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At least 19 recordsLinked to original sources
PubMed1989

Idiopathic aldosteronism masquerading as discrete aldosterone-secreting adrenal cortical neoplasms among patients with primary aldosteronism.

The medical records of 32 patients with primary aldosteronism who underwent adrenalectomy at the University of Michigan Medical Center from January 1975 to February 1988 were reviewed. All 32 patients had the preoperative diagnosis of aldosterone-secreting adrenal cortical neoplasms. Based on pathology reports, however, 21 of 32 (66%) patients were confirmed to have adrenal cortical neoplasms. Ten of 32 (31%) patients had nodular hyperplasia, and 1 of 32 (3%) had diffuse hyperplasia. This report focuses on the results in 11 patients with idiopathic aldosteronism. In six of nine (67%) patients, aldosterone levels rose within 4 hours of patients assuming an upright posture after salt loading. Seven patients had selective adrenal venous aldosterone/cortisol ratios that were interpreted to lateralize to one adrenal gland; however, only four of seven (57%) had ratios of 3:1 or greater than the contralateral adrenal gland. In 6 of 11 (55%) patients, adrenal scans (NP-59) initially demonstrated unilateral uptake. Three of four computerized axial tomographic scans demonstrated a unilateral adrenal mass. Only 3 of 11 (27%) patients with idiopathic aldosteronism were normotensive after surgery. Four of 11 (36%) patients' conditions were improved, in that they became normotensive with antihypertensive medication. These data suggest that if both imaging and functional studies lateralize to one adrenal gland, it is reasonable to expect either a cure or an improvement after adrenalectomy among patients with primary aldosteronism caused by idiopathic aldosteronism. Unilateral adrenalectomy may be the treatment of choice in carefully selected patients with nodular hyperplasia causing primary aldosteronism.

Adrenal Cortex↗
PubMed1976

Effect of aldosterone antagonist canrenone on plasma aldosterone concentration and plasma renin activity, and on the excretion of aldosterone and electrolytes by man.

Canrenone was administered in doses of 2 x 82 mg and 2 x 164 mg per day over a period of 10 days to diabetic patients without cardiovascular, liver or kidney involvement. Aldosterone excretion and plasma aldosterone increased only slightly during both regimes. There was a clear-cut increase in aldosterone excretion only after discontinuation of canrenone. Excretion of sodium, potassium and fluid was not significantly changed either during or after treatment. The lack of effect of canrenone on the kidney was in contrast to the significant decrease in serum sodium and increase in serum potassium, and the significant, dose-dependent rise in plasma renin activity following canrenone administration. The increased plasma renin activity persisted for some days after discontinuation of canrenone. It is suggested that canrenone primarily exerted its effect in the distal part of the large intestine where ionic movements are most affected by aldosterone. The disproportionately slight increase in plasma aldosterone concentration and aldosterone excretion, in spite of the greatly elevated plasma renin activity and serum potassium level, is considered to be due to a direct inhibitory effect of canrenone on aldosterone production in the adrenals.

Aldosterone↗
PubMed1991

An unexpected rise in plasma aldosterone to furosemide-upright test in primary aldosteronism due to aldosterone producing adenoma.

This paper documents an unexpected rise in plasma aldosterone concentration (PAC) to the furosemide-upright test despite a decrease in adrenocorticotropin (ACTH) by dexamethasone, and an unresponsiveness in plasma renin activity to this stimulus in a patient with aldosterone producing adenoma. Furthermore, this patient showed an appropriate response in PAC to a rapid ACTH test, and an insensitivity in PAC to angiotensin-II (Ang-II) infusion. Other factor(s) besides ACTH or Ang-II may play a role in the plasma aldosterone response to ambulation after intravenous furosemide administration in patients with primary aldosteronism.

Adenoma↗
PubMed1979

Effects of prolonged infusions of potassium chloride, adrenocorticotrophin or angiotensin II upon serum aldosterone concentration and the conversion of corticosterone to aldosterone in rats.

The temporal relation between alterations in serum aldosterone and in the conversion of labelled corticosterone to aldosterone by incubated adrenal tissue was studied in conscious rats receiving long-term infusions of KCl, ACTH or angiotensin II. When potassium-deficient rats were given KCl, a marked increase in serum aldosterone was observed only after 12 h, i.e. at a time when the conversion of corticosterone to aldosterone had become normal. After 24 h of ACTH infusion into sodium- and potassium-replete rats the serum aldosterone was markedly elevated, whereas the conversion of corticosterone to aldosterone was significantly decreased. After 48 h of continued ACTH infusion the serum aldosterone returned to normal and there was a further decrease in the conversion rate. A 24-h angiotensin II infusion into sodium- and potassium-replete rats induced significant increases in both the serum aldosterone and the conversion. After 48 h of continued angiotensin infusion the serum aldosterone returned to normal while the conversion and the blood pressure remained elevated. These results indicate that the activity of the enzymes involved in the final steps of aldosterone biosynthesis may become rate-limiting for the secretion of aldosterone during potassium deficiency and during prolonged ACTH treatment. On the other hand, the observed transiency of aldosterone stimulation by exogenous angiotensin II was not due to a suppression of the final steps of aldosterone biosynthesis and remains unexplained.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Reduced urinary aldosterone excretion rates with normal plasma concentrations of aldosterone in the very elderly.

Although aldosterone production declines with age, so does the aldosterone metabolic clearance rate (MCR), and the net effect of age on the circulating level of aldosterone may be less than can be predicted from production rates alone. The effect of age on aldosterone production and plasma levels was studied in a group of elderly individuals at a very advanced age when susceptibility to the impacts of age might be particularly pronounced. Seventeen nursing home patients, ages 75-99 (mean age 86 years), had aldosterone production assessed from the urinary excretion rate of the acid hydrolyzable 18-glucuronide conjugate of aldosterone. Aldosterone excretion was low in the elderly when compared to a group of healthy, young to middle-aged subjects: 123 +/- 19 (SEM) vs. 234 +/- 18 ng/h (P less than 0.001). However, plasma aldosterone concentrations in the elderly were well within a range observed in much younger and fully ambulatory subjects: 14.1 +/- 1.3 in the elderly vs. 15.9 +/- 1.8 ng/dL in the young. The plasma aldosterone concentration was apparently maintained at a normal level by a coincident decrease in both the metabolic clearance rate and the aldosterone production rate. In conclusion, an aldosterone deficiency state resulting from an age-correlated reduction in aldosterone production is probably uncommon in the elderly.

Aged↗
PubMed1977

Effect of a spirolactone on plasma and urinary aldosterone in primary aldosteronism.

In primary aldosteronism due to an adrenal adenoma (n=2), treatment with a spirolactone (160 mg Canrenone/day for 7 days) decreased plasma aldosterone and urinary aldosterone-18-glucuronide. However, in the presence of a normalization in urinary aldosterone 18-glucuronide plasma aldosterone remained elevated above normal. Continued therapy with higher doses (320 mg/day for 7 days and 480 mg/day for 28 days) did not significantly alter plasma aldosterone, while urinary aldosterone-18-glucuronide returned to values comparable to those obtained before therapy. Cessation of the drug resulted in a marked increase in plasma aldosterone and urinary aldosterone-18-glucuronide. The results indicate that in primary aldosteronism due to an adrenal adenoma, the spirolactone (Canrenone) inhibits aldosterone biosynthesis and seems to influence aldosterone degradation.

Adenoma↗
PubMed1976

Aldosterone regulation in primary aldosteronism: differences between adenoma and bilateral hyperplasia.

1. The diurnal patterns of plasma aldosterone, plasma renin activity (PRA), cortisol and adrenocorticotrophic hormone (ACTH) in the supine and in the upright position have been studied in fourteen patients with primary aldosteronism, five with adenoma and nine with bilateral hyperplasia. Blood samples were drawn at intervals from 6 h to 30 min. 2. Supine patients with an adenoma showed marked diurnal variations of aldosterone, with maximal values at 08.00 hours and minimal values of 18.00 hours and secretory spurts beginning after 02.00 hours. Plasma cortisol paralleled aldosterone, and ACTH seemed to anticipate aldosterone and cortisol variations; PRA remained unchanged. In patients with hyperplasia, aldosterone was significantly lower than in the adenoma group at 08.00 hours, and its decline during the day was less marked; fluctuations rather than secretory episodes were seen. 3. After patients assumed the upright posture, aldosterone remained unchanged or decreased in patients with adenoma, whereas it significantly increased in hyperplasia; PRA remained low, although a slight increment was seen in the latter group. The different response of aldosterone in the two groups was not modified by the administration of propranolol, apparently excluding a renin-dependent mechanism. On the other hand, dexamethasone seemed to affect the response of aldosterone to the upright posture in both groups; in adenoma there was a slight but significant increase, and in hyperplasia the usual rise was partially suppressed. 4. It is concluded that ACTH has a predominant role in regulating aldosterone secretion in primary aldosteronism due to adenoma, whereas its action in bilateral hyperplasia is only permissive.

Adenoma↗
PubMed1975

Regulation of aldosterone secretion in primary aldosteronism.

Plasma aldosterone, plasma renin activity and plasma cortisol were determined in patients with primary aldosteronism in response to posture and at short-time intervals overnight while the patient were supine. In the 5 patients with an aldosterone-producing adenoma postural changes in plasma aldosterone were paralleled by those in cortisol while plasma renin activity was generally undetectable indicating an ACTH-dependent secretion of aldosterone. This concept was supported by the observation that in 3 of these patients who were tested overnight 1. episodic secretion of plasma aldosterone was paralleled by those of cortisol and 2. episodic secretion of plasma aldosterone could be blunted by dexamethasone. In the patient with idiopathic adrenal hyperplasia concomittant changes in plasma aldosterone and plasma renin activity occurred. The assumption that in this patient the fluctuations in plasma aldosterone were mediated through changes in renal renin secretion was supported by the finding that episodic secretion of plasma aldosterone persisted under suppression of ACTH-secretion by dexamethasone. Our results indicate, that the described procedures may all serve as diagnostic criteria to differentiate between aldosterone-producing adenoma and idiopathic adrenal hyperplasia.

Adenoma↗
PubMed1976

Circadian rhythm and effect of posture on plasma aldosterone concentration in primary aldosteronism.

The effect of circadian rhythm and alterations in posture on plasma aldosterone concentration was studied in 13 patients with primary aldosteronism (six adenoma, five idiopathic hyperplasia, two carcinoma) to define the regulatory mechanism in each of these pathologic subtypes. Blood samples for aldosterone, cortisol, renin, and potassium concentrations were obtained every 4 h during prolonged recumbency (32 h) and upright posture (16 h). During recumbency, aldosterone and cortisol followed a normal circadian pattern in patients with adenoma and hyperplasia, with peak values at 0400-0800 h and the nadir at 1600-2400 h. Normalized aldosterone and cortisol values correlated significantly in both groups (adenoma r=+0.66, P less than 0.001; hyperplasia r=+0.42, P less than 0.01). With upright posture, aldosterone levels declined parallel to the normal circadian fall in cortisol in patients with adenoma (r=+0.68, P less than 0.001); whereas aldosterone levels increased in patients with hyperplasia parallel to small increments in renin (r=+0.65, P less than 0.001) and potassium (r=+0.64, P less than 0.001). During the administration of dexamethasone, aldosterone no longer correlated with cortisol in patients with adenoma but continued to correlate with renin during upright studies in patients with hyperplasia (r=+0.77, P less than 0.01). Aldosterone circadian rhythm was abnormal in patients with carcinoma and no effect of posture was noted. Unilateral adrenalectomy restored the normal postural relationship in four patients with adenoma. These studies suggest that aldosterone secretion is under continuous ACTH control regardless of posture in patients with adenoma, whereas persistent adrenal responsiveness to small increments in renin and/or potassium mediate the postural increase in plasma aldosterone in patients with hyperplasia. True adrenal autonomy occurs only in patients with adrenal carcinoma and when ACTH is suppressed in those with adenoma.

Adult↗
PubMed1977

The effects of temperature and plasma cortisol on distribution of aldosterone between plasma and red blood cells: influence on metabolic clearance rate and on hepatic and renal extraction of aldosterone.

Aldosterone enters red blood cells (RBC) to a greater extent at 37 C than at lower temperatures. The ratio of 3H-aldosterone concentration in RBC to that in plasma increases from 0.2 at 4 C to 0.7 at 37 C when cortisol concentration is low. Increasing plasma cortisol increases the RBC/plasma aldosterone ratio. When plasma transcortin (CBG) is saturated with cortisol, the RBC/plasma ratio of 3H-aldosterone approaches 0.93, the ratio observed in RBC incubated in 4% albumin solution. The effects of plasma cortisol and temperature on the RBC/plasma ratio reflect an affinity of aldosterone for plasma CBG greater than the affinity for plasma albumin or RBC. Hepatic extraction averages 92% of plasma and RBC aldosterone. Neither hepatic extraction nor renal extraction (less than or equal to 20%) is significantly altered by changing plasma cortisol concentration. Whole blood MCR of aldosterone is unaffected by redistribution of aldosterone from plasma to RBC when plasma cortisol increases, but both plasma cortisol and the temperature at which blood is separated affect the RBC/plasma ratio of 3H-aldosterone and thus change the calculated plasma MCR. The RBC transport of aldosterone, and its dependence on temperature and plasma cortisol, must be taken into account in the evaluation of plasma aldosterone concentration.

Aldosterone↗
PubMed2026

Aldosterone fuels the progression of cardiovascular-kidney -metabolic syndrome: focus on primary aldosteronism spectrum.

In 2023, the American Heart Association (AHA) introduced the Cardiovascular-Kidney-Metabolic (CKM) syndrome concept to address the substantial burden of interrelated cardiovascular, kidney, and metabolic disorders. The framework highlights that chronic kidney disease (CKD) significantly accelerates CKM syndrome progression and increases cardiovascular risk, an effect that may be closely paralleled by aldosterone excess. Excess aldosterone can arise from renin-dependent aldosteronism (RDA), a primarily physiological state (not discussed in this review), or from renin-independent aldosteronism (RIA). RIA is a pathophysiologically relevant condition characterized by persistent autonomous activation, bypassing normal renin-angiotensin-aldosterone system (RAAS) regulation. Its most recognized form is PA, a prevalent, multidimensional disorder spanning a continuum from subclinical to overt autonomous aldosterone production. This leads to inappropriately elevated aldosterone relative to suppressed renin and sodium levels. PA is a leading cause of secondary hypertension and elevates the risk of metabolic and cardiorenal disorders, showing substantial overlap with CKM syndrome. Despite its clinical significance, the specific relationship between PA and CKM syndrome remains insufficiently investigated. This review synthesizes evidence from three key perspectives: (1) Epidemiology and clinical data show that PA spans a spectrum from subclinical to overt stages and is strongly associated with driving and accelerating the progression of CKM syndrome; (2) Therapeutically, targeted treatment of PA mitigates the adverse effects of aldosterone on CKM syndrome progression; and (3) Pathophysiologically, inappropriately elevated aldosterone primarily interacts with widely distributed mineralocorticoid receptors in tissues relevant to CKM syndrome, exacerbating key pathogenic pathways akin to adding fuel to the fire. Building on this synthesis, we emphasize that inappropriately elevated aldosterone is not merely a simple biomarker but an active driver and accelerator of CKM syndrome progression. This review also proposes future directions for integrated PA-CKM screening and management. Incorporating PA into the CKM syndrome framework could not only refine CKM syndrome care but also address the critical underdiagnosis of PA, whose screening rate regrettably remains below 2% in high-risk populations.

Humans↗
PubMed1979

Dissociation in the excretion of different aldosterone metabolites and unmetabolized ('free') aldosterone in hypertension.

1. The determination of aldosterone-18-glucuronide (pH 1-labile aldosterone) was complemented by concomitant measurements of free urinary aldosterone and tetrahydroaldosterone in 307 patients, most of whom were hypertensive. In 38 cases (12.3%) the normal, aldosterone-18-glucuronide concentration was clinically misleading, but increased free aldosterone and/or tetrahydroaldosterone values suggested the presence of hyperaldosteronism, which in many of these cases was confirmed by elevated excretion of the possible major aldosterone precursor 18-hydroxycorticosterone (18-OH-B). 2. Of 224 patients with essential hypertension and normal or low plasma renin activity 18 had an elevated free aldosterone and/or tetrahydroaldosterone excretion without increased aldosterone-18-glucuronide. These cases may represent early or pre-symptomatic forms of primary hyperaldosteronism. In other cases, particularly when tetrahydroaldosterone was increased alone, abnormalities of aldosterone metabolism were suspected. 3. In two out of 15 patients with primary hyperaldosteronism, aldosterone-18-glucuronide values were frequently found to be normal, although elevations were noted in other variables. However, no relation to the morphological abnormality (adenoma versus hyperplasia) was seen.

18-Hydroxycorticosterone↗
PubMed1990

Pituitary peptides other than ACTH may not be aldosterone secretagogue in primary aldosteronism.

In order to elucidate whether pituitary peptides other than ACTH which are derived from the proopiomelanocortin (POMC) are involved for aldosterone secretion in primary aldosteronism, we administered ovine corticotropin releasing factor (CRF), beta-endorphin and naloxone to seven patients with aldosterone producing adenoma. One hundred micrograms of CRF produced an augmented aldosterone response in patients with aldosteronism, while 500 micrograms of beta-endorphin infusion failed to cause any significant changes in neither normal subjects nor patients. An opioid antagonist, naloxone (10 mg, iv) produced no noticeable change in plasma aldosterone in normal subjects, while it caused a slight increase in patients with primary aldosteronism. Plasma cortisol increased to a similar degree in response to CRF and naloxone in normal subjects and patients. In three patients with isolated ACTH deficiency, neither aldosterone nor cortisol responded to these stimuli. The present results indicate that POMC-derived pituitary peptides other than ACTH are unlikely to participate in the aldosterone secretion in normal subjects or in patients with primary aldosteronism.

Adenoma↗
PubMed1989

Racial differences in aldosterone excretion and plasma aldosterone concentrations in children.

Blacks are more likely to have hypertension, have lower levels of plasma renin activity, and typically consume less potassium than whites. Whether blacks and whites secrete different amounts of aldosterone is less clear. We estimated aldosterone secretion indirectly in 715 children, 249 of whom were black, by measuring their nocturnal rates of urinary excretion of aldosterone. Dietary sodium and potassium intakes were estimated from their excretion rates. The mean (+/- SE) aldosterone-excretion rate was lower in the black children than in the white children (0.045 +/- 0.003 vs. 0.078 +/- 0.004 nmol per micromole of creatinine per kilogram of body weight; P less than 0.001). The potassium-excretion rate was also lower in the black children than in the white children (0.13 +/- 0.01 vs. 0.18 +/- 0.01 mmol per micromole of creatinine per kilogram; P less than 0.001). Aldosterone excretion was highly correlated with potassium excretion (P less than 0.001), but the lower aldosterone-excretion rate in blacks was explained only in part by their lower dietary intake of potassium. Systolic blood pressure was higher in black children (P less than 0.001), as was diastolic pressure (P = 0.037). In a second study of 99 children, the plasma aldosterone level was found to be significantly lower in black children than in white children (230 +/- 30 vs. 400 +/- 30 pmol per liter; P less than 0.001). Plasma renin activity and plasma cortisol levels were the same in both groups. In summary, we found that black children secrete about 40 percent less aldosterone than white children. The role of the lower aldosterone-secretion rate in the genesis of the higher blood pressures observed in black children is not known.

Aldosterone↗
PubMed1979

Effects of metoclopramide and bromocriptine on the renin-angiotensin-aldosterone system in man. Dopaminergic control of aldosterone.

This study was designed to investigate the possible role of dopaminergic mechanisms in the control of the renin-angiotensin-aldosterone system in normal man. Six normal male subjects in metabolic balance at 150 meq sodium, 60 meq potassium constant intake received the specific dopamine antagonist, metoclopramide, 10 mg i.v. or placebo followed by angiotensin II infusion 1 h later on 2 consecutive days. Metoclopramide increased plasma aldosterone concentration from 8.2+/-2.2 to 21.0+/-3.3 ng/100 ml (P < 0.005) and plasma prolactin concentration from 18.0+/-4.0 to 91.7+/-4.0 ng/ml (P < 0.001) within 15 min of its administration. At 1 h, plasma aldosterone and prolactin concentrations remained elevated at 16.8+/-2.1 ng/100 ml (P < 0.01) and 86.8+/-15.9 ng/ml (P < 0.005), respectively. Angiotensin II at 2, 4, and 6 pmol/kg per min further increased plasma aldosterone concentration to 27.2+/-3.4, 31.9+/-5.7, and 36.0+/-6.7 ng/100 ml (P < 0.02), respectively. Placebo did not alter plasma aldosterone or prolactin concentrations, but angiotensin II increased plasma aldosterone concentration to 13.7+/-2.4, 19.0+/-1.9, and 23.3+/-3.2 ng/100 ml (P < 0.005). The increment of plasma aldosterone concentration in response to angiotensin II was similar after metoclopramide or placebo. The six subjects also received the dopamine agonist, bromocriptine, 2.5 mg or placebo at 6 p.m., midnight, and 6 a.m. followed by angiotensin II infusion on 2 consecutive d. Bromocriptine suppressed prolactin to <3 ng/ml. After placebo, plasma aldosterone concentration increased from 5.2+/-1.4 to 12.3+/-1.7, 17.2+/-2.2, and 21.8+/-3.5 ng/100 ml (P < 0.01) and after bromocriptine from 7.2+/-1.0 to 14.7+/-3.0, 19.8+/-3.2, and 23.4+/-1.6 ng/100 ml (P < 0.001) with each respective angiotensin II dose. No difference in the response to angiotensin II after bromocriptine or placebo was observed. Plasma renin activity, free 11-hydroxycorticoid concentration, and serum potassium concentration were unchanged by metoclopramide or bromocriptine. The results suggest that aldosterone production is under maximum tonic dopaminergic inhibition which can be overridden with stimulation by angiotensin II in normal man.

11-Hydroxycorticosteroids↗
PubMed1977

[A simplified radioimmunoassay for serum aldosterone--non-extraction method with 125I-labeled aldosterone (author's transl)].

A simplified direct radioimmunoassay system for serum aldosterone measurement was developed by using radio iodine-labeled aldosterone and highly specific antiserum to aldosterone. 8-anilino-1-naphthalene sulfonic acid(ANS) was used to prevent the binding of aldosterone to serum proteins. Polyethylene glycol was used to separate the antibody-bound aldosterone from the free aldosterone as the precipitant. The minimum measurable concentration of aldosterone is 30pg/ml of serum by short incubation method (at 25 degrees C for 3hr incubation) and 15pg/ml of serum by long incubation method (at 4 degrees C for 20 hr incubation) respectively. Present radioimmunoassay eliminates extraction of the aldosterone from serum and chromatographic separation procedures, and requires only 0.1ml of serum sample for assay. The intra-assay precision was C. V. 6.9% (average of 4 samples) and the inter-assay precision was C. V. 10.7% (average of 4 samples). There is an excellent correlation between the extraction method and this direct method in serum aldosterone value obtained (correlation coefficient, 0.96). The normal value was 36.8+/-25.9pg/ml (recumbent) and 113.6+/-6.15pg/ml (upright).

Aldosterone↗
PubMed1979

The effect of extremely high sodium intake on plasma renin activity, plasma aldosterone concentration, and urinary excretion of aldosterone metabolites.

The effect of sodium intake on aldosterone production was examined in eight healthy men whose urinary sodium excretion approached their dietary sodium intake at levels of 10, 300, 800 and 1500 mEq sodium/day. Aldosterone secretion was estimated from the excretion rate of two aldosterone metabolites: Thaldo and aldosterone-18-glucuronide. Maximal suppression of aldosterone secretion appeared to have been reached when sodium intake was 800 mEq/day, since no further decrease in aldosteron metabolite excretion rates was observed at 1500 mEq/day dietary sodium. Both plasma renin activity and plasma aldosterone concentration were suppressed and approached or were below the detection limits of the respective radioimmunoassays when sodium intake reached 800 and 1500 mEq/day. Body weight and blood pressure significantly increased at each increment of sodium intake. Our findings show that when sodium intake is extremely high, aldosterone secretion does not decrease to zero but continues at a rate we estimate to be 10 to 30 microgram/day. We suggest that this nonsuppressible secretion of aldosterone may have contributed to the observed increases in weight and blood pressure.

Adult↗