scholarly journals Aldosterone secretion in patients with septic shock: a prospective study

2013 ◽  
Vol 57 (8) ◽  
pp. 636-641 ◽  
Author(s):  
Rafael Barberena Moraes ◽  
Gilberto Friedman ◽  
Marina Verçoza Viana ◽  
Tiago Tonietto ◽  
Henrique Saltz ◽  
...  
Keyword(s):  
Septic Shock ◽  
Serum Levels ◽  
Zona Glomerulosa ◽  
High Dose ◽  
Zona Fasciculata ◽  
Cortisol Secretion ◽  
Aldosterone Secretion ◽  
Acth Stimulation ◽  
Aldosterone Production ◽  
A Prospective Study

OBJECTIVE: To assess serum levels of the main factors that regulate the activation of the zona glomerulosa and aldosterone production in patients with septic shock, as well as their response to a high-dose (250 µg) adrenocorticotropic hormone (ACTH) stimulation test. SUBJECTS AND METHODS: In 27 patients with septic shock, baseline levels of aldosterone, cortisol, ACTH, renin, sodium, potassium, and lactate were measured, followed by a cortrosyn test. RESULTS: Renin correlated with baseline aldosterone and its variation after cortrosyn stimulation. Baseline cortisol and its variation did not correlate with ACTH. Only three patients had concomitant dysfunction of aldosterone and cortisol secretion. CONCLUSIONS: Activation of the zona glomerulosa and zona fasciculata are independent. Aldosterone secretion is dependent on the integrity of the renin-angiotensin-aldosterone system, whereas cortisol secretion does not appear to depend predominantly on the hypothalamic-pituitary-adrenal axis. These results suggest that activation of the adrenal gland in critically ill patients occurs by multiple mechanisms.

Detection of Na+ and K+ in the Rat Adrenal Cortex with the Electron Microprobe

1977 ◽  
Vol 53 (5) ◽  
pp. 423-430 ◽  
Author(s):  
C. Decorzant ◽  
A. M. Riondel ◽  
M.-J. Philippe ◽  
J. Bertrand ◽  
M. B. Vallotton
Keyword(s):  
Adrenal Cortex ◽  
Electron Microprobe ◽  
Electrolyte Concentration ◽  
Zona Glomerulosa ◽  
Plasma Aldosterone ◽  
Zona Fasciculata ◽  
Aldosterone Secretion ◽  
Dietary Regimen ◽  
High K ◽  
Aldosterone Production

1. In order to demonstrate whether modification of aldosterone secretion is mediated by parallel changes of K+ in the adrenal zona glomerulosa, the total (intracellular + extracellular) Na+ and K+ content of the rat adrenal cortex was determined with the electron microprobe. 2. Groups of rats were submitted to one of the following dietary regimens: standard, low Na+, high K+ or high Na+. 3. Distribution of Na+ and K+ across the zona glomerulosa and zona fasciculata was compared. Standards of known electrolyte concentration were also analysed. 4. The [Na+] was found to be greater in the zona glomerulosa than in the zona fasciculata but K+ was distributed evenly in both zones. This was independent of dietary regimen. 5. Aldosterone production, assessed by plasma aldosterone concentrations, could not be correlated with zona glomerulosa K+ content.

Effect of adrenocorticotrophin on cortisol and androstenedione secretion from dispersed cells of guinea-pig adrenal zonae fasciculata and reticularis

1986 ◽  
Vol 109 (3) ◽  
pp. 399-404 ◽  
Author(s):  
W. R. Robertson ◽  
B. Davison ◽  
D. C. Anderson ◽  
J. Frost ◽  
A. Lambert
Keyword(s):  
Body Weight ◽  
Guinea Pig ◽  
Adrenal Cortex ◽  
Zona Glomerulosa ◽  
Adrenal Weight ◽  
Zona Fasciculata ◽  
Cortisol Secretion ◽  
Acth Stimulation ◽  
17 Hydroxyprogesterone ◽  
Dispersed Cells

ABSTRACT We have studied cortisol and androstenedione secretion by dispersed cells of the outer zona fasciculata (ZF) plus zona glomerulosa, and the inner zona reticularis (ZR) plus medulla of the guinea-pig adrenal. The ZF and ZR were microdissected apart, the cells dispersed and incubated (200 000 cells/ml) for 90 min in the presence of adrenocorticotrophin (ACTH; 500 ng/l), dibutyryl cyclic AMP (dbcAMP; 1 mmol/l), pregnenolone, 17-hydroxypregnenolone, 17-hydroxyprogesterone, 11-deoxycortisol and 21-deoxycortisol. The steroid concentrations were 5–25 μmol/l. Cortisol secretion was assayed by radioimmunoassay. There was no detectable cortisol secretion ( < 50 nmol/l) from the ZR in the controls (no additive) or after dbcAMP stimulation. Adrenocorticotrophin-stimulated cortisol secretion was also low (range < 50–340 nmol/l). In contrast the ZF secreted 177–379 (control), 828–2052 (dbcAMP) and 2863–9735 (ACTH) nmol cortisol/l. There was no detectable (i.e. < 2 nmol/l) cAMP production by ZR or ZF either basally (no ACTH) or after ACTH stimulation (500 ng/l). Challenge of the ZR cells with each cortisol precursor steroid (5 μmol/l) increased (P < 0·05) cortisol secretion over that seen with the corresponding basal and ACTH-stimulated controls. Thus pregnenolone, 17-hydroxypregnenolone, 17-hydroxyprogesterone, 11-deoxycortisol and 21-deoxycortisol (converted directly to cortisol by 21-hydroxylase) gave rise to (mean ± s.d., n = 4) 406 ± 86, 680 ± 180, 1307 ± 111, 1141 ± 234 and 3160 ± 419 nmol cortisol/l respectively. The corresponding figures for the ZF prepared from the same adrenal cortex were 3919 ± 309, 4122 ± 97, 5766 ± 615, 5035 ± 260 and 6954 ± 755 nmol cortisol/l. With pregnenolone (25 μmol/l), cortisol secretion increased to 7847 ± 1424 (ZR) and 12880 ± 982 nmol/l (ZF), a ZR:ZF ratio of 0·6 compared with 0·1 for pregnenolone at 5 μmol/l. Androstenedione was secreted in the basal state by both ZF and ZR in similar quantities, i.e. 3·7 ± 0·3 and 3·7 ± 0·4 nmol/l (n = 9 and 14 respectively). Both cell types were ACTH sensitive, with androstenedione secretion increasing to 28 ± 4·8 (ZF) and 12·5 ± 0·9 (ZR) nmol/l. There was a direct correlation (r = 0·924, P < 0·05) between total adrenal weight and body weight, between the percentage ZR in the cortex and adrenal weight (r = 0·96, P < 0·05) and between the percentage ZR and body weight (r = 0·981, P< 0·05). In a mature animal (800–1000 g) the ZR may occupy > 66% of the adrenal cortex. The mean diameters of cells from the ZF and ZR were 21 and 25 μm respectively. J. Endocr. (1986) 109, 399–404

scholarly journals Regulation of aldosterone secretion by mineralocorticoid receptor–mediated signaling

2017 ◽  
Vol 232 (3) ◽  
pp. 525-534 ◽  
Author(s):  
Cherish Chong ◽  
Anis Hamid ◽  
Tham Yao ◽  
Amanda E Garza ◽  
Luminita H Pojoga ◽  
...  
Keyword(s):  
Mineralocorticoid Receptor ◽  
Ex Vivo ◽  
Zona Glomerulosa ◽  
Zona Fasciculata ◽  
Aldosterone Secretion ◽  
Aldosterone Synthase ◽  
Adrenal Steroidogenesis ◽  
Corticosterone Secretion ◽  
Aldosterone Production ◽  
Male Wistar Rats

We posit the existence of a paracrine/autocrine negative feedback loop, mediated by the mineralocorticoid receptor (MR), regulating aldosterone secretion. To assess this hypothesis, we asked whether altering MR activity in zona glomerulosa (ZG) cells affects aldosterone production. To this end, we studied ex vivo ZG cells isolated from male Wistar rats fed chow containing either high (1.6% Na+ (HS)) or low (0.03% Na+ (LS)) amount of sodium. Western blot analyses demonstrated that MR was present in both the ZG and zona fasciculata/zona reticularis (ZF/ZR/ZR). In ZG cells isolated from rats on LS chow, MR activation by fludrocortisone produced a 20% and 60% reduction in aldosterone secretion basally and in response to angiotensin II (ANGII) stimulation, respectively. Corticosterone secretion was increased in these cells suggesting that aldosterone synthase activity was being reduced by fludrocortisone. In contrast, canrenoic acid, an MR antagonist, enhanced aldosterone production by up to 30% both basally and in response to ANGII. Similar responses were observed in ZG cells from rats fed HS. Modulating glucocorticoid receptor (GR) activity did not alter aldosterone production by ZG cells; however, altering GR activity did modify corticosterone production from ZF/ZR/ZR cells both basally and in response to adrenocorticotropic hormone (ACTH). Additionally, activating the MR in ZF/ZR/ZR cells strikingly reduced corticosterone secretion. In summary, these data support the hypothesis that negative ultra-short feedback loops regulate adrenal steroidogenesis. In the ZG, aldosterone secretion is regulated by the MR, but not the GR, an effect that appears to be secondary to a change in aldosterone synthase activity.

Endothelin-1 potentiation of angiotensin II stimulation of aldosterone production

1992 ◽  
Vol 262 (1) ◽  
pp. R85-R89 ◽  
Author(s):  
E. N. Cozza ◽  
S. Chiou ◽  
C. E. Gomez-Sanchez
Keyword(s):  
Angiotensin Ii ◽  
Zona Glomerulosa ◽  
Receptor Subtype ◽  
Ang Ii ◽  
Aldosterone Secretion ◽  
Acth Stimulation ◽  
Endothelin 1 ◽  
Aldosterone Production ◽  
Glomerulosa Cells ◽  
Stimulation Of

Endothelin-1 (ET-1) binds to specific receptors in cultured bovine adrenal glomerulosa cells and stimulates aldosterone secretion with a 50% effective concentration (EC50) of 300 +/- 80 pM (mean +/- SE). The relative stimulatory potency for ET-1 is significantly less than that of angiotensin II (ANG II). The incubation of calf zona glomerulosa cells in primary culture with ET-1 and ANG II resulted in a significant potentiation of ANG II effect on aldosterone secretion. The EC50 of ET-1 potentiation of ANG II-induced stimulation of aldosterone secretion was 40 +/- 5 pM (mean +/- SE, n = 4), which is lower than the EC50 for ET-1 stimulation of aldosterone secretion. Adrenocorticotropic hormone (ACTH) stimulation of aldosterone secretion, but not that of potassium, was also potentiated by ET-1, but to a lesser degree. ET-1 and ET-1-mediated potentiation of ANG II-stimulated aldosterone biosynthesis increased both the early and late pathways of aldosterone biosynthesis, but the potentiation was greater for the early pathway. Preincubation with ET-1 for at least 15 min, followed by extensive washing to remove bound ET-1, also resulted in persistent potentiation of ANG II-mediated aldosterone secretion. ET-2, sarafotoxin, and vasoactive intestinal contractor potentiation of ANG II action were very similar to that of ET-1. ET-3 and Big-ET-1 potentiated ANG II stimulation only at the highest doses tested and the proendothelin-(110-130) fragment was inactive. ET-1 potentiation of ANG II action is likely to be mediated through an ETB receptor subtype.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Quantitative assessment of CYP11B1 and CYP11B2 expression in aldosterone-producing adenomas

2002 ◽  
pp. 795-802 ◽  
Author(s):  
F Fallo ◽  
V Pezzi ◽  
L Barzon ◽  
P Mulatero ◽  
F Veglio ◽  
...  
Keyword(s):  
Real Time ◽  
Secretory Activity ◽  
Zona Glomerulosa ◽  
Zona Fasciculata ◽  
Mrna Levels ◽  
Rt Pcr ◽  
Pathophysiological Role ◽  
Aldosterone Production

BACKGROUND: The presence and pathophysiological role of CYP11B1 (11beta-hydroxylase) gene in the zona glomerulosa of human adrenal cortex is still controversial. METHODS: In order to specifically quantify CYP11B1, CYP11B2 (aldosterone synthase) and CYP17(17alpha-hydroxylase) mRNA levels, we developed a real-time RT-PCR assay and examined the expression in a series of adrenal tIssues, including six normal adrenals from patients adrenalectomized for renal cancer and twelve aldosterone-producing adenomas (APA) from patients with primary aldosteronism. RESULTS: CYP11B1 mRNA levels were clearly detected in normal adrenals, which comprised both zona glomerulosa and fasciculata/reticularis cells, but were also measured at a lower range (P<0.05) in APA. The levels of CYP11B2 mRNA were lower (P<0.005) in normal adrenals than in APA. CYP17 mRNAlevels were similar in normal adrenals and in APA. In patients with APA, CYP11B2 and CYP11B1 mRNA levels were not correlated either with basal aldosterone or with the change from basal aldosterone in response to posture or to dexamethasone. No correlation between CYP11B1 mRNA or CYP11B2 mRNA and the percentage of zona fasciculata-like cells was observed in APA. CONCLUSIONS: Real-time RT-PCR can be reliably used to quantify CYP11B1 and CYP11B2 mRNA levels in adrenal tIssues. Expression of CYP11B1 in hyperfunctioning zona glomerulosa suggests an additional formation of corticosterone via 11beta-hydroxylase, providing further substrate for aldosterone biosynthesis. CYP11B1 and CYP11B2 mRNA levels in APA are not related to the in vivo secretory activity of glomerulosa cells, where post-transcriptional factors might ultimately regulate aldosterone production.

ADRENAL POTASSIUM AND SODIUM IN EXPERIMENTAL HYPER- AND HYPOALDOSTERONISM IN THE RAT. DETERMINATION BY ELECTRON PROBE X-RAY MICROANALYSIS

1975 ◽  
Vol 80 (1) ◽  
pp. 114-125 ◽  
Author(s):  
Katalin Sz. Szalay ◽  
Ernö Bácsy ◽  
Ervin Stark
Keyword(s):  
Electron Probe ◽  
Sodium Content ◽  
Zona Glomerulosa ◽  
Potassium Content ◽  
Zona Fasciculata ◽  
Aldosterone Secretion ◽  
X Ray ◽  
Intracellular Potassium

ABSTRACT Potassium and sodium contents in the various adrenal zones were determined in experimental hyper- and hypoaldosteronism in the rat by electron probe X-ray microanalysis. The analysis aimed at revealing intracellular values. There was no change in the potassium content of the zona glomerulosa, zona fasciculata and medulla neither in hyperaldosteronism, induced by Na-deficiency, nor in hypoaldosteronism, elicited by Na-rich diet. The sodium content in the zona glomerulosa and zona fascicularis was increased in the Na-loaded rats, while that of the medulla was not changed. Our data are not consistent with the hypothesis that a change of adrenal intracellular potassium would act as a final stimulus in the regulation of aldosterone secretion.

Steroid characteristics of mineralocorticoid adrenocortical hypertension

1991 ◽  
Vol 37 (10) ◽  
pp. 1843-1848 ◽  
Author(s):  
E G Biglieri ◽  
C E Kater
Keyword(s):  
Plasma Renin ◽  
Zona Glomerulosa ◽  
Zona Fasciculata ◽  
Hydroxylase Deficiency ◽  
Aldosterone Production ◽  
Apparent Mineralocorticoid Excess ◽  
Tomography Scan ◽  
Apparent Mineralocorticoid Excess Syndrome ◽  
Hydroxy Steroid ◽  
Steroid Dehydrogenase

Abstract Adrenocortical causes of hypertension are established by examining the mineralocorticoid hormones produced in the zona glomerulosa and zona fasciculata. In the zona glomerulosa, aldosterone excess leads to hypertension, hypokalemia, and suppressed plasma renin activity, with increased concentrations of urinary aldosterone (either as the 18-glucuronide or free aldosterone) as an index of its production. Identifying a tumor by computed tomography scan verifies the diagnosis of a correctable lesion. If no tumor is found, several maneuvers are used to identify primary adrenal hyperplasia, a disorder with autonomous aldosterone production, for which reduction of adrenal mass is curative. The zona fasciculata has two major pathways: the 17-deoxy pathway, where deoxycorticosterone (DOC) and corticosterone are the significant steroids, and the 17-hydroxy pathway, which leads to cortisol production. Tumors of the 17-deoxy pathway, DOC-producing adenomas, have increased concentrations of DOC and its precursor steroids, normal concentrations of cortisol, and suppression of aldosterone production secondary to suppression of the renin system. Two enzymatic defects in the zona fasciculata, 11 beta- and 17 alpha-hydroxylase deficiency, can be first readily identified by the virilization in the former, hypogonadal features in the latter. Steroid patterns are diagnostic. DOC is produced in excess in both deficiencies and is the cause of the hypertension. Deficient or impaired 11 beta-hydroxy steroid dehydrogenase in the apparent mineralocorticoid excess syndrome or after licorice ingestion retards the conversion of cortisol to inactive cortisone in the kidney, leading to mineralocorticoid hypertension; this leads to suppression of the renin system and subsequently of aldosterone.

Electrical responses in cat adrenal cortex: possible relation to aldosterone secretion.

1979 ◽  
Vol 237 (2) ◽  
pp. E158 ◽  
Author(s):  
E Natke ◽  
E Kabela
Keyword(s):  
Membrane Potential ◽  
Angiotensin Ii ◽  
Adrenal Cortex ◽  
Adrenal Glands ◽  
Membrane Depolarization ◽  
Zona Glomerulosa ◽  
Membrane Potentials ◽  
Zona Fasciculata ◽  
Aldosterone Secretion ◽  
Stimulus Secretion Coupling

The effects of secretagogues for aldosterone release were studied on the membrane potential of cells in the adrenal cortex of the cat. Adrenal glands were excised, sliced, and continuously superfused. Membrane potentials were recorded from both zona glomerulosa and zona fasciculata-reticularis. Secretagogues, angiotensin II (1 microgram/ml) and 20 mM KCl, were found to depolarize cells rapidly. Ouabain (10(-5) M) also depolarized the membrane potential although the response was sluggish. Samples of the superfusate were collected and analyzed by radioimmunoassay for their aldosterone and cortisol content. Depolarizing concentrations of angiotensin II, KCl, and ouabain seemed to increase aldosterone release. Cortisol output was more variable. Saralasin blocked the effects of angiotensin II on the membrane potential. These experiments suggest that membrane depolarization plays a role in the stimulus-secretion coupling of mineral corticoids.

scholarly journals Hypothalamic-pituitary-adrenal axis in lethal canine Staphylococcus aureus pneumonia

2014 ◽  
Vol 307 (11) ◽  
pp. E994-E1008 ◽  
Author(s):  
Irene Cortés-Puch ◽  
Caitlin W. Hicks ◽  
Junfeng Sun ◽  
Steven B. Solomon ◽  
Peter Q. Eichacker ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Septic Shock ◽  
Hpa Axis ◽  
Strong Relationship ◽  
High Dose ◽  
Acth Stimulation ◽  
Hypothalamic Pituitary Adrenal ◽  
Free Cortisol ◽  
Poor Outcomes ◽  
Staphylococcus Aureus Pneumonia

The clinical significance and even existence of critical illness-related corticosteroid insufficiency is controversial. Here, hypothalamic-pituitary-adrenal (HPA) function was characterized in severe canine Staphylococcus aureus pneumonia. Animals received antibiotics and titrated life-supportive measures. Treatment with dexamethasone, a glucocorticoid, but not desoxycorticosterone, a mineralocorticoid, improves outcome in this model. Total and free cortisol, adrenocorticotropic hormone (ACTH). and aldosterone levels, as well as responses to exogenous ACTH were measured serially. At 10 h after the onset of infection, the acute HPA axis stress response, as measured by cortisol levels, exceeded that seen with high-dose ACTH stimulation but was not predictive of outcome. In contrast to cortisol, aldosterone was largely autonomous from HPA axis control, elevated longer, and more closely associated with survival in early septic shock. Importantly, dexamethasone suppressed cortisol and ACTH levels and restored ACTH responsiveness in survivors. Differing strikingly, nonsurvivors, sepsis-induced hypercortisolemia, and high ACTH levels as well as ACTH hyporesponsiveness were not influenced by dexamethasone. During septic shock, only serial measurements and provocative testing over a well-defined timeline were able to demonstrate a strong relationship between HPA axis function and prognosis. HPA axis unresponsiveness and high aldosterone levels identify a septic shock subpopulation with poor outcomes that may have the greatest potential to benefit from new therapies.

scholarly journals Oxygen-dependence of ACTH-stimulated aldosterone and corticosterone synthesis in the rat adrenal cortex: developmental aspects

2002 ◽  
Vol 172 (3) ◽  
pp. 595-604 ◽  
Author(s):  
ED Bruder ◽  
AK Nagler ◽  
H Raff
Keyword(s):  
Enzyme Activity ◽  
Age Groups ◽  
Maximal Activity ◽  
Zona Glomerulosa ◽  
Zona Fasciculata ◽  
Steroid Synthesis ◽  
Camp Generation ◽  
Aldosterone Production ◽  
Health And Disease

The control of ACTH-stimulated steroidogenesis under decreasing levels of O(2) is not fully understood. The purpose of this study was to examine the effects of decreased O(2) in vitro on rat adrenocortical steroid synthesis at different stages of development. Of interest was the evaluation of the effect of low O(2) on steroidogenesis during the stress hyporesponsive period of the neonate. Rats were killed at 7, 14, or 42 days of age, adrenals collected and capsules (zona glomerulosa, ZG) separated from subcapsules (zona fasciculata/reticularis, ZFR). Cells were dispersed and placed into glass vials each gassed with a different level of O(2) (21, 5, 2, 1, or 0% O(2)). The entire steroidogenic pathway was analyzed by measuring ACTH-stimulated cAMP, corticosterone and aldosterone production during a 2 h incubation. In addition, the early (P450 scc) and late (P450c11 beta and P450 aldo) pathway activities were examined in the presence of cyanoketone. The PO(2) for half-maximal activity (P(50)) for aldosterone synthesis in ZG cells from 7- and 42-day-old rats was approximately 28 mmHg and 7 mmHg respectively, indicating that cells from older rats were more resistant to inhibition by low O(2). The P(50) for cAMP production from the ZG was approximately 14 mmHg for both age groups. The P(50) for corticosterone synthesis was approximately 28 mmHg and <7 mmHg in ZFR cells from 7- and 42-day-old cells respectively. The only enzyme activities affected by low O(2) (<35 mmHg) were P450 aldo and P450 scc. Moderate decreases in O(2) (from approximately 150 mmHg) decreased aldosteronogenesis, possibly due to observed decreases in cAMP generation, but not due to decreases in steroidogenic enzyme activity (7-day-old). Severe decreases in O(2) presumably inhibited P450 aldo through a direct effect on enzyme activity (both ages). P450 scc activity (including cholesterol transport) also seems to be decreased by very low O(2) (7-day-old). These findings illustrate a novel developmental alteration in O(2)-regulated steroid production, and may have implications for neonatal health and disease.

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