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PubMed2004

Aldosterone and aldosterone antagonism in systemic hypertension.

Aldosterone mediates both water and electrolyte balance by acting on the renal mineralocorticoid receptors. Recent experimental studies have also documented the presence of these receptors in other body organs, including the brain, blood vessels, and heart, suggesting that aldosterone plays a larger role in normal physiologic function and in cardiovascular diseases such as systemic hypertension and congestive heart failure (CHF). The nonspecific aldosterone inhibitor spironolactone, and the selective aldosterone inhibitor eplerenone, are both approved for clinical use in treating patients with hypertension and/or symptomatic CHF. Studies have shown that spironolactone lowers blood pressure, improves endothelial function, reduces myocardial hypertrophy and fibrosis, and lowers the incidence of fatal arrhythmias. Eplerenone, which is more specific for the mineralocorticoid receptor, appears to provide all the beneficial effects of spironolactone in hypertensive patients, with the potential to modify many of the side effects related to nonspecific steroid-receptor blockade. Hyperkalemia remains a potential problem with all aldosterone antagonists.

Aldosterone↗
PubMed1982

Characterisation of aldosterone metabolites cross reacting with aldosterone and tetrahydroaldosterone antibodies.

Metabolites of aldosterone were extracted from human urine collected over three days following the intravenous injection of a tracer dose of tritium labelled hormone. After enzymic hydrolysis, steroids were separated by column, paper and thin-layer chromatography and the polarities of the labelled metabolites were compared with the chromatographic properties of known aldosterone products. The pattern of metabolites changed over the three days, from that associated with typical aldosterone metabolites, to less polar metabolites. Materials in the organic extract from a pH-1 hydrolysate of pooled pregnancy urine, were located by their ability to bind with aldosterone and tetrahydroaldosterone antisera and exhibited similar chromatographic properties to the radioactive metabolites. Using GC-MS, the identity of this immunoactive material could not be established in extracts after purification from 200 ml pregnancy urine but some synthetic derivatives of aldosterone as candidate compounds, were excluded.

Adrenal Cortex Neoplasms↗
PubMed1984

Circadian rhythm of plasma aldosterone and time dependent alterations of aldosterone regulators.

In order to investigate the relative contribution of ACTH, the renin angiotensin and dopaminergic system to the circadian rhythm of plasma aldosterone, hormone levels were determined at hourly intervals over a 24 h span in four supine healthy men. Blood was withdrawn under basal conditions (control), after either dexamethasone, captopril or bromocriptine++ (CB-154) administration. Plasma aldosterone rhythmicity was abolished in dexamethasone treated groups but not in captopril or CB treated groups. Time dependent alterations of aldosterone regulators were analyzed by multiple regression methods at 3 hourly intervals. These results indicate that plasma aldosterone rhythmicity is predominantly under the control of ACTH whereas the renin angiotensin or dopaminergic system plays a little role. In supine, sodium repleted states, ACTH is a potent stimulus of aldosterone at 000-0600 h and 1700-1900 h clocktime, whereas during daytime renin-angiotensin is an additional regulator.

Adrenocorticotropic Hormone↗
PubMed2001

Screening for primary aldosteronism without discontinuing hypertensive medications: plasma aldosterone-renin ratio.

The traditional workup for primary aldosteronism is cumbersome and requires discontinuing antihypertensive medications, which is inconvenient and potentially dangerous. A simple and accurate screening test that can be used without modifying medications is needed. The plasma aldosterone-renin ratio (ARR) is a valid screening assay for primary aldosteronism, but antihypertensives are usually discontinued before obtaining this ratio, limiting its utility. The present prospective study is designed to examine the validity of the ARR as a screening test for primary aldosteronism if the ratio is measured randomly while patients continue antihypertensive therapy. During the 18-month study period, 90 patients were referred to the hypertension clinic with poorly controlled hypertension. ARR was measured in random blood samples in all 90 patients while maintaining their prescribed antihypertensive medications. Those with elevated ARRs (>100 ng/dL / ng/mL/h) underwent further diagnostic workup, including adrenal computed tomography and/or magnetic resonance imaging and adrenal iodine 131 norcholesterol uptake scan. Fifteen patients (17%) had elevated ARRs greater than 100:1. Ten of 15 patients were found to have adrenal adenoma on diagnostic workup, and adenoma was later confirmed by histological examination after surgical removal in these 10 patients. Five patients were found to have adrenal hyperplasia; all 5 patients responded to antialdosterone treatment. Thus, all 15 patients had good control of blood pressure after surgery and/or antialdosterone medications. No patient showed a falsely elevated ARR. Data suggest that the ARR is a valid screening assay for primary aldosteronism in patients with poorly controlled blood pressure, and discontinuation of antihypertensive medications is not needed for this test.

Adenoma↗
PubMed1986

Metoclopramide fails to stimulate aldosterone secretion and inhibits serotonin-mediated aldosterone secretion in the rat.

The acute and chronic effects of metoclopramide on aldosterone secretion in the rat model were examined. Metoclopramide 50 micrograms iv in dexamethasone-treated rats did not increase plasma aldosterone concentration. Chronic infusion of metoclopramide (72 micrograms/hr) over 5 days also did not show any increase in the plasma or urinary aldosterone concentration when compared with control rats. Metoclopramide in vitro showed no effect on aldosterone secretion from rat adrenal capsular cells but it inhibited serotonin-mediated aldosterone secretion from the same cells significantly.

Adrenal Glands↗
PubMed1981

Effect of metoclopramide on plasma aldosterone in normal subjects, primary aldosteronism and hypopituitarism.

The behaviour of plasma renin, aldosterone, cortisol and prolactin after administration of a drug with antidopaminergic action, metoclopramide, was evaluated in 6 normal subjects, 8 patients affected by primary aldosteronism and in 5 patients affected by anterior hypopituitarism. In the first two groups, besides the predictable increase of prolactin under metoclopramide, a significant aldosterone increase was noted. Cortisol remained unchanged, and PRA was not significantly increased. A similar pattern of aldosterone, cortisol and PRA was also found in patients with hypopituitarism. However, the plasma prolactin did not increase in this group. The comparative examination of three groups of patients leads us to conclude that aldosterone increase is not imputable to ACTH, renin or to prolactin. This may be explained by a possible direct effect of the antidopaminergic drug at the adrenal level, which is more likely than an effect through some yet undetermined factor.

Aldosterone↗
PubMed1974

Renal aldosterone receptors: studies with (3H)aldosterone and the anti-mineralocorticoid (3H)spirolactone (SC-26304).

In vivo, a spirolactone (SC-26304) inhibited the effects of aldosterone on urinary K(+):Na(+) ratios and the binding of [(3)H]aldosterone to renal cytoplasmic and nuclear receptors. Cytoplasmic binding of [(3)H]aldosterone and [(3)H]spirolactone (SC-26304) was similar in magnitude and involved the same set of sites. Under three sets of conditions-(i) in the intact rat, (ii) in kidney slices, and (iii) in reconstitution studies (mixing prelabeled cytoplasm with either purified renal nuclei or chromatin), [(3)H]spirolactone (SC-26304) did not yield specific nuclear complexes in contrast to the reproducible generation of these complexes with [(3)H]aldosterone. In glycerol density gradients, cytoplasmic [(3)H]aldosterone receptor complexes sedimented at 8.5 S and 4 S in low concentrations of salt and at 4.5 S in high concentrations of salt. Cytoplasmic [(3)H]spirolactone (SC-26304) receptor complexes sedimented at 3 S in low concentrations of salt and 4 S in high concentrations of salt. These results are discussed in terms of an allosteric model of the receptor system.

Adrenalectomy↗
PubMed2005

Plasma aldosterone to renin ratio predicts treatment response in primary aldosteronism: is volume loading needed?

Volume loading is considered the golden standard of the confirmatory tests in the diagnostics of primary aldosteronism (PA). However, it is time-consuming, and it is unclear to what extent it improves the diagnostics of PA in comparison to simple screening tests. To study this question, the diagnostics with and without oral sodium loading (OSL) were evaluated by receiver operating characteristic curves analyses in 77 consecutive OSL patients. The final diagnosis was essential hypertension in 39 cases and PA in 38 cases, determined by review of the patient records, biochemical tests, imaging findings, and the response to therapy with spironolactone and/or operation. Plasma aldosterone-to-renin-activity ratio (ARR) and daily urinary aldosterone had a good diagnostic ability that did not significantly improve by accomplishing OSL. Cut-off values with optimal sensitivity and specificity were >or=1050 pmol/l per ng/ml/h for upright ARR, and >or=45 nmol/day for daily urinary aldosterone. To conclude, carefully conducted outpatient tests are sufficient for the diagnostics of PA, when the diagnosis is justified by the positive response to treatment. However, volume loading serves as an additional diagnostic tool in the most problematic cases, improving slightly the discriminative ability of urinary aldosterone determination.

Aldosterone↗
PubMed1990

Some aldosterone-producing adrenal tumours also secrete cortisol, but present clinically as primary aldosteronism.

1. Two patients with angiotensin-responsive aldosterone-producing adenoma (APA) and one with adrenal cortical carcinoma demonstrated autonomous secretion of cortisol as well as of aldosterone. 2. The response of cortisol and of aldosterone to ACTH did not differentiate between the two APA which secreted cortisol and the eight which demonstrated normal suppression with dexamethasone. 3. Concurrent autonomous secretion of cortisol as well as aldosterone may occur in patients who present clinically with primary aldosteronism. 4. Biochemical distinctions between adenomas may reflect differences in their cellular composition.

Adenoma↗
PubMedDate not supplied

Studies of impaired aldosterone response to spironolactone-induced renin and potassium elevations in adenomatous but not hyperplastic primary aldosteronism.

Spironolactone (SPL) corrects hypertension, hypokalemia, and hyporeninemia in patients with primary hyperaldosteronism (PHA) by blocking mineralocorticoid (MCH) receptors. We evaluated the effect of continuous SPL treatment (100 to 300 mg/day for 7 days to 9 years) on plasma renin (PRC), potassium, aldosterone (PA), 18-hydroxycorticosterone (18-OHB), deoxycorticosterone (DOC), and corticosterone (B) concentrations and 24-hour urinary excretion of aldosterone (UA) in 24 patients with PHA (15 with an aldosterone-producing adenoma [APA] and nine with idiopathic PHA [IHA]). Despite the normalization of PRC and K in both APA and IHA patients by SPL, UA and PA failed to increase in APA (55.8 +/- 8.8 to 51.4 +/- 7.3 micrograms/24 hr and 54.0 +/- 9.4 to 44.6 +/- 6.2 ng/dl, respectively) in contrast to rises in IHA patients (22.3 +/- 2.5 to 69.3 +/- 10.3 micrograms/24 hr and 16.0 +/- 1.0 to 49.9 +/- 9.9 ng/dl). Similar corrections with amiloride (20-40 mg/day for 2 months) in one patient with APA produced a three- to fourfold increase in UA and PA. In addition, while on SPL the characteristic fall or no change in PA and 18-OHB during upright posture persisted in all APA patients despite further increases in PRC (4.48 +/- 1.15 to 7.86 +/- 1.89) and K (4.0 +/- 0.1 to 4.3 +/- 0.1). The patterns of the aldosterone precursors, DOC, B, and 18-OHB, and their ratios to acute stimulation with cosyntropin were not altered by SPL. Thus, SPL treatment causes a sustained impairment of the aldosterone secretory response to normalized PRC and K, but not to ACTH stimulation, only in patients with APA.

Adenoma↗
PubMed1993

Reduced response to metoclopramide and anomalous rising response to upright posture of plasma aldosterone concentration in Japanese patients with aldosterone-producing adenoma.

We examined the changes in plasma aldosterone concentration (PAC) during 3 kinds of postural stimulation tests and a metoclopramide test in 20 Japanese patients with surgically proven aldosterone-producing adenoma. In the 2-h upright test (n = 16), PAC increased (P < 0.01) in 14 of 16 patients, with a mean percent change of 135 +/- 42% (+/- SD) of the supine levels without any significant change in plasma cortisol. In the furosemide-upright test (n = 17), PAC increased (P < 0.01) in 15 of 17 patients by 131 +/- 27%, with a significant increase in cortisol. However, in the furosemide upright test after dexamethasone pretreatment, which suppressed plasma cortisol during the test, PAC also increased (P < 0.01) in all 9 patients examined by 158 +/- 36%. Angiotensin-II infusion failed to increase PAC in all 4 patients examined whose PAC increased with postural stimulation tests. Injection of 10 mg metoclopramide (n = 13) induced a significant, but less marked, increase (P < 0.01) in PAC to 157 +/- 59% of basal levels, which was lower than those in previously reported series in Western countries. These results suggest that 1) there is a difference in PAC responsiveness to postural stimulation tests and to metoclopramide injection between Japanese and Western patients; and 2) the difference in the metoclopramide-induced aldosterone response implies a relative reduction of tonic dopaminergic inhibition of aldosterone secretion in our Japanese patients with aldosterone-producing adenoma.

Adrenal Cortex↗
PubMed1996

Aldosterone-producing adenomas do not contain glucocorticoid-remediable aldosteronism chimeric gene duplications.

In glucocorticoid-remediable aldosteronism (GRA) a chimeric gene has been described with the activity of aldosterone synthase, but the promoter of 11 beta-hydroxylase leading to ectopic expression of aldosterone synthase activity in the zona fasciculata. Similar to GRA, in aldosterone-producing adenomas (APA), the primary regulation of aldosterone production is ACTH, and there is increased production of the 18-oxygenated cortisol compounds, 18-oxocortisol and 18-hydroxycortisol. Because of these hormonal similarities, we tested whether a chimeric GRA-like gene was present in APA from 11 patients. A GRA-like chimeric gene was not found in the DNA from these tumors and, therefore, is not the mechanism responsible for hyperaldosteronism in APA.

Adenoma↗
PubMed1977

Urinary aldosterone excretion rate and plasma aldosterone concentration in the rat: effect of ACTH, DOC, furosemide and of changes in sodium balance.

In rats kept under standard conditions urinary aldosterone exretion rate (UAER) and plasma aldosterone concentration (PAC) showed a circadian rhythm with peak values at the beginning of the dark perioith a single dose of DOC (2 mg/kg sc) or given saline as drinking water UAER and PAC decreased to very low levels. Restriction of dietary sodium for 5 weeks increased UAER and PAC 60-fold and 100-fold, respectively. Treatment with ACTH (250 or 500 microng/kg iv) stimulated UAER 8 h following injection and PAC 1 h after injection. In rats treated with a single dose of furosemide (25 mg/kg sc) PAC increased to maximal values within 90 min and reached control values within 24 h. Twenty-four hours-UAER also increased after furosemide treatment. UAER paralleled PAC under all experimental conditions tested. Therefore, our results suggest that UAER is a reliable index of the activity of the renin-angiotensin-aldosterone system in rats under conditions of low and high aldosterone secretion. Measurement of UAER is a useful tool for studies on aldosterone levels in rats over a long period of time.

Adrenocorticotropic Hormone↗
PubMed1985

Primary aldosteronism with normal aldosterone levels in blood and urine.

A 47 year old women examined for hypertension (200/100 mmHg) was normokalaemic, and had low plasma renin activity (PRA) (0.1 ng/ml X h) and normal aldosterone levels in both plasma (7-13 ng/dl) and urine (4.7-7.4 micrograms/day). Computed tomography (CT) and scintiscan indicated an adenoma on the right adrenal gland, which was then removed. The histology of the adenoma and analysis of the aldosterone content were compatible with the criteria for an aldosterone-producing adenoma. Three months after surgery, her hypertension had improved, serum potassium levels had increased slightly, and PRA had normalized. This was an unusual form of primary aldosteronism which showed normal levels of aldosterone in both blood and urine.

Adenoma↗
PubMed1976

Triamterene-induced changes in aldosterone and renin values in essential hypertension. Evidence of a role for aldosterone in preventing blood pressure reduction.

The effect of triamterene, a potassium-retaining natriuretic and diuretic agent, on arterial blood pressure was studied in 31 patients with essential hypertension; there were seven patients with low plasma renin activity and 24 patients with normal plasma renin activity. Triamterene exhibited mild antihypertensive action, somewhat more pronounced in the low-renin group. The patients were also analyzed by considering them in terms of their blood pressure response. Of the 21 patients in the nonresponder group, no blood pressure decrease occurred, despite induced volume depletion accompanied by an increased plasma renin activity and a concomitant rise in the aldosterone excretion. In contrast, the ten patients in the responder group exhibited a fall in blood pressure, but the aldosterone excretion rate did not change significantly, even though plasma renin activity increased significantly. Moreover, only in the nonresponder group did the stimulated aldosterone excretion rate correlate significantly with the stimulated plasma renin activity. Thus, the failure of triamterene to lower blood pressure in the nonresponder group can be closely related to a significant increase in aldosterone excretion rate. The data suggest the operation of a reactive pressor action mediated by aldosterone, independent of its sodium-retaining effect.

Aldosterone↗
PubMed2004

The role of aldosterone and aldosterone-receptor antagonists in heart failure.

Prolonged overactivation of neurohormonal mechanisms in heart failure produces deleterious effects on the cardiovascular system and leads to poor prognosis. Angiotensin-converting enzyme (ACE) inhibitors and beta-blockers have been shown to interrupt this excessive overactivity and improve survival. Activation of the renin-angiotensin system leads to increased synthesis of aldosterone in heart failure. Some aldosterone production is independent of ACEs; therefore, ACE inhibition does not entirely suppress the excessive formation of aldosterone. An excess of aldosterone in heart failure leads to sodium retention and myocardial fibrosis. The use of aldosterone antagonists, combined with standard therapy for heart failure, improves morbidity and mortality.

Aldosterone↗
PubMed1991

Aldosterone-producing adenoma--variable serum aldosterone response to postural change: a case report.

A 25-year-old female was admitted for evaluation of hypertension and hypokalemia. Plasma renin activity was suppressed and plasma aldosterone level was higher than normal. The CT scan of adrenal gland revealed a 2.5cm in size low density tumor mass over right adrenal area, and NP-59 adrenal scan showed early and persistent uptake of radioactivity in the right adrenal gland. Interestingly, the plasma aldosterone level was elevated, decreased and unchanged to postural change on three different occasions. After right adrenalectomy, the plasma aldosterone level decreased to 4.77ng/dl, blood pressure, serum potassium, and plasma aldosterone returned to normal response to postural change. Histologically, it was compatible with the picture of cortical adenoma. However, the tumor cell may not have reached autonomous function yet, since different responses of plasma aldosterone to postural change were observed clinically.

Adenoma↗
PubMed1991

Effect of captopril on aldosterone response to potassium infusion in primary aldosteronism.

The effect of captopril on the aldosterone response to potassium was studied in 6 patients with idiopathic adrenal hyperplasia (IAH) and in 4 patients with an aldosterone-producing adenoma (APA), who all have suppressed activity of circulating renin-angiotensin system (RAS). Precaptopril, KCl infusion induced a significant increase in aldosterone in both groups. This increment was significantly blunted by captopril in IAH, but not in APA. Decreased potassium-stimulated aldosterone secretion after captopril in IAH supports the hypothesis that adrenal RAS plays a role in aldosterone production under potassium stimulation.

Adenoma↗