycorticosterone, although not of corticosterone or 18-hydroxy-DOC. This preparation has been used to study further the mechanism of secretion of corticosterone and 18-hydroxy-DOC. Thus, production of these two steroids was measured at different perfusion flows, varying between 0·1 and 0·6 ml/min, with different levels of ACTH stimulation. Corticosterone production was significantly (P < 0·001) increased by increasing flows both under control conditions and when ACTH was administered at constant rates of 50 μu./min or 1 mu./min. Production of 18-hydroxy-DOC was not affected by flow either under control conditions or with 50 μu. ACTH/min. However, when ACTH was administered at 1 mu./min, 18-hydroxy-DOC production was also significantly (P < 0·001) increased by flow. The results are consistent with those obtained in previous in-vitro studies and have been interpreted as suggesting that the main mechanism of corticosterone secretion is simple diffusion. In contrast, 18-hydroxy-DOC secretion, at least at sub-maximal levels of stimulation, appears to require a more complex process.

scholarly journals Intra-adrenal mechanisms in the response to chronic stress: investigation in a rat model of emotionality

2006 ◽  
Vol 189 (2) ◽  
pp. 211-218 ◽  
Author(s):  
O Kosti ◽  
P W Raven ◽  
D Renshaw ◽  
J P Hinson
Keyword(s):  
Chronic Stress ◽  
Rat Model ◽  
Restraint Stress ◽  
Adrenocortical Function ◽  
Acth Stimulation ◽  
Corticosterone Response ◽  
Rat Strain ◽  
First Time ◽  
Adrenocortical Responses

The exploratory behaviour of the genetically derived Maudsley rat model of emotionality has been well characterized. Maudsley reactives (MR) present with more ‘anxious-like’ behaviour than Maudsley nonreactives (MNR). Although this behaviour is assumed to be associated with altered adrenocortical function, the few studies addressing this issue have produced inconsistent findings. We therefore set out to investigate the adrenal endocrinology of the MR and MNR strains. Control Wistars, the ancestors of the Maudsleys, have been used for the first time to set the baseline for all the experiments carried out. It was found that the MNR strain had a significantly blunted adrenocorticotrophic hormone (ACTH) response to restraint stress compared with Wistars, but a normal corticosterone response. Conversely, the MR had a significantly exaggerated ACTH response to restraint stress, but a normal corticosterone response. This finding suggested that the MR adrenal is less sensitive to ACTH than the MNR. This was confirmed by investigating the corticosterone dose–response to ACTH in adrenals from the two strains incubated in vitro. Several possible intra-adrenal regulators were investigated, but the only significant molecular difference in the adrenal glands from the two strains was the level of expression of neuropeptide Y (NPY), which is known to be a stress-responsive peptide in the adrenal. We propose that intra-adrenal NPY is responsible for blunting adrenocortical responses to ACTH stimulation in the MR strain. The observed changes in adrenal NPY suggest that this rat strain may serve as a model of chronic stress, with the MR phenotype representing maladaptation.

Testosterone receptor blockade after trauma and hemorrhage attenuates depressed adrenal function

2000 ◽  
Vol 279 (5) ◽  
pp. R1841-R1848 ◽  
Author(s):  
Zheng F. Ba ◽  
Ping Wang ◽  
Douglas J. Koo ◽  
Mian Zhou ◽  
William G. Cioffi ◽  
...  
Keyword(s):  
Adrenal Function ◽  
Male Rats ◽  
Ringer Lactate ◽  
Acth Stimulation ◽  
Camp Content ◽  
Morphological Alterations ◽  
Shed Blood ◽  
Corticosterone Response ◽  
Corticosterone Release ◽  
Adrenal Corticosterone

Although the testosterone receptor antagonist flutamide restores the depressed immune function in males after trauma and hemorrhage, it remains unknown whether this agent has any salutary effects on adrenal function. To study this, male rats underwent laparotomy and were bled to and maintained at a blood pressure of 40 mmHg until 40% of the shed blood volume was returned in the form of Ringer lactate. Animals were then resuscitated and flutamide (25 mg/kg body wt) was administered subcutaneously. Plasma adrenocorticotropic hormone (ACTH) and corticosterone, as well as adrenal corticosterone and cAMP were measured 20 h after resuscitation. In additional animals, ACTH was administered and ACTH-induced corticosterone release and adrenal cAMP were determined. The results indicate that adrenal contents of corticosterone and cAMP were significantly decreased and morphology was altered after hemorrhage. Administration of flutamide improved corticosterone content, restored cAMP content, and attenuated adrenal morphological alterations. Flutamide also improved the diminished ACTH-induced corticosterone release and adrenal cAMP response at 20 h after hemorrhage and resuscitation. Furthermore, the diminished corticosterone response to ACTH stimulation in the isolated adrenal preparation was improved with flutamide. These results suggest that flutamide is a useful adjunct for improving adrenal function in males following trauma and hemorrhage.

Control of zona glomerulosa function in the isolated perfused rat adrenal gland in situ

1985 ◽  
Vol 104 (3) ◽  
pp. 387-395 ◽  
Author(s):  
J. P. Hinson ◽  
G. P. Vinson ◽  
B. J. Whitehouse ◽  
G. Price
Keyword(s):  
Angiotensin Ii ◽  
Zona Glomerulosa ◽  
Adrenocortical Function ◽  
Specific Marker ◽  
Dependent Manner ◽  
Aldosterone Secretion ◽  
In Vitro Techniques ◽  
Corticosterone Secretion

ABSTRACT The extent to which results obtained using in-vitro techniques can be taken to reflect in-vivo physiological responses in the study of adrenocortical function has not been subjected to systematic study. Some evidence suggests that in-vitro preparative methods may affect the secreted steroid profile. For this reason it seemed desirable to study adrenal function using an isolated perfused whole gland technique, and this study reports results obtained with known aldosterone stimulants. Angiotensin II, ACTH and potassium ions all stimulated aldosterone secretion in a dose-dependent manner. The stimulation thresholds of these substances were compatible with their normal circulating concentrations. For angiotensin II stimulation this preparation was two orders of magnitude more sensitive than any in-vitro preparation. Most importantly, the specific glomerulosa effectors, angiotensin II and potassium, selectively stimulated aldosterone output, and had no consistent effect on corticosterone secretion at any dose used. On the other hand, ACTH stimulated both corticosterone and aldosterone output at all effective concentrations. The actions of α-MSH were also studied using this preparation. Low doses of α-MSH selectively stimulated aldosterone secretion, while higher doses were needed to stimulate corticosterone. The onset of response to all stimulants was invariably seen within the first 10 min after administration of stimulants. Maximal aldosterone output was achieved within the first 10 min whereas corticosterone secretion usually peaked 10–20 min later. The amount of aldosterone produced by this preparation was much higher than the amount produced by dispersed cell preparations, and closely approximated to the levels of aldosterone obtained in adrenal vein blood. The data indicate that the isolated circulation perfused gland system is a sensitive preparation which approximates to the physiological condition. In particular, aldosterone is the prominent glomerulosa product, and corticosterone is, in this system, a more specific marker for inner zone function. J. Endocr. (1985) 104, 387–395

Metabolism of cortisol in anorexia nervosa

1990 ◽  
Vol 122 (6) ◽  
pp. 753-758 ◽  
Author(s):  
H. Vierhapper ◽  
A. Kiss ◽  
P. Nowotny ◽  
S. Wiesnagrotzki ◽  
C. Monder ◽  
...  
Keyword(s):  
Anorexia Nervosa ◽  
Urinary Excretion ◽  
Plasma Concentrations ◽  
Adrenocortical Function ◽  
Acth Stimulation ◽  
Healthy Women ◽  
Rate Limiting Step ◽  
Enhanced Secretion ◽  
Excretion Rates ◽  
Steroid Excretion

Abstract. In patients with anorexia nervosa 24-h mean plasma concentration of cortisol were 0.44± 0.09 μmol/l (normal < 0.28 μmol/l). Following stimulation by ACTH (1–24) urinary excretion rates of cortisol were stimulated from 0.22 ± 0.08 to 4.85 ± 2.78 μmol/24 h. Similarly, plasma concentrations of the glucocorticoid metabolite, tetrahydrocortisone, increased from 23.3 ± 9.0 to 47.3 ± 30.2 nmol/l; urinary excretion rates of tetrahydrocortisone increased from 3.61 ± 0.90 to 8.40 ± 1.72 μmol/24 h. The relative share of the sulphate, glucuronide and free fractions of tetrahydrocortisone in the patients' urine did not indicate any defect in metabolization of this steroid metabolite. Excretion rates of the four glucocorticoid tetrahydro-metabolites, tetrahydrocortisone, allotetrahydrocortisone, tetrahydrocortisol, and allo-tetrahydrocortisol, expressed as percent of total steroid excretion, were similar in patients with anorexia and in healthy women under basal conditions (24 ± 6 vs 23 ± 6%) and during stimulation by ACTH (1–24) (36 ± 10 vs 45 ± 6%). The share of the two androgen metabolites, androsterone and etiocholanolone, was 24 ± 5% of total steroid excretion (basal; healthy women: 27 ± 8%) and 13 ± 2% (ACTH stimulation; healthy women: 12 ± 4%) in patients with anorexia nervosa. Thus, analysis of urinary steroid excretion rates did not indicate a shift in adrenocortical function. The results confirmed enhanced secretion of cortisol in patients with anorexia nervosa under basal conditions and during/following stimulation by ACTH. The ACTH-induced increase in the concentrations of the tetrahydro-glucocorticoid metabolites in urine was less pronounced than that of cortisol. The data strongly suggest a rate-limiting step in the transformation of cortisol into its main metabolites, most likely an impaired reduction of the double bond in positions C4/C5.

ADRENOCORTICAL FUNCTION IN FOETAL, NEONATAL AND YOUNG PIGS

1972 ◽  
Vol 54 (3) ◽  
pp. 473-481 ◽  
Author(s):  
M. DVOŘÁK
Keyword(s):  
Blood Plasma ◽  
Adrenal Cortex ◽  
Developmental Stages ◽  
Plasma Concentrations ◽  
Adrenal Weight ◽  
Adrenocortical Function ◽  
Adult Level ◽  
Adrenocortical Activity ◽  
Young Pigs

SUMMARY Absolute and relative adrenal weight, blood plasma concentrations of 17-hydroxycorticosteroids and their production in vitro on incubation of adrenal slices with corticotrophin (ACTH), were measured in foetal pigs, piglets and older pigs. These criteria all indicated that adrenocortical activity was highest on the day of birth. It developed intensely in about the last 10 days of intra-uterine life. After birth it decreased progressively with age, approaching the adult level after weaning in the second month of life. The adrenal cortex of pigs of all developmental stages investigated in this study was capable of responding markedly to stimulation with ACTH. No significant differences in adrenocortical activity were found between sexes up to 90 days of age.

131I-19-IODOCHOLESTEROL SCINTIGRAPHY OF THE ADRENAL CORTEX

1975 ◽  
Vol 80 (1) ◽  
pp. 81-94 ◽  
Author(s):  
H. Dige-Petersen ◽  
T. Munkner ◽  
J. Fogh ◽  
M. Blichert-Toft ◽  
J. O. Lund
Keyword(s):  
Adrenal Cortex ◽  
Cushing’S Syndrome ◽  
Cushing's Syndrome ◽  
Adrenocortical Function ◽  
Adrenocortical Adenoma ◽  
Acth Stimulation ◽  
Small Tumour ◽  
The Third ◽  
The Right

ABSTRACT 131I-19-iodocholesterol scintigraphy of the adrenal cortex has been carried out in 26 patients. In 4 patients with normal adrenocortical function the tracer was equally accumulated on the two sides. In 7 patients with untreated Cushing's syndrome, bilateral uptake was found in 4 patients with bilateral hyperplasia whereas unilateral visualization was obtained in three cases of cortisol producing adenomas. The side localization was confirmed at operation. Eight patients had been operated for Cushing's syndrome prior to the scintigraphy. Remnant adrenocortical tissue with negligible or subnormal function (4 patients) could not be visualized. Normo- or hyperfunctioning remnant tissue was visualized in 3 patients. One patient had recurrent hypercorticism due to metastases from a previously removed adrenocortical carcinoma; a single pelvic accumulation was seen, whereas several metastases in the abdomen and thorax were not visualized. Four patients with aldosteronism were investigated. Three had primary aldosteronism due to an adrenocortical adenoma. In two of these, the site of the adrenal lesion was localized pre-operatively. In the third patient, equal bilateral accumulation of iodocholesterol was seen even after suppression with dexamethasone. At operation a small tumour was found. In 1 patient with indeterminate aldosteronism both glands were visualized and at a second examination the uptake was equally suppressed by dexamethasone. Finally 3 patients were investigated. One had a testosterone producing tumour of the right ovary. The tumour was not visualized on the scintigram in spite of a slight accumulation of activity as measured in vitro. Another patient with a cyst of the right adrenal gland presented a defect in the activity on the affected side. In the third patient previously subjected to hypophysectomy, the adrenal cortex was visualized only after ACTH-stimulation. The 131I-19-iodocholesterol scintigraphy is a valuable method for the diagnosis and localization of cortisol and aldosterone producing tumours, and for the localization of normo- and hyperfunctioning adrenocortical remnants. The interpretation of the scintigrams must be based on relevant biochemical assays.

Adrenocortical function in response to myocardial necrosis in exercise-trained rats

1978 ◽  
Vol 44 (1) ◽  
pp. 104-108 ◽  
Author(s):  
J. A. Severson ◽  
R. D. Fell ◽  
D. R. Griffith
Keyword(s):  
Myocardial Necrosis ◽  
Plasma Corticosterone ◽  
Treadmill Running ◽  
Male Rats ◽  
Adrenocortical Function ◽  
Subcutaneous Injections ◽  
Corticosterone Secretion ◽  
Virgin Male ◽  
And Control

Plasma corticosterone concentrations and in vitro adrenal secretion of corticosterone was determined in exercise-trained rats. Virgin, male rats, 100 days of age, were trained for an 11-wk period by treadmill running. Following the training program, rats were subjected to two subcutaneous injections of l-isoproterenol 24 h apart and killed 24 h after the second injection. All exercise-trained rats survived isoproterenol treatment, while 44% of the control rats died. Plasma corticosterone concentrations were elevated only in exercise-trained rats treated with isoproterenol. Control rats treated with isoproterenol had plasma corticosterone concentrations similar to that in control and exercise-treated rats given placebo injections. Exercise training reduced adrenocortical responsiveness to ACTH in vitro, but isoproterenol treatment increased in vitro responsiveness to ACTH in exercise-trained and control rats. Total unstimulated corticosterone secretion rates in vitro were similar. The reason for better rat survival in exercise-trained rats is unknown; however, improved energy metabolism, depressed aldosterone secretion, or both are suggested as reasons for the better survival of exercise-trained rats.

Inhibition by omeprazole of adrenocortical response to ACTH: Clinical studies and experiments on bovine adrenal cortex in vitro

1986 ◽  
Vol 70 (1) ◽  
pp. 99-102 ◽  
Author(s):  
C. W. Howden ◽  
C. J. Kenyon ◽  
G. H. Beastall ◽  
J. L. Reid
Keyword(s):  
Adrenal Cortex ◽  
Adrenocortical Function ◽  
High Dose ◽  
Acth Stimulation ◽  
Double Blind ◽  
Zollinger Ellison Syndrome ◽  
Dependent Inhibition ◽  
Cortisol Levels ◽  
Cortisol Release

1. Omeprazole, a substituted benzimidazole, is a potent inhibitor of gastric acid secretion which is currently being evaluated in patients with peptic ulcer and Zollinger-Ellison syndrome. 2. Drugs which possess an imidazole nucleus have previously been shown to inhibit cortisol release from the adrenal cortex, secondary to inhibition of mitochondrial cytochrome P-450 dependent hydroxylation reactions. 3. In a double-blind placebo-controlled crossover study in healthy male volunteers, omeprazole (60 mg daily for 7 days) did not alter basal cortisol levels. The peak cortisol response to ACTH stimulation was significantly reduced. Cortisol levels 60 min after ACTH were 824 ± 27 nmol/l on omeprazole (mean ± sem), and 929 ± 35 on placebo (P < 0.005). 4. In vitro, omeprazole caused a concentration-dependent inhibition of ACTH-stimulated cortisol release from isolated bovine adrenal cells (ED50 = 20 μg/ml). This was associated with a decrease in deoxycortisol synthesis. Therefore, unlike some other imidazole-containing drugs, the inhibitory effects of omeprazole are not entirely due to steroid 11 β-hydroxylase inhibition. 5. Substantial inhibition occurred at omeprazole concentrations which are higher than plasma levels normally achieved in clinical use. However, impairment of adrenocortical function may occur in patients on long-term high dose omeprazole treatment for Zollinger-Ellison syndrome.

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