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PubMedDate not supplied

A study on human adrenal secretion. Measurement of epinephrine, norepinephrine, dopamine and cortisol in peripheral and adrenal venous blood under surgical stress.

Epinephrine (E), norepinephrine (NE), dopamine (DA) and cortisol (F) were measured in samples drawn simultaneously by direct venepuncture from the brachial and the adrenal vein of 12 patients undergoing surgery for left kidney diseases. In 7 patients the influence of anesthesia on peripheral plasma levels was also assessed. Catecholamines were measured by a radioenzymatic assay and F by radioimmunoassay. Compared to basal values (mean +/- SE) (E: 53.6 +/- 6.2 pg/ml; NE: 209.4 +/- 24.4 pg/ml; DA: 24.5 +/- 3.3 pg/ml; F: 12.9 +/- 1.2 micrograms/dl) only NE peripheral levels were significantly modified by anesthesia (NE: 343.7 +/- 67.4 pg/ml p less than 0.05), whereas under surgery a significant increase in the peripheral levels was found for every substance measured (mean +/- SE) (E: 332.5 +/- 46.6 pg/ml p less than 0.001; NE: 633.6 +/- 114.2 pg/ml p less than 0.005; DA: 85.8 +/- 15.7 pg/ml p less than 0.005; F: 21.3 +/- 1.9 micrograms/dl p less than 0.01). Catecholamine and F levels in adrenal vein showed a high variability suggesting an intermittent secretion. In the adrenal venous blood E levels were, in the mean, 381 times higher, NE levels 45 times, DA levels 27 times and F levels 23 times higher than in peripheral blood. E, NE and DA concentrations in the adrenal vein were all significantly correlated to the others but not to cortisol, suggesting that the medulla secrets E, NE and DA in rather constant ratios and that the cortex and the medulla respond differently to surgical stress.

Adrenal Glands↗
PubMed1998

Ultrastructural and hormonal changes in the contralateral adrenal gland in unilateral adrenal gland ischemia: an experimental study in rats.

While it is well known that unilateral tissue ischemia may result in contralateral damage in some paired organs, there is no universally accepted mechanism to explain why these contralateral changes occur. The aim of the present study was to investigate the ultrastructural and hormonal changes that occur in the contralateral nonischemic adrenal gland after unilateral ischemia of an adrenal gland in a rat model. The animals were divided into four groups of four rats each; namely, a control group which received a sham operation without any ischemic insult, a 2-h ischemic group, a 4-h ischemic group, and an 8-h ischemic group. The left adrenal blood vessels were ligated in all ischemia groups and blood samples were taken for hormonal study 2, 4, and 8 h later, after which bilateral adrenalectomy was performed to determine the ultrastructural changes. The plasma concentrations of aldosterone and cortisol were determined by radioimmunoassays. There was an increase in both aldosterone and cortisol levels related to the duration of the ischemia, but the differences among the groups were not statistically significant. Contralateral ultrastructural damage such as heterochromatin in nuclei, mitochondrial degeneration, endoplasmic reticulum cisternal widening, increased lipid droplets, and lysosomes, were demonstrated electron-microscopically after unilateral adrenal ischemia.

Adrenal Glands↗
PubMed1989

The role of sterol carrier protein 2 in stimulation of steroidogenesis in rat adrenal mitochondria by adrenal cytosol.

Cholesterol side-chain cleavage (CSCC) in isolated rat adrenal mitochondria is enhanced by prior corticotropin (ACTH) stimulation in vivo (8-fold). Part of this stimulation is retained in vitro by addition of cytosol from ACTH-stimulated adrenals to mitochondria from unstimulated rats (2.5- to 6-fold). In vivo cycloheximide (CX) treatment fully inhibits the in vivo response and resolves the in vitro cytosolic stimulation into components: (i) ACTH-sensitive, CX-sensitive; (ii) ACTH-sensitive, CX-insensitive; and (iii) ACTH-insensitive, CX-insensitive. These components contribute approximately equally to stimulation by ACTH cytosol. Components (i) and (iii) most probably correspond to previously identified cytosolic constituents steroidogenesis activator peptide and sterol carrier protein 2 (SCP2). SCP2, as assayed by radioimmunoassay or ability to stimulate 7-dehydrocholesterol reductase, was not elevated in adrenal cytosol or other subcellular fractions by ACTH treatment. Complete removal of SCP2 from cytosol by treatment with anti-SCP2 IgG decreased cytosolic stimulatory activity by an increment that was independent of ACTH or CX treatment. Addition of an amount of SCP2, equivalent to that present in cytosol, restored activity to SCP2-depleted cytosol but had no effect alone or when added with intact cytosol, suggesting the presence of a factor in cytosol that potentiates SCP2 action. Pure hepatic SCP2 stimulated CX mitochondrial CSCC 1.5- to 2-fold (EC50 0.7 microM) but was five times less potent than SCP2 in adrenal cytosol. Two pools of reactive cholesterol were distinguished in these preparations characterized, respectively, by succinate-supported activity and by additional isocitrate-supported activity. ACTH cytosol and SCP2 each stimulated cholesterol availability to a fraction of mitochondrial P450scc that was reduced by succinate but failed to stimulate availability to additional P450scc reduced only by isocitrate.

Adrenal Glands↗
PubMed1989

Actions of somatostatin on perfused bovine adrenal glands and cultured bovine adrenal medullary cells.

The effects of somatostatin on catecholamine secretion and inositol phosphate accumulation have been studied using isolated perfused bovine adrenal glands and cultured bovine adrenal medullary cells. Somatostatin had no effect on basal adrenaline or noradrenaline secretion from either preparation. At concentrations above 1 microM, somatostatin inhibited the secretion of both catecholamines induced by 5 microM nicotine from cultured chromaffin cells. In contrast, over the concentration range 0.1 nM-10 microM, somatostatin had no effect on the secretory responses produced by 10 nM angiotensin II or 1 microM histamine. Inositol phosphate accumulation in cultured bovine adrenal medullary cells was unaffected by 0.1 nM-0.1 microM somatostatin, however at 1 and 10 microM somatostatin it was significantly increased, by 23% and 103% respectively. The effects of somatostatin (0.1 nM-10 microM) and of 50 microM muscarine on inositol phosphate accumulation were simply additive. Similarly, somatostatin at 0.1 nM and 10 nM together with 10 nM angiotensin II or 1 microM histamine produced additive inositol phosphate responses. In contrast, 1 microM somatostatin gave significantly more-than-additive (synergistic) inositol phosphate responses with angiotensin II and histamine. The results suggest that some adrenal medullary cells possess several types of receptors, and that these receptors may interact to produce non-additive responses.

Adrenal Glands↗
PubMed1989

Decreased adrenal medullary catecholamines in adrenal transplanted parkinsonian patients compared to nephrectomy patients.

Adrenal medullary catecholamines were measured in tissue samples from eight patients who underwent autologous transplantation of the adrenal medulla to the caudate nucleus as a treatment for Parkinson's disease. These adrenal catecholamine levels were compared to a group of patients of similar age who underwent unilateral nephrectomy for renal cell carcinoma. The levels of each catecholamine, expressed as nanomoles per milligram wet weight tissue, were significantly lower (P less than or equal to 0.005) in the parkinsonian patients than in the nephrectomy patients. These observations support data reported previously from autopsy specimens and suggest that the adrenal medullae of parkinsonian patients may be a compromised source of dopamine-producing tissue; this may limit its effectiveness in eliciting maximum clinical improvement following transplantation.

Adrenal Medulla↗
PubMed1979

Evidence for 6-keto-PGF1 alpha in adrenal cortex of the rat and effects of 6-keto-PGF1 alpha and PGI2 on adrenal cAMP levels and steroidogenesis.

Both intact cortical tissue and isolated cortical cells from the adrenal gland of the rat were analyzed for 6-keto-PGF1 alpha, the hydrolysis metabolite of PGI2, using high-performance liquid chromatography and gas chromatography-mass spectrometry. 6-Keto-PGF1 alpha was present in both incubations of intact tissue and isolated cells of the adrenal cortex, at higher concentrations than either PGF2 alpha or PGE2. Thus, the cortex does not depend upon vascular components for the synthesis of the PGI2 metabolite. Studies in vitro, using isolated cortical cells exposed to 6-keto-PGF1 alpha (10(-6)-10(-4)M), show that this PG does not alter cAMP levels or steroidogenesis. Cells exposed to PGI2 (10(-6)-10(-4)M), however, show a concentration-dependent increase of up to 4-fold in the levels of cAMP without altering cortico-sterone production, ACTH (5-200 microU/ml) increased cAMP levels up to 14-fold, and corticosterone levels up to 6-fold, in isolated cells. ACTH plus PGI2 produced an additive increase in levels of cAMP, however, the steroidogenic response was equal to that elicited by ACTH alone. Adrenal glands of the rat perfused in situ with PGI2 showed a small decrease in corticosterone production, whereas ACTH greatly stimulated steroid release. Thus, while 6-keto-PGF1 alpha is present in the rat adrenal cortex, its precursor, PGI2, is not a steroidogenic agent in this tissue although it does stimulate the accumulation of cAMP.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

Effect of prolonged physical training on the histochemically demonstrable catecholamines in the sympathetic neurons, the adrenal gland and extra-adrenal catecholamine storing cells of the rat.

The effect of daily physical training for 24 months on the sympathetic neurons, adrenal gland, extra-adrenal catecholamine storing cells and on the heart was investigated in rats. The tissue catecholamine fluorescence intensity was determined by microfluorimetric quantitation of catecholamines. The maximal and final body weights were significantly lower in trained animals. The trained rats showed prominent increase of heart weight relative to body weight, while the adrenals did not enlarge. The adrenergic nerve fiber density of the heart and the fluorescence intensity of the terminal axons were significantly increased. There were no changes in the fluorescence intensity of the perikarya of the sympathetic neurons and the amount of extra-adrenal catecholamine storing cells after physical exercise. The volume of the superior cervical ganglion was doubled and the neuronal perikarya were enlarged in trained animals. The prolonged physical training throughout the life span of the rat gave new information about the reactions of the sympathetic nervous system to physical exercise.

Adrenal Medulla↗
PubMed1990

Diminished adrenal steroidogenic activity in aging rats: new evidence from adrenal cells cultured from young and aged normal and hypoxic animals.

Adrenal cells from 2-6-month-old young rats (Y cells) and from 19-25-month-old aged male rats (O cells) were adapted to primary monolayer culture. The cultures of Y and O cells appeared to be primarily epithelial and rounded up in response to stimulation with adrenocorticotropic hormone (ACTH). The general morphology of O cells was comparable to that observed in Y cells except for the presence of lipofuscin-like granules, a cellular marker of aging, in O cells, but not in Y cells. ACTH-stimulated steroid production by O cells was 52% lower than that by Y cells. Exposure of intact young rats to hypoxia (0.5 atmosphere) for 21 days prior to sacrifice and culture resulted in a 122% increase of ACTH-stimulated adrenal steroidogenic activity in the cultured cells, but this effect was not observed in adrenal cells cultured from hypoxic aged rats. The results suggest that there is an age-related diminution in rat adrenal steroidogenic capacity in response to ACTH stimulation in culture derived from Y and O animals; hypoxic stress magnifies this difference.

Adrenal Cortex↗
PubMed1999

11beta-hydroxyandrostenedione and delta5-androstenediol as markers of adrenal androgen production in patients with 21-hydroxylase-deficient nonclassic adrenal hyperplasia.

OBJECTIVE: To determine the sensitivity of 11beta-hydroxyandrostenedione (11-OHA4) and delta5-androstenediol (ADIOL) as markers of excessive adrenal androgen production. DESIGN: Prospective study. SETTING: Academic medical centers. PATIENT(S): Thirteen women with untreated 21-hydroxylase-deficient nonclassic adrenal hyperplasia (NCAH) and 18 healthy, eumenorrheic, nonhirsute controls matched for age and body mass index. INTERVENTION(S): All subjects were studied before and after acute adrenal stimulation with 0.25 mg of IV ACTH-(1-24). MAIN OUTCOME MEASURE(S): Basal levels of total testosterone, sex hormone-binding globulin, DHEAS, and free testosterone were measured. Levels of androstenedione (A4), DHEA, 11-OHA4, and ADIOL were determined before (Steroid0) and 60 minutes after (Steroid60) acute ACTH-(1-24) stimulation. RESULT(S): Patients with NCAH had higher median basal levels of DHEAS and total and free testosterone than controls. Patients with NCAH had higher median A4(0), A460, DHEA(0), DHEA60, 11-OHA4(0), ADIOL0, and ADIOL60 levels but similar 11-OHA4(60) levels compared with controls. Among patients with NCAH, 30%, 54%, 15%, and 85% had 11-OHA4(0), ADIOL0, 11-OHA4(60), and ADIOL(60) levels, respectively, above the 95th percentile of controls. CONCLUSION(S): Overall, serum levels of 11-OHA4 did not appear to be a very sensitive marker of excessive adrenal androgen production, at least in patients with NCAH. Although ACTH-stimulated ADIOL levels were elevated in 85% of the patients studied, they did not appear to have any advantage over the measurement of A4 or DHEA levels.

Adrenal Hyperplasia, Congenital↗
PubMed1999

Adrenal and gonadal contributions to urinary excretion and plasma concentration of epitestosterone in men--effect of adrenal stimulation and implications for detection of testosterone abuse.

OBJECTIVE: The ratio of urinary testosterone (T) to epitestosterone (EpiT) is used to detect T abuse in sport. Also, plasma or urinary concentrations of EpiT have been measured to assess testicular steroidogenesis during hormonal male contraception. Further investigations are required to evaluate the relative contributions of the testis and adrenal to EpiT production. To this purpose, we have compared basal urinary EpiT glucuronide and plasma EpiT and the response to synthetic adrenocorticotrophic hormone (ACTH) stimulation between eugonadal and hypogonadal men. DESIGN AND SUBJECTS: The basal urinary excretion rate of EpiT glucuronide was determined in 34 eugonadal men. Six men, clinically diagnosed as hypogonadal, and 6 out of the 34 eugonadal men previously described, received an intramuscular injection of synthetic ACTH depot (1 mg) at 0800 h on two consecutive days. Blood samples were collected prior to and then at 1.5, 8, 24, 25.5, 32 and 48 h with respect to the first administration (0 h). 24-h urine specimens were collected from 0800 h on days 1 and 2 (baseline) and 3 and 4 (stimulation). MEASUREMENTS: Plasma EpiT, T and cortisol were measured by RIA and urinary EpiT and T, following glucuronide hydrolysis, by gas chromatography-mass spectrometry (extract combines aglycones with a minor amount of urinary free steroids). RESULTS: Basal excretion rates of EpiT glucuronide in eugonadal men (range: 62-751 nmol/24 h) were considerably greater than in hypogonadal men (range: 3-34 nmol/24 h). Mean basal plasma EpiT in eugonadal men (1.32 +/- 0.08 nmol/l) were greater than in hypogonadal men (0.68 +/- 0.04 nmol/l). In each group, synthetic ACTH stimulation increased plasma cortisol 4-fold. In eugonadal men, plasma and urinary EpiT were unchanged whereas plasma and urinary T glucuronide decreased in response to ACTH. In hypogonadal patients, ACTH increased plasma and urinary EpiT while plasma T remained unchanged. CONCLUSION: The testes are the major source of epitestosterone, the adrenal contribution being relatively modest. Following adrenal stimulation, urinary epitestosterone glucuronide increases considerably in hypogonadal men but this increase is masked in eugonadal men because testicular production is probably suppressed by the ACTH-induced rise in cortisol. Activation of the adrenal cortex results in no change or only a small decrease in the urinary T/EpiT ratio in eugonadal men.

Adrenal Glands↗
PubMed1999

Prolonged hypoxic stress increases adrenal cholesterol reserve in rats without causing adrenal hypertrophy.

1. It is known that, in rats, hypoxia stimulates adrenal steroidogenesis, but our understanding of the hypoxic effect on the glandular parameters remains incomplete. 2. Adrenals were collected and analysed from rats that had been exposed to hypoxic conditions for 3 weeks. 3. The results reveal increased adrenal concentrations of corticosterone, free cholesterol and total cholesterol without a change in glandular weight and protein concentration. The increased total cholesterol is primarily associated with enriched cholesteryl adrenate (CE22: 4), cholesteryl arachidonate (CE20: 4) and cholesteryl oleate (CE18: 1).

Adrenal Cortex↗
PubMed1979

[Adrenal and extra-adrenal phaeochromocytoma: diagnostic features and localisation by determining plasma catecholamines (author's transl)].

Urinary catecholamines and urinary excretion of vanillylmandelic acid confirmed the diagnosis of phaeochromocytoma in ten patients. In two of seven a modified glucagon test significantly aided confirmation of the diagnosis. In all patients the tumour was localised both by catecholamine determination in blood from the vein draining into the inferior vena cava (IVC) and by adrenal phlebography. Site of the adrenal tumour was definitively determined by the high catecholamine level in the adrenal veins and by phlebography. Three extra-adrenal tumours, a thoracic and two abdominal ones, were localised by high catecholamine levels in blood from other veins draining into the IVC. Vanillylmandelic acid determinaion was unreliable in the diagnosis of small phaeochromocytomas.

Abdominal Neoplasms↗
PubMed1999

Teratoma in the region of adrenal gland: a unique entity masquerading as lipomatous adrenal tumor.

BACKGROUND: The aim of this study was to establish the clinical and pathologic aspects of 3 atypical lipomatous lesions in the region of the adrenal gland. METHODS: Three young Chinese patients (ages 18, 18, and 37 years) were seen for nonspecific back pain. Radiologic examination revealed a lipomatous lesion in the region of the adrenal gland, and hormonal assessment was normal. Calcification was noted in 2 of the 3 lesions. Adrenalectomy was performed because of the size (diameter 7.5, 10, 11 cm) of the tumors with suspected local symptoms. RESULTS: On gross examination 2 tumors were cystic and 1 was solid. In all 3 patients the diagnosis was mature teratomas. The tumors were composed of mature tissues arising from more than 1 germinal layer. There was no evidence of immature elements or malignancy. Adipose tissue was the predominant component in the tumors. There was no evidence of recurrent diseases in all these patients during follow-up. CONCLUSIONS: To our knowledge, this is the first report of teratomas occurring in the adrenal region. Teratoma should clinically and radiologically be included in the differential diagnoses of lipomatous adrenal lesions. Excision of the teratoma is advocated.

Adolescent↗
PubMed1984

Congenital adrenal tissue in the lung with adrenal cytomegaly. Case report and review of the literature.

Adrenal cytomegaly is a cellular abnormality found in the fetal and neonatal adrenal gland. It is characterized by large polyhedral cells with granular eosinophilic cytoplasm and irregular pleomorphic nuclei. A case of bilateral adrenal cytomegaly in five-day-old infant with two foci of pulmonary involvement is reported with a review of the literature. The question of whether the pulmonary lesion represents metastasis or cytomegalic change in ectopic adrenal tissue is discussed.

Adrenal Cortex↗
PubMed1998

Role of the adrenal gland and adrenal-mediated chemosignals in suppression of estrus in the house mouse: the lee-boot effect revisited.

Mature female mice, grouped in the absence of a male stimulus, exhibit a suppressed estrous cycle (the so-called Lee-Boot effect). We have designed a series of experiments to elucidate the involvement of the adrenal gland in this phenomenon. Our initial results indicate that adrenalectomized mice exhibit a regular estrous cycle in either isolated or grouped conditions. A single, intact mouse caged with five adrenalectomized females showed repeated normal cycles. When the urine samples from group-caged intact mice or group-caged adrenalectomized mice were applied to the external nares of singly caged females, estrous cycles were inhibited in the animals receiving urine from the intact mice but not from the adrenalectomized mice. In addition, corticosterone therapy restored the function of estrus suppression in grouped, adrenalectomized mice. We had previously shown that the urinary excretion of several volatile compounds (2-heptanone, trans-5-hepten-2-one, trans-4-hepten-2-one, pentyl acetate, cis-2-penten-1-yl acetate, and 2,5-dimethylpyrazine) was adrenal mediated (Science 1986; 231:722-725). A further testing of these compounds in relation to estrus suppression has now revealed that a mixture of these compounds is effective, but removing 2, 5-dimethylpyrazine from the mixture abolished the biological response. The overall results of this study show conclusively an important role of the adrenal gland and adrenal-mediated urinary metabolites in estrus suppression.

Adrenal Glands↗
PubMed1986

Macronodular adrenal hyperplasia with hypothalamic-pituitary-adrenal suppression by ultra-high-dose dexamethasone: regression following hypophysectomy.

Cushing's syndrome associated with macronodular adrenal hyperplasia (MAH) may present with high-dose dexamethasone (dex) nonsuppressible hypercortisolemia. This has been interpreted as suggesting a primary adrenal disorder, leading to recommendations for curative adrenalectomy in these cases. The present case of MAH demonstrates high urinary and serum cortisol levels, sufficiently suppressed only by ultra-high-dose (32 mg/day X 2 day) dex, with parallel reduction of plasma adrenocorticotrophin noted as well. Subsequent clinical cure by transsphenoidal hypophysectomy and identification of a pituitary adenoma confirmed the secondary nature of adrenal cortical hypersecretion. The conceptual evolution of macronodules and altered feedback dynamics of the hypothalamo-pituitary-adrenal axis in MAH are briefly discussed.

Adrenal Gland Diseases↗
PubMed1986

Increased sympatho-adrenal tone and adrenal medulla reactivity in DOCA-salt hypertensive rats.

Sympatho-adrenal tone and reactivity were evaluated in anaesthetized normotensive and DOCA-salt hypertensive rats, by measuring arterial plasma concentrations of norepinephrine and epinephrine under basal conditions and following bilateral carotid occlusion. Baseline norepinephrine levels were significantly higher in DOCA-salt hypertensive animals than in their respective normotensive controls, whether they were studied with intact vagi or following bilateral vagotomy. The possibility of a relationship between the increased basal sympathetic fibres and the maintenance of DOCA-salt hypertension is strongly suggested by the finding of a significant correlation between mean arterial pressure (MAP) and basal circulating norepinephrine values in those animals. Furthermore, the epinephrine increase following carotid occlusion was found to be markedly potentiated in hypertensive animals (intact or vagotomized), suggesting adrenal medullary hyperreactivity to baroreflex activation in this model of hypertension. In normotensive rats the epinephrine increase induced by the carotid occlusion was greatly potentiated by the administration of an alpha 2-antagonist (yohimbine), and completely abolished by administration of an alpha 2-agonist (clonidine). In contrast, the epinephrine response to carotid occlusion, which is already enhanced in hypertensive animals, was unaffected by the same treatments. These results therefore suggest that adrenal medullary hyperreactivity observed in DOCA-salt hypertensive rats may be due to a dysfunction of an alpha 2-adrenergic mechanism modulating adrenal medullary secretion.

Adrenal Medulla↗
PubMed1995

IL-1 is expressed in human adrenal gland in vivo. Possible role in a local immune-adrenal axis.

IL-1 is an important mediator in the dialogue between the immune system and the hypothalamo-pituitary-adrenal axis. A direct influence of IL-1 upon adrenal steroidogenesis has been demonstrated in experimental animals. We therefore designed a study to see if IL-1 is expressed within the normal human adrenal gland. The combination of in situ hybridization and specific immunostaining to IL-1 beta was eminently suited to demonstrate both mRNA and protein production. The specific immunostaining of the different cells combined with in situ hybridization (IL-1) allowed us to identify the exact cellular source of IL-1. IL-1 mRNA occurred in the zona reticularis in 17 alpha-hydroxylase positive steroid cells surrounding the adrenomedullary cells. Some CD68+ macrophages in this zona showed a positive signal. A weak signal was seen to IL-1 mRNA in few chromaffin cells, while IL-1-like immunoreactivity was more frequent. We conclude that in the normal situation in man IL-1 is mainly expressed in specialized cortical cells. The occurrence of the major glucocorticoid inducing factor in the normal human adrenal gland itself provides evidence for an autocrine or paracrine reaction under physiological conditions.

Adrenal Glands↗