Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Aldosterone”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

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↗
PubMed1969

Activation of aldosterone secretion in primary aldosteronism.

Angiotensin infusion evokes marked increases in aldosterone secretion in primary aldosteronism and little change in secondary aldosteronism. The low plasma renin activity of primary aldosteronism and the elevated plasma renin activity of secondary aldosteronism are thought to account for this differential response. The effect of angiotensin on aldosterone and 18-hydroxycorticosterone secretion was studied during adrenal vein catheterization in seven patients with primary aldosteronism (whose plasma renin activity had been elevated following spironolactone therapy), one hypertensive patient with normal plasma renin activity and normal aldosterone secretion, two patients with secondary aldosteronism who had elevated plasma renin activity, and one anephric patient whose plasma renin activity was 0. Adrenal venous aldosterone and 18-hydroxycorticosterone were measured before and after a ten min sub-pressor angiotensin infusion. The cells of the aldosterone-producing adenoma (APA) respond to small increases in plasma angiotensin with large increases in secretion of aldosterone and 18-hydroxycorticosterone. The dose of angiotensin capable of evoking this response from the aldosterone-producing adenoma produces little or no change in the secretion of the steroids from nontumorous glands. The augmentation of aldosterone secretion, induced by angiotensin, in primary aldosteronism is due solely to increased secretion by the adenoma and not by the contralateral zona glomerulosa. The increased sensitivity of the aldosterone-producing adenoma is characteristic of the tumor. This response is independent of fluctuations in endogenous plasma renin activity. This sensitivity is not blunted by high plasma renin activity, nor is it a function of tumor mass for the effect is observed in aldosterone-producing adenomas regardless of size. ACTH injection after angiotensin infusion resulted in a marked increase in aldosterone concentration in the effluent from the nontumorous adrenal, but was not capable of producing further increases in aldosterone concentration in the effluent from the APA. In view of this exquisite sensitivity to infused angiotensin, it may be that the small variations in endogenous plasma renin activity that have been observed in primary aldosteronism may be capable of evoking large changes in aldosterone secretion in patients with aldosterone-producing adenomas.

Adrenal Gland Neoplasms↗
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↗
PubMed1982

Effect of aldosterone antagonists on mineralocorticoid synthesis in vitro. Inhibition of aldosterone production by prorenoate-K.

A perifusion technique using frog adrenal glands has been applied to investigate the effects of long-term administration of a new aldosterone antagonist (potassium prorenoate; SC 23992) on mineralocorticoid production. Whatever the duration of administration of potassium prorenoate, at a constant concentration of 5 X 10(-4) M, a significant inhibition of aldosterone output occurred during the passage of the compound. The inhibition was immediate (lag period less than 10 min); the amplitude of the inhibition was constant during the whole experiment and ranged from 77 to 89%; the aldosterone output returned to a regular basal value 80-100 min after the end of infusion of potassium prorenoate. We have also investigated the effect of a concentration gradient of potassium prorenoate (similar to the concentration gradient of aldosterone antagonist observed in plasma after a single oral administration of the molecule) upon aldosterone production over 12 h. From this study, we have established the existence of a highly significant correlation between the extent of the inhibition of aldosterone production and the concentration of the aldosterone antagonist. Finally we have observed that potassium prorenoate blocked the stimulation of aldosterone secretion induced by synthetic ACTH and significantly reduced the angiotensin-induced aldosterone stimulation. The present results indicate that, besides the well-known competitive inhibition of aldosterone binding exerted by potassium prorenoate at the renal receptor site, a direct inhibition of aldosterone biosynthesis also accounts for the pharmacological activity of this aldosterone antagonist.

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↗
PubMed1969

Stimulation and suppression of aldosterone in plasma of normal man and in primary aldosteronism.

The effect of stimulating and suppressive influences on plasma aldosterone in normal man and in patients with primary aldosteronism were studied using a sensitive double-isotope derivative assay for aldosterone. In normal sitting subjects, values were 9.2+/-0.9 (SE) mmug/100 ml and in subjects supine for 1 hr plasma aldosterone was 5.2+/-0.4 (SE) mmug/100 ml. Adrenocorticotropic hormone (ACTH), 0.5 U/hr, produced a rise of 46.8+/-22 (SE) mmug which was similar to the 1-hr effect of an infusion of a synthetic ACTH (beta(1-24), Cortrosyn). Angiotensin II in pressor amounts also increased plasma aldosterone 21.5+/-2.9 (SE) without change in plasma cortisol, whereas a subpressor dose ([unk]) had minimal effect.Fludrocortisone, 1.2 mg/day for 3 days, suppressed plasma aldosterone levels to 1.8+/-0.7 (SE) mmug/100 ml in five normal sitting subjects (P < 0.01); however, dexamethasone, 2 mg/day for 1-2 days, did not lower aldosterone concentration in plasma. In six patients with primary aldosteronism, plasma aldosterone on a normal sodium diet was 39.1+/-4.4 (SE) which differed significantly from normal sitting or supine subjects (P < 0.001). In contrast to the normal subjects, neither a pressor infusion of angiotensin II for 1 hr, nor fludrocortisone, 1.2 mg/day for 3 days, impressively altered plasma aldosterone levels. This approach appears to be useful for the study of the acute physiology and control mechanisms of aldosterone production in normal and hypertensive man.

Adrenal Cortex Hormones↗
PubMed1984

Renal receptor-binding activity of reduced metabolites of aldosterone: evidence for a mineralocorticoid effect outside of the classic aldosterone receptor system.

Reduced metabolites of aldosterone have been shown to have antinatriuretic and kaliuretic effects. We have studied the ability of four reduced metabolites of aldosterone to compete with [3H]aldosterone and [3H]dexamethasone for binding to the mineralocorticoid and glucocorticoid receptors of the kidney using adrenalectomized rat renal slices and cytosol, respectively, as sources of the binding proteins. 5 alpha-Dihydroaldosterone had 18.9% the ability to compete with [3H]aldosterone for binding to the cytoplasmic receptor of adrenalectomized rat renal slices in comparison to unlabeled aldosterone. Its antinatriuretic potency varied between 7-17%. Its ability to compete with [3H]dexamethasone for binding to the renal glucocorticoid receptor was only 1.9% in comparison to unlabeled dexamethasone. The relative competitive activities of 3 beta,5 alpha-tetrahydroaldosterone and 3 beta,5 beta-tetrahydroaldosterone with [3H]aldosterone to adrenalectomized rat renal slices cytosol were 1.26% and 0.05%, respectively, in comparison to unlabeled aldosterone. Their reported mineralocorticoid activities using the adrenalectomized rat bioassay (antinatriuresis) were 0.1-0.4% and 0.15%, respectively, in comparison to aldosterone. The most important aldosterone metabolite 3 alpha,5 beta-tetrahydroaldosterone showed negligible competitive activity with [3H]aldosterone or [3H]dexamethasone for the renal corticoid type I or type II receptors, respectively. However, this compound has been reported and confirmed to have weak but clear-cut mineralocorticoid activity (approximately 1/100th that of aldosterone). The mineralocorticoid activity of 3 alpha,5 beta-tetrahydroaldosterone cannot be explained by a mechanism involving the classic renal mineralocorticoid receptor. The mechanism could involve an alternative receptor system, a nonreceptor-mediated renal mechanism, or the conversion to a metabolite that would interact with classic receptors.

Adrenalectomy↗
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↗
PubMed1983

Effects of metoclopramide, a dopamine antagonist, on secretion of aldosterone and renin release in patients with primary aldosteronism.

To assess the interaction between dopamine and aldosterone secretion in primary aldosteronism, the dopamine antagonist, metoclopramide (methoxy-2-chloro-5-procainamide), was given as an i.v. bolus (10 mg) to 5 patients with primary aldosteronism and 5 normal subjects treated with dexamethasone (2 mg/day) to eliminate an influence of ACTH. Metoclopramide increased plasma aldosterone concentration (PAC) in primary aldosteronism from 39.1 +/- 15.5 to 42.5 +/- 15.9 ng/100 ml (p less than 0.05) and also from 12.9 +/- 2.3 to 23.6 +/- 3.4 ng/100 ml (p less than 0.01) in normal subjects at 15 min. Plasma renin activity (PRA), and plasma concentrations of cortisol, potassium, and sodium did not significantly change with metoclopramide in either primary aldosteronism or normal subjects. Plasma prolactin increased by 12- and 20-fold in primary aldosteronism and in normal subjects, respectively, but there was no significant positive correlation between changes in PAC and in plasma prolactin in either primary aldosteronism or normal subjects. It is suggested that dopamine inhibits the secretion of aldosterone in primary aldosteronism as well as in normal subjects. It seems unlikely that dopamine affects the release of renin in primary aldosteronism.

Adrenocorticotropic Hormone↗
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↗