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At least 19 recordsLinked to original sources
PubMed1998

Diagnosis of glucocorticoid-remediable aldosteronism in primary aldosteronism: aldosterone response to dexamethasone and long polymerase chain reaction for chimeric gene.

Aldosterone suppression by dexamethasone, and high 18-hydroxycortisol and 18-oxocortisol levels are used to differentiate glucocorticoid-remediable aldosteronism (GRA) from other forms of primary aldosteronism. These methods are time consuming, expensive, and impractical for large studies. Moreover, diagnosis of GRA requires a confirmatory genetic test. We evaluated 117 patients with primary aldosteronism referred to our centers by the use of a long PCR technique to reveal the chimeric gene of GRA. In 60 of 117 patients, the response of aldosterone to dexamethasone (2 mg/day for 4 days) was also assessed. None of our patients, including 2 pairs of siblings, was positive for the chimeric gene. The results of long PCR were confirmed by Southern blotting. Despite a negative genetic test, 6 patients (1 with aldosterone-producing adenoma and 5 with idiopathic hyperaldosteronism) had plasma aldosterone suppressed by dexamethasone (i.e. < or = 2 ng/dL). Of 117 patients, 43 were identified as having aldosterone-producing adenoma and 74 as having idiopathic hyperaldosteronism. In our experience, the long PCR technique is a reliable and simple test to at least exclude GRA in patients with primary aldosteronism. A short term dexamethasone suppression test of aldosterone can be misleading in identifying GRA. The prevalence of GRA in primary aldosteronism remains to be established.

Adult↗
PubMed1995

Zona fasciculata-like cells determine the response of plasma aldosterone to metoclopramide and aldosterone synthase messenger ribonucleic acid level in aldosterone-producing adenoma.

The different responses of plasma aldosterone to ACTH and angiotensin II in aldosterone-producing adenoma (APA) is thought to be due to the various cellular compositions of the tumors. To investigate whether the dopaminergic regulation of aldosterone in APA is also dependent on the cellular types, we studied the effects of metoclopramide on plasma aldosterone in six patients with APA. The messenger RNA (mRNA) levels of aldosterone synthase (P450aldo), 11 beta-hydroxylase (P450(11) beta), and 17 alpha-hydroxylase (P450(17) alpha) of APA and normal adrenal glands were determined by competitive polymerase chain reaction. After administration of metoclopramide (an antagonist of dopamine-2 receptor), the increment of plasma aldosterone correlated inversely with the percentage of zona fasciculata cells of APA. The mRNA level of P450aldo in the tumorous portion was much higher, whereas the levels of P450(11) beta and P450(17) alpha mRNAs were lower, than those of the nontumorous portion and normal adrenals. There was a correlation of the percentage of zona fasciculata cells in APA with the levels of P450aldo and P450(11) beta mRNAs, but not with P450(17) alpha mRNA. These results suggest that differential responsiveness of plasma aldosterone to metoclopramide may be due to various proportions of different cell types in APA that may have different expression of dopamine-2 receptor. In addition, this histologically dependent expression was present at the transcriptional level of the gene responsible for aldosterone biosynthesis.

Adenoma↗
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↗
PubMed2002

Is aldosterone the missing link in refractory hypertension?: aldosterone-to-renin ratio as a marker of inappropriate aldosterone activity.

Use of the random aldosterone-to-renin ratio (ARR) as a reliable marker of inappropriate aldosterone activity has led to primary aldosteronism (PA) being increasingly diagnosed in hypertensive patients. At least 10% of hypertensives have been found to have PA, the majority of whom presumably have bilateral adrenal hyperplasia or idiopathic hyperaldosteronism as an aetiology for PA. Whilst these patients clearly have excess aldosterone activity, they have in common many features that are found in hypertensive patients in general, amongst which include heightened angiotensin II adrenal sensitivity. Whether these individuals belong within the spectrum of 'essential hypertension' is being debated, but is probably irrelevant clinically since they appear to respond favourably to spironolactone treatment. In addition, there is recent evidence suggesting that these patients overexpress a key enzyme involved in aldosterone production, the aldosterone synthase, the activity of which appears to relate to its genotypic variation.

Aldosterone↗
PubMed1981

Factors relating to aldosterone secretion rate, the excretions of aldosterone 18-glucuronide, and the plasma aldosterone concentration in cirrhosis.

In a group of eight patients with cirrhosis the rate of renal excretion of the 18-glucuronide metabolite of aldosterone (U Aldo V) was found to be closely related to the aldosterone secretion rate (ASR). U Aldo V was therefore used as an index of ASR in a further group of fifty patients in order to evaluate the possible importance of factors known to regulate aldosterone secretion. U Aldo V showed statistically significant relationships to both plasma renin activity (PRA) and the plasma sodium concentration (P Na), but not to the plasma potassium concentration (PK) or the renal excretion of cortisol (U Cort V), the latter sued as an index of adrencorticotrophic hormone activity. The plasma aldosterone concentration (P Aldo) was determined in fifty-eight patients and also found to show statistically significant relationships to PRA and P Na. P Aldo showed a weak, though statistically significant, relationship to PK, but not to U Cort V. These findings are in keeping with a role for the renin-angiotensin system in the control of aldosterone secretion in cirrhosis although evidence from other studies suggest other factors to be involved also. Whether P Na was another determinant of ASR, or whether aldosterone was a determinant of P Na through regulating sodium reabsorption by the proximal tubule of the nephron, is uncertain.

Adult↗
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↗
PubMed1995

Increased disorderliness and amplified basal and pulsatile aldosterone secretion in patients with primary aldosteronism.

To investigate the pathophysiology of altered aldosterone secretion in patients with primary aldosteronism, the pulsatile mode of in vivo aldosterone and cortisol release was examined by quantitative deconvolution analysis in 5 normal subjects (controls) and 10 patients with aldosterone-producing adenomas (APA) under conditions of sodium (150 meq/day) balance. Episodic release of aldosterone and cortisol was assessed by sampling blood at 10-min intervals for 24 h. A waveform-independent deconvolution algorithm was used to calculate endogenous aldosterone and cortisol secretion rates on a sample by sample basis in each subject. There were no differences in the number of aldosterone or cortisol secretory bursts per day or their mean interpulse intervals between normal subjects and patients with primary aldosteronism. A 24-h rhythmicity in serum aldosterone concentrations was maintained in APA patients. Patients with primary aldosteronism had significantly higher (P < 0.01) aldosterone mean secretory rates, mean mass of aldosterone secreted per burst, maximal aldosterone secretion rates attained within each burst, and mean basal (nadir) aldosterone secretion rates. A recently introduced regularity statistic, approximate entropy (ApEn), was used to test for orderliness (small ApEn) vs. randomness (large ApEn) in the aldosterone time series. ApEn was significantly larger for the APA patients (1.433 +/- 0.148) than for normal subjects (0.306 +/- 0.098; P < 0.001), with complete group segmentation yielding 100% sensitivity and specificity. In contrast, a scale-invariant form of this measure, normalized ApEn, showed no significant distinction between tumoral and normal aldosterone release patterns. These ApEn findings taken together are consistent with the deconvolution results from an entirely distinct perspective, reinforcing an amplitude difference, but no frequency difference, between normal subjects and APA patients. Unexpectedly, patients with APA had significantly lower mean cortisol secretory rates, reduced cortisol secretory burst mass, and attenuated maximal cortisol secretory rates than normal subjects (P < 0.01). Plasma cortisol and aldosterone concentrations in patients remained positively correlated over short time lags. In summary, the present findings demonstrate that in normal subjects and patients with APA, both aldosterone and cortisol are secreted in a burst-like mode. The presence of substantial basal aldosterone release and increased irregularity of serial aldosterone concentrations distinguishes APA from normal subjects.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1982

Urinary free 18-hydroxycorticosterone, plasma aldosterone, and urinary aldosterone metabolites in normal pregnancy.

The final steps in aldosterone biosynthesis are unclear. Undecided is whether 18-hydroxycorticosterone is a precursor of aldosterone or an end product. 18-Hydroxycorticosterone is secreted in close relationship to aldosterone. To get adequate information on the status of aldosterone in pregnancy, determination of more than one parameter of aldosterone seems to be necessary. Urinary excretion of free 18-hydroxycorticosterone, tetrahydroaldosterone, aldosterone-18-glucuronide, free aldosterone, and the plasma concentration of aldosterone were measured by radioimmunoassay in 16 primigravid women in the last trimester of normal pregnancy and in 13 healthy nonpregnant women. All steroids measured were significantly increased in pregnancy. The ratios of aldosterone-18-glucuronide to tetrahydroaldosterone in the two groups were not significantly different, so that significant changes in renal or hepatic aldosterone metabolism could not be demonstrated in pregnancy. When pregnant women with ankle edema (n = 7) were compared to pregnant women without edema (n = 9), no differences in steroid patterns could be found. The increased excretion of 18-hydroxycorticosterone in pregnancy confirms the state of hyperaldosteronism in normal pregnancy which is associated with an increase in biologically active, free aldosterone. Dissociation in the excretion of the two aldosterone metabolites and free aldosterone was found in three pregnant women, in whom excretion of aldosterone-18-glucuronide was increased but excretion of tetrahydroaldosterone and free aldosterone was in the normal nonpregnant range.

18-Hydroxycorticosterone↗
PubMed1980

[A simple method for measuring aldosterone secretion rate using 125I-aldosterone (authors' transl)].

A simplified radioimmunoassay system for aldosterone secretion rate was developed by using radioiodine-labelled aldosterone and highly specific antiserum to aldosterone. An antibody was produced in rabbits by injecting aldosterone-oxime coupled with bovine gamma-globulin once a month. Aldosterone-oxime was labelled with 125I by using the chloramine T method described by Hunter and Greenwood. 3 ml of a twenty-four-hour urine specimen was used for the radioimmunoassay. Following CH2Cl2 extraction, pH 1 hydrolysis was carried out for twenty-four hours. Separation of the aldosterone extract was achieved by paper chromatography (hexane:benzene:methanol:water = 1:9:5:2.5). The minimum measurable concentration was under 1pg, and adequate intraassay and interassay precision were obtained. Aldosterone secretion rate was 89.6 +/- 25.8 (mean +/- SD)mug/day in normal subjects and was similar in low- and normal-renin essential hypertension. Significant high values (806.4 +/- 65.8mug/day) were obtained in primary aldosteronism and were slightly high in secondary aldosteronism and high-renin essential hypertension. The aldosterone secretion rate correlated positively with plasma aldosterone level (r = 0.731, p < 0.01). Aldosterone secretion rates were obviously higher than plasma levels in primary and idiopathic aldosteronism. From these results, it is concluded that this method is a very useful and reliable one for measuring aldosterone secretion rate and for discriminating primary aldosteronism from low-renin essential hypertension. it is superior in its simplicity, and there is no need to use a liquid scintillation counter.

Aldosterone↗
PubMed1982

Direct radioimmunoassays for "aldosterone" and "18-hydroxycorticosterone" in unprocessed urine, and their use in screening to distinguish primary aldosteronism from hypertension.

For distinguishing primary aldosteronism from essential hypertension, we use simple direct radioimmunoassays for "aldosterone" (aldosterone and other materials that react with the antibody to aldosterone) and "18-hydroxycorticosterone" (similarly) in unprocessed urine. Patients with primary aldosteronism have high values for "aldosterone." This diagnosis can be validated by assays of further urine samples from the same person and by additional direct assays for "18-hydroxycorticosterone." In none of 65 urine samples from 26 patients with primary aldosteronism were both "aldosterone" and "18-hydroxycorticosterone" values within their reference intervals. However, a few "aldosterone" and "18-hydroxycorticosterone" values for patients with essential hypertension and normal aldosterone excretion were also (moderately) increased. Thus, when high values are found, true aldosterone values must be estimated by extraction and chromatography, to eliminate false positives. The "aldosterone" and "18-hydroxycorticosterone" values by our procedure are much higher than the corresponding values for urinary free aldosterone and 18-hydroxycorticosterone. Although not identified, the immunoactive materials are probably metabolites of aldosterone and 18-hydroxycorticosterone.

18-Hydroxycorticosterone↗
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↗