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PubMed1982

Primary aldosteronism: effects of inhibition of ACTH and potassium administration on plasma aldosterone concentration.

The relative roles of ACTH, angiotensin and potassium in influencing aldosterone secretion in primary aldosteronism were assessed by direct or indirect means. In untreated patients with primary aldosteronism caused either by adrenal adenoma or hyperplasia plasma aldosterone and cortisol concentrations fluctuated in unison and dexamethasone reduced both hormones markedly. Only when renin-angiotensin system was greatly activated and plasma potassium normalized by medical treatment was dexamethasone less successful in lowering plasma aldosterone concentration. Potassium infusion of 10,20 and 30 mEq/hr in patients with adenoma failed to elicit any increase in plasma aldosterone concentration despite significant increases in plasma potassium levels. These results suggest that patients with primary aldosteronism due to adrenal adenoma are relatively more sensitive to small changes in plasma ACTH level than those in plasma angiotensin or potassium levels. In recumbent patients with adrenal hyperplasia ACTH also modulates plasma aldosterone concentration.

Adenoma↗
PubMed2001

Screening for primary aldosteronism--normal ranges for aldosterone and renin in three South African population groups.

OBJECTIVE: To establish normal ranges for plasma aldosterone, renin and aldosterone/renin (A/R) ratio in South African normotensives under typical outpatient conditions, and to estimate the prevalence of primary aldosteronism (PA) among hypertensives in primary care settings. DESIGN AND METHODS: One hundred and thirty-six normotensive subjects and 154 sex- and age-matched hypertensives at three primary care clinics had measurements of blood pressure, plasma creatinine, K+, aldosterone, plasma renin activity, and spot urine for urinary Na+/creatinine ratio. Medication was not withdrawn before testing. RESULTS: Mean plasma renin activity in black normotensive subjects (0.95 +/- 1.25 ng/ml/h, mean +/- standard deviation (SD)) was significantly lower than in white (2.09 +/- 1.12 ng/ml/h; P < 0.0001) and coloured (1.81 +/- 1.86 ng/ml/h, P = 0.013) normotensives. Mean plasma aldosterone in black normotensives (306 +/- 147 pmol/l) was also significantly lower than in white (506 +/- 324 pmol/l, P = 0.0002) and coloured (418 +/- 304 pmol/l, P = 0.0148) normotensives. In hypertensives, there were no significant differences in renin or aldosterone levels between the three population groups. Urinary Na+/creatinine ratios, an index of Na+ intake, were not significantly different in the three population groups. None of the normotensives had an A/R ratio > or = 1,000 plus aldosterone > or = 750, while 7.1% of hypertensives exceeded these levels, suggesting that they are appropriate criteria for screening for PA. CONCLUSIONS: A large fraction of black normotensive subjects had low renin and aldosterone levels compared with whites, suggesting a salt-retaining tendency in black subjects. These results have important implications for the interpretation of plasma renin and aldosterone levels in hypertensive patients. In primary care settings, 7.1% of hypertensives had biochemical results indicating the need for investigation of PA.

Aldosterone↗
PubMed1976

The dexamethasone-modified adrenal scintiscan in hyporeninemic aldosteronism (tumor versus hyperplasia). A comparison with adrenal venography and adrenal venous aldosterone.

The dexamethasone-modified adrenal scintiscan, a noninvasive procedure, is described for the preoperative distinction between primary aldosteronism (aldosterone-producing ademona) and idiopathic aldosteronism (bilateral hyperplasia) and for the preoperative localization of aldostersone-producing adenomas. This procedure has been carried out on 17 subsequently proved cases of primary aldosteronism and nine cases (four unexplored) of idiopathic aldosteronism. In the tumor cases, it indicated correctly the side of the tumor in 88 per cent. It was correct in predicting the existence of bilateral hyperplasia in all of the five cases explored. It produced the same response in four more cases believed to have bilateral hyperplasia, in which surgical exploration has not been carried out. Many of the same patients had, in addition, standard adrenal scintiscans (SS), adrenal venography, and determinations of aldosterone in adrenal venous blood. These results are compared with those of the dexamethasone scintiscan (DS). In tumor localization, the 88 per cent figure for the DS was only moderately better than that of the other three (71 per cent, SS; 80 per cent, venography; 80 per cent, adrenal venous aldosterone levels). However, in predicting bilateral hyperplasia, the DS was 100 per cent correct, as were the levels of aldosterone in adrenal venous blood. The SS and adrenal venography failed in bilateral hyperplasia and gave many false-positive results indicating tumor. The DS, a relatively simple outpatient procedure, appears to be at least as effective, both in lateralizing tumors and distinguishing between tumor and bilateral hyperplasia, as the more difficult, expensive, and sometimes hazardous invasive procedure of bilateral adrenal vein catheterization.

Adolescent↗
PubMed2005

Analysis of unilateral adrenal hyperplasia with primary aldosteronism from the aspect of messenger ribonucleic acid expression for steroidogenic enzymes: a comparative study with adrenal cortices adhering to aldosterone-producing adenoma.

Unilateral adrenal hyperplasia with primary aldosteronism is very rare and shows similar endocrine features to aldosterone-producing adenoma and bilateral adrenal hyperplasia. In this study, the mRNA expression of steroidogenic enzymes in unilateral adrenal hyperplasia was examined by in situ hybridization. We found subcapsular micronodules composed of spironolactone body-containing cells, which showed intense expression for 3beta-hydroxysteroid dehydrogenase, 11beta-hydroxylase, 18-hydroxylase, and 21-hydroxylase but not 17alpha-hydroxylase, indicating aldosterone production. This expression pattern was the same as that in unilateral multiple adrenocortical micronodules, reported recently. Additionally, it was noted that a nodule with active aldosterone production was closely adjacent to one showing intense 17alpha-hydroxylase expression. In the adrenal cortices adhering to aldosterone-producing adenoma, the majority of hyperplastic zona glomerulosa and hyperplastic nodules demonstrated a decreased steroidogenic activity. However, minute nodules indicative of active aldosterone production were found at high frequency. These results suggest that the subcapsular micronodules observed might be the root of aldosterone-producing adenoma. Furthermore, we emphasize the need for long-term follow-up after unilateral adrenalectomy or enucleation of the adenoma because of the possibility that buds with autonomous aldosterone production may still be present in the contralateral or remaining adrenal tissue.

3-Hydroxysteroid Dehydrogenases↗
PubMed1986

Abnormality of circulatory reflex and aldosterone response during head-up tilting in patients with primary aldosteronism.

Abnormality of the circulatory reflexes has been reported in patients with primary aldosteronism. However, changes in blood pressure, heart rate, plasma renin activity (PRA), and plasma aldosterone concentration (PAC) after head-up tilting in primary aldosteronism have not yet been reported. Seven patients with primary aldosteronism were tilted to a 65 degree head-up position which was maintained for 30 min. Systolic blood pressure decreased significantly 5 min after tilting and remained at this level during the period of tilting. Diastolic blood pressure did not change during the tilting. Heart rate increased after 5 min of tilting and this level of heart rate was maintained for 30 min. Plasma renin activity was low and did not change during tilting. However, plasma aldosterone concentration increased significantly 20 min after tilting. Plasma cortisol concentration and plasma ACTH concentration also increased significantly. These results suggest that primary aldosteronism causes abnormalities of the circulatory reflexes. The increase of endogenous ACTH may increase plasma aldosterone concentration in patients with primary aldosteronism.

Adrenocorticotropic Hormone↗
PubMed2001

Validity of the aldosterone-renin ratio used to screen for primary aldosteronism.

OBJECTIVE: To determine whether the calculated ratio of plasma aldosterone concentration (PAC) to plasma renin activity (PRA), a proposed screening test for primary aldosteronism, provides a renin-independent measure of circulating aldosterone that is suitable to judge whether PAC is inappropriately elevated relative to PRA. SUBJECTS AND METHODS: This study consisting of 221 black and 276 white subjects with previously diagnosed essential hypertension was conducted between 1996 and 2000. Antihypertensive drugs were withdrawn for at least 4 weeks; PAC and PRA were measured while subjects were supine and then seated after 30 minutes of ambulation. The seated measurements were repeated after 4 weeks of oral diuretic therapy with hydrochlorothiazide (25 mg/d). RESULTS: The variation in the aldosterone-renin ratio was strongly and inversely dependent on PRA (R2=0.71; P<.001). When subjects changed position from supine to seated, the increase in mean +/- SD PRA (from 1.18 +/- 1.06 to 1.31 +/- 1.19 ng x mL(-1) x h(-1); P<.001) was associated with an increase in the mean ratio (from 18.6 +/- 52.8 to 25.8 +/- 38.1 h x 10(2); P<.001), whereas the increase in mean +/- SD PRA in response to diuretic therapy (from 1.31 +/- 1.19 to 2.72 +/- 2.67 ng x mL(-1) x h(-1); P=.007) was associated with a decrease in the mean ratio (from 25.8 +/- 38.1 to 16.4 +/- 31.6 h 10(2); P<.001). CONCLUSION: In patients with previously diagnosed essential hypertension, calculation of the aldosterone-renin ratio does not provide a renin-independent measure of circulating aldosterone that is suitable for determining whether PAC is elevated relative to PRA. Because elevation of the aldosterone-renin ratio is predominantly an indicator of low PRA, its perceived value in screening for primary aldosteronism most likely derives from additional diagnostic tests being done in patients with low-renin hypertension.

Age Distribution↗
PubMed1993

Different effects of three aldosterone treatments on plasma aldosterone and salt intake.

Adrenalectomized male rats received a nominal dose of 47.6 micrograms/day aldosterone for 14 days by daily injections, osmotic minipumps, or controlled-release pellets. Plasma aldosterone concentrations were barely detectable (< 20 pg/ml) 24 h after rats received aldosterone by injection, remained constant at 200 pg/ml in rats with osmotic minipumps, and dropped from > 500 to 75 pg/ml during the first week after implantation of controlled-release pellets. For the most part, the effects of the different treatments on NaCl intake were related to their effects on plasma aldosterone levels according to a U-shaped function. However, NaCl intake was dissociated from plasma aldosterone levels when treatment first began or was discontinued. NaCl intake may be a function of the amount of aldosterone delivered but not necessarily plasma aldosterone concentration.

Adrenal Glands↗
PubMedDate not supplied

The effects of infusions of ring-A-reduced derivatives of aldosterone on the antinatriuretic and kaliuretic actions of aldosterone.

Infusion of Ring-A-reduced metabolites of aldosterone in adrenalectomized male rats for 4 days revealed that 5 alpha-Ring-A-reduced derivatives, 5 alpha-dihydroaldosterone (5 alpha-DHAldo; 2.5-5.0 micrograms/day), 3 alpha,5 alpha-tetrahydroaldosterone (3 alpha,5 alpha-THAldo; 5-25 micrograms/day), and 3 beta,5 alpha-THAldo (50-175 micrograms/day) possessed intrinsic Na+-retaining activity. The same infusions of 5 alpha-DHAldo, 3 alpha,5 alpha-THAldo, and 3 beta,5 alpha-THAldo, also lowered the urinary excretion of potassium. The 5 beta-Ring-A-reduced derivative 3 alpha,5 beta-THAldo did not demonstrate either of these biological properties. In another set of experiments, on the fourth day of infusion, aldosterone (0.1 microgram/rat) was administered acutely subcutaneously; none of the Ring-A-reduced derivatives altered the Na+-retaining activity of aldosterone. However, in a dose-dependent manner, both 3 alpha,5 alpha-THAldo and 3 beta,5 alpha-THAldo blunted the urinary K+-secretory effect of aldosterone; low dosages of 5 alpha-DHAldo and larger dosages of 3 alpha,5 beta-THAldo did not. Thus, the 5 alpha-reduced derivatives of aldosterone not only lowered urinary Na+ and K+ excretion in their own right, but two of them blunted the kaliuretic response of the parent mineralocorticoid, aldosterone. Further experiments will be required to determine whether these aldosterone metabolites are further metabolized or interconverted during the expression of the regulatory properties described here and whether these properties are physiologically relevant.

Aldosterone↗
PubMed2003

Endothelin receptor blockade lowers plasma aldosterone levels via different mechanisms in primary aldosteronism and high-to-normal renin hypertension.

BACKGROUND: Endothelin (ET)-1 contributes to raising blood pressure (BP) and inducing cardiovascular disease by vasoconstriction and potent stimulation of aldosterone secretion. In the rat this latter effect occurs via ET(B) receptors; in humans in vitro studies implicated both ET(A) and ET(B) receptors, but there is no conclusive evidence in vivo. METHODS: We recruited 13 consenting hypertensive patients: six with primary aldosteronism (PA) and seven with high-to-normal renin hypertension (HNRH). They were infused with a low dose (200 nmol/min for 5 min followed by 100 nmol/min for 10 min) of the ET(A)-selective antagonist BQ-123 either alone or, on a different day, together with an identical dose of the ET(B)-selective antagonist BQ-788. Plasma aldosterone, cortisol and ACTH concentration and plasma renin activity (PRA) were measured with radioimmunoassay at -15, 0, 30, 60, 120, 240, 360 min, while BP was recorded non-invasively. RESULTS: BQ-123 alone and combined with BQ-788 significantly lowered mean BP in both PA and HNRH patients (by 6-10 mmHg at nadir; P<0.01). In PA patients, a short-lived decrease of aldosterone was elicited by combined BQ-123 and BQ-788 (-14%; P<0.05), but not by BQ-123 alone; cortisol, ACTH, and PRA were unaffected by either treatment. In HNRH patients, BQ-123 both alone and combined with BQ-788 lowered aldosterone (-39 and -28%, respectively) and PRA (-43 and -16%, respectively), while cortisol and ACTH were unaffected. CONCLUSIONS: Endogenous ET-1 contributes to maintaining the high BP values and the aldosterone secretion in both PA and HNRH patients. In the former patients, the aldosterone secretagogue effect of ET-1 is mediated via ET(B) receptors, while in the latter it occurs mainly via ET(A)-mediated stimulation of renin production.

Adrenocorticotropic Hormone↗
PubMed1986

Endogenous dopaminergic inhibition of aldosterone and prolactin secretion is apparently not increased in primary aldosteronism.

To examine the previous suggestion that the endogenous dopaminergic activity would be increased in patients with primary aldosteronism, dose-response curves of aldosterone and prolactin stimulation by the dopamine antagonist metoclopramide were established in a pilot study by injecting metoclopramide 1, 2.5, and 10 mg i.v. consecutively at hourly intervals to 6 patients with primary aldosteronism and 14 healthy volunteers. All three metoclopramide doses induced clear-cut rises in aldosterone levels both in patients with primary aldosteronism and healthy controls. Basal aldosterone concentration was higher in range in the patients but the dose-response curves were nearly parallel one with the other. Prolactin responsiveness was also very similar. Thus, the present findings do not support the hypothesis of an increase in endogenous dopaminergic activity in primary aldosteronism.

Adult↗
PubMed2004

Active renin versus plasma renin activity to define aldosterone-to-renin ratio for primary aldosteronism.

BACKGROUND: In recent years, the assessment of the plasma aldosterone-to-renin ratio (ARR) has become an established screening method for the diagnosis of primary aldosteronism. Plasma renin activity (PRA) is usually measured to define ARR although, increasingly, renin concentration alone is often measured in clinical routine. OBJECTIVE: To determine the threshold of ARR using active renin concentration to screen for primary aldosteronism. DESIGN AND PARTICIPANTS: To determine the ARR threshold based on plasma immunoreactive renin concentration (irR), we measured plasma aldosterone concentration (PAC), irR and PRA in 36 hypertensive patients, nine thereof with adrenal adenoma, and compared ARRs calculated from irR and PRA, respectively. SETTING: Single-centre, hypertension clinic in a tertiary care hospital. RESULTS: PRA ranged from 0.41-14.9 ng/ml per h and irR from 1.1-72 ng/l. There was an excellent correlation between PRA and irR (r = 0.98, P < 0.0001) and between ARRPRA and ARRirR (r = 0.96, P < 0.0001). An ARRPRA > 750 pmol/l per ng/ml per h was previously found to be highly predictive of primary aldosteronism because 90% of the corresponding patients failed to suppress PAC upon saline infusion or fludrocortisone. The corresponding threshold value for ARRirR was 150 pmol/ng in our patients. Using these cut-offs, nine subjects had both increased ARRPRA and ARRirR while, in three patients, either ARRPRA or ARRirR were increased. The nine patients with increased ARRPRA and ARRirR also had PAC > 650 pmol/l. Only these patients had adrenal adenomas. CONCLUSIONS: The ARR threshold to screen for primary aldosteronism may be based on measurement of irR. An ARRirR > 150 pmol/ng may indicate primary aldosteronism.

Adenoma↗
PubMed2007

Aldosterone as a key mediator of the cardiometabolic syndrome in primary aldosteronism: an observational study.

OBJECTIVE: Primary aldosteronism (PA) is characterized by the onset of both cardiac and gluco-metabolic alterations. The aim of this study was to evaluate the impact of aldosterone excess on the development of such complications, and the effects of surgical and pharmacological treatment on their long-term outcome. METHODS: We prospectively re-examined 61 patients: 25 with aldosterone-producing adenoma (APA), after surgery, and 36 patients with idiopathic hyperaldosteronism (IHA) on pharmacological treatment. The lipid, fasting and dynamic glucose profiles and the echocardiographic parameters were evaluated at diagnosis and at follow-up. RESULTS: After adrenalectomy all patients had normalization of aldosterone levels and were cured of hypokalaemia, and a resolution of hypertension was achieved in 12 of 25 patients. APA patients showed a significant reduction of both plasma glucose (P=0.017) and insulin levels (P=0.001) after 75 g oral glucose tolerance test. Stabilization of glucose metabolism complications was observed in IHA patients. Multiple regression analysis at diagnosis showed a positive correlation between homeostasis model assessment (HOMA) insulin resistance index and HOMA beta cell and serum aldosterone levels in both APA and IHA. Echocardiographic parameters were improved in both APA and IHA at follow-up and the difference was statistically significant for left ventricular mass index (P=0.017) and interventricular septum thickness (P=0.007) in APA patients. CONCLUSIONS: The removal of aldosterone excess in APA patients induces the regression of both cardiac and gluco-metabolic complications, indicating aldosterone as a main determinant of such alterations. In IHA patients the medical treatment seems to avoid the possible progression of the these alterations that appear to be stable.

Adenoma↗
PubMed1980

Aldosterone regulation in primary aldosteronism: influence of salt balance, posture and ACTH.

The response of aldosterone to manipulations of the renin-angiotensin and hypothalamic-pituitary-adrenal systems has been studied in thirteen patients with primary aldosteronism due to a single adenoma (ten patients) or bilateral hyperplasia (three patients). The aldosterone response to dietary sodium restriction was small and variable, although urinary aldosterone excretion increased in nine out of twelve studies. The response of patients with hyperplasia could not be distinguished from those with adenoma. All patients were unresponsive to salt loading. By contrast, plasma aldosterone fell in all patients after overnight dexamethasone (1 mg) and increased after brief (1 h) physiological ACTH stimulation. During prolonged erect posture, plasma aldosterone increased in the three patients with hyperplasia and decreased or remained unchanged in patients with ademona. Changes in plasma renin activity were similar in both groups. These studies show that patients with primary aldosteronism, while largely unresponsive to manipulations of sodium balance, retain sensitivity to small and acute changes in ACTH. The different behaviour of patients with hyperplasia to prolonged erect posture cannot be explained by insensitivity to ACTH, but could be due to a relative increase in sensitivity to angiotensin.

Adenoma↗
PubMed2003

Short-term aldosterone action on Na,K-ATPase surface expression: role of aldosterone-induced SGK1?

Aldosterone controls extracellular volume and blood pressure by regulating Na(+) reabsorption across epithelial cells of the aldosterone-sensitive distal nephron (ASDN). This effect is mediated by a coordinate action on the luminal channel ENaC (generally rate limiting) and the basolateral Na,K-ATPase. Long-term effects of aldosterone (starting within 3 to 6 hours and increasing over days) are mediated by the direct and indirect induction of stable elements of the Na(+) transport machinery (e.g., Na,K-ATPase alpha subunit), whereas short-term effects appear to be mediated by the upregulation of short-lived elements of the machinery (e.g., ENaC alpha subunit) and of regulatory proteins, such as the serum- and glucocorticoid-regulated kinase SGK1. We have recently shown that in cortical collecting duct (CCD) from adrenalectomized (ADX) rats, the increase in Na,K-ATPase activity (approximately threefold in 3 h), induced by a single aldosterone injection, can be fully accounted for by the increase in Na,K-ATPase cell-surface expression. Using the model cell line mpkCCD(cl4), we showed that the parallel increase in Na,K-ATPase function [assessed by Na(+) pump current (I(p)) measurements] and cell-surface expression depends on transcription and translation, and that it is not secondary to a change in apical Na(+) influx. As a first approach to address the question whether the aldosterone-induced regulatory protein SGK1 might play a role in mediating Na,K-ATPase translocation, we have used the Xenopus laevis expression system. SGK1 coexpression indeed increased both the Na(+) pump current and the surface expression of pumps containing the rat alpha1 subunits. In summary, aldosterone controls Na(+) reabsorption in the short term not only by regulating the apical cell-surface expression of ENaC but also by coordinately acting on the basolateral cell-surface expression of the Na,K-ATPase. Results obtained in the Xenopus oocyte expression system suggest the possibility that this effect could be mediated in part by the aldosterone-induced kinase SGK1.

Aldosterone↗
PubMed1996

Hypoxia in vivo inhibits aldosterone synthesis and aldosterone synthase mRNA in rats.

Hypoxia leads to a decrease in aldosterone that cannot be entirely explained by extrinsic controllers of adrenal function. We have shown that acute hypoxia attenuates aldosterone synthesis via a direct inhibition of the function of the aldosterone enzyme pathway. The mechanism of the sustained decrease in aldosterone during chronic hypoxia is unknown. The present study evaluated the hypothesis that chronic hypoxia leads to a decrease in the expression of the steroidogenic enzyme P-450c11AS unique to the aldosterone pathway. Rats were exposed to 3 days of normoxia, moderate hypoxia (12% O2), or severe hypoxia (10% O2). Adrenal glands were removed and prepared for biochemical analysis of steroidogenesis in vitro (dispersed capsular cells) and for measurement of steady-state enzyme mRNA levels by reverse-transcription competitive polymerase-chain reaction (RT-cPCR) and by in situ hybridization histochemistry (ISHH). Moderate hypoxia had no effect on steroidogenesis. Adrenal cells from rats exposed to severe hypoxia demonstrated a decreased conversion of corticosterone to aldosterone (late pathway catalyzed by P-450c11AS) without a change in the other mitochondrial cytochrome P-450 enzyme activities. Adrenal cells from rats exposed to hypoxia also demonstrated a three- to fourfold decrease in P-450c11AS mRNA without a change in the other mitochondrial cytochrome P-450 enzymes mRNAs, as determined by either RT-cPCR or ISHH. We conclude that relatively short-term chronic hypoxia in rats leads to a decrease in aldosteronogenesis by decreasing the expression of the gene for the late-pathway enzyme unique to the aldosterone pathway (P-450c11AS).

Aldosterone↗
PubMed1978

Studies of plasma aldosterone in anephric people: evidence for the fundamental role of the renin system in maintaining aldosterone secretion.

When plasma aldosterone (PA) was measured in 32 predialysis samples from 18 anephric subjects more than 3 months postnephrectomy, all but two values were subnormal, 16 measurements were undetectable, i.e. below 0.35 ng/100 ml, and PA averaged only 1.7 ng/100 ml +/- 0.5 (SE) in the remaining 16. In contrast, PA averaged 29.7 +/- 5.6 ng/100 ml in 12 dialysis patients with kidneys. Plasma renin activity was undetectable in 15 assays of anephric subjects and averaged 0.5 +/- 0.1 ng/ml/h in the remaining 17. However, these latter measurements appeared to be an artifact caused by the presence of plasma prorenin. Serum potassium fell during dialysis and appeared responsible for the concurrent 75% fall in PA observed in six nephric patients (delta 14 ng/100 ml), and in three anephric patients (delta 3.3 ng/100 ml) with low but measurable PA values. Overt hyperkalemia was required for potassium to stimulate aldosterone into the normal range in anephric subjects. The angiotensin II analog, saralasin, also increased PA slightly in five studies. Renin and PA fell after nephrectomy and increased after transplantation. Decreases and increases in renin always preceded those of aldosterone. Usually it took several weeks for aldosterone to fall to undetectable levels and several days to return to normal levels after renal transplantation. These observations suggest that the baseline plasma level of angiotensin determines both the baseline level of aldosterone secretion and its capacity to respond either to more angiotensin or to other stimuli. In the absence of renin, the adrenal almost loses its capacity to generate aldosterone. The data support the view that the renin system plays a fundamental role in maintaining aldosterone secretion in man.

Aldosterone↗
PubMed1992

Endothelin stimulates aldosterone secretion in vitro from normal adrenocortical tissue, but not adenoma tissue, in primary aldosteronism.

In addition to vasoconstriction, endothelin (ET) has been reported to show various endocrine actions in animals. However, no data have emerged concerning the effect of ET on adrenal function in humans. We, therefore, investigated the effects of ET on aldosterone and cortisol secretion from adrenocortical tissues obtained from normal subjects (n = 6) and patients with primary aldosteronism (n = 5). Adrenal tissue slices were incubated at 37 C for 120 min in modified Krebs-Ringer solution containing glucose and HEPES. ET increased aldosterone secretion from normal adrenocortical tissue in a dose-dependent manner, with an ED50 of 0.036 nmol/L, although the maximum response was small compared with that to angiotensin-II. ET also stimulated aldosterone secretion from tissues adjacent to the adenoma, but not from the adenoma, in patients with primary aldosteronism. The effects of ET on aldosterone secretion were significantly suppressed by calcium channel blockade with nicardipine. ET did not affect cortisol secretion from the adrenal tissues. These results suggest that ET is one of the factors that regulates aldosterone secretion in humans.

Adenoma↗
PubMed1997

Impaired potassium-stimulated aldosterone production: a possible explanation for normokalemic glucocorticoid-remediable aldosteronism.

Unlike other forms of primary aldosteronism, recent prospective studies have paradoxically revealed that glucocorticoid-remediable aldosteronism (GRA) is usually characterized by normal potassium (K+) levels. To evaluate this paradox we studied 10 GRA subjects and 14 healthy controls in two protocols: 1) the renal K+ excretory response to acute oral administration of 50 mmol K+ chloride and to fludrocortisone, 0.2 mg p.o. q12 h x 4 doses; and 2) the aldosterone response to administration of 50 mmol K+ chloride. The K+ excretion rate (KER) in GRA subjects (n = 6) at baseline (45.6 +/- 8.3 microEq/min), after K+ (134 +/- 34.2 microEq/min), and after fludrocortisone (100 +/- 35.0 microEq/min) was not significantly different than that seen in the control (n = 8) subjects (54.9 +/- 19.0, 154 +/- 35.5, 112 +/- 45.8 microEq/min, respectively). Thus the renal kaliuretic response to K+ ingestion and exogenous mineralocorticoid is normal in GRA. Serum aldosterone increased from 5.0 +/- 3.8 at baseline to a maximum of 13.1 +/- 6.6 ng/dL 60 min after K+ ingestion in control subjects (n = 7), but failed to increase in GRA subjects (n = 14), going from 8.7 +/- 3.8 (baseline) to 8.8 +/- 5.4 ng/dL at 60 min (P = 0.004 vs. control). The blunted aldosterone response to K+ in GRA in association with the sharp diurnal decline in aldosterone in this ACTH-regulated syndrome probably results in a milder degree of hyperaldosteronism compared with other forms of primary aldosteronism, thereby producing volume expansion with minimal renal K+ wasting.

Adult↗