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PubMed1982

Regulation of aldosterone secretion by a new aldosterone stimulating factor.

The site of action in the steroidogenic pathway of aldosterone stimulating factor (ASF), isolated from human urine, was studied in collagenase-dispersed rabbit adrenal capsular cells and compared with those of beta-lipotropin (beta-LPH), angiotensin II (A II) and adrenocorticotropic hormone (ACTH). When incubated with adrenal cell suspension at 37 degrees C for 2 hours, ASF, beta-LPH and ACTH induced dose-related increases in aldosterone production. ASF was less potent (ED50 = 10(-9) M) than ACTH but was more potent than beta-LPH. When ASF was added to the incubation with low dose of A II or ACTH, its effect on aldosterone production was additive, while no additional effect of ASF on aldosterone production was obtained in the presence of high dose of A II or ACTH. ASF increased the conversion of corticosterone to aldosterone like ACTH and beta-LPH. We have reported that ASF is a true aldosterone secretagogue and readily distinguishable from ACTH, A II and beta-LPH. The present study suggests ASF shares a common rate-limiting final pathway of steroidogenesis, which may be the step between corticosterone to aldosterone, with ACTH, A II and beta-LPH.

Adrenal Glands↗
PubMed1987

Effects of corticotropin-releasing factor (CRF) on aldosterone and 18-hydroxycorticosterone in essential hypertension and primary aldosteronism.

The effects of ovine corticotropin releasing factor (o-CRF) on plasma aldosterone, 18-OH-corticosterone (18-OHB), plasma adrenocorticotropin (ACTH) and cortisol were determined in eight patients with primary aldosteronism, six with aldosterone-producing adenoma (APA) and two with idiopathic hyperaldosteronism (IHA). The results were compared with those in six normal subjects and eleven patients with essential hypertension (EHT, 5 with low renin and 6 with normal renin). In patients with APA, the peak plasma aldosterone and 18-OHB responses to 100 micrograms iv of o-CRF (226% and 113% increase from baseline, respectively) were greater than those in EHT and normal subjects. The net integrated aldosterone and 18-OHB responses (840 +/- 156, and 419 +/- 121 ng/dl.hr, respectively) were also significantly greater (p less than 0.01) in APA than those in normals and EHT. In two patients with IHA, both the peak and net integrated aldosterone response were smaller than those in APA, in spite of nearly identical plasma ACTH and cortisol responses. These results suggest that augmented responses of mineralocorticoids to o-CRF may be characteristic of aldosteronism due to APA, mediated by CRF-induced ACTH, and possibly other proopiomelanocortin (POMC)-derived peptides.

18-Hydroxycorticosterone↗
PubMed1978

Primary aldosteronism: inability to differentiate unilateral from bilateral adrenal lesions by various routine clinical and laboratory data and by peripheral plasma aldosterone.

In 31 patients with primary aldosteronism routine clinical and laboratory data, the effect of orthostasis on plasma aldosterone (PA), plasma renin activity (PRA) and cortisol (PC), effect of fludrocortisone or high sodium intake on basal PA and night-day fluctuations of basal PA and PC with and without suppression of pituitary ACTH by dexamethasone were determined to differentiate patients with a unilateral aldosterone producing tumour (adenoma, APA, n=20; carcinoma, CA, n=1) from those with idiopathic bilateral adrenal hyperplasia (IAH, n=10). Mean systolic and diastolic blood pressure, age, serum potassium and urinary excretion of sodium and potassium were not significantly different in both groups of patients. Normokalaemic primary aldosteronism occurred both in patients with APA (n=2) and in patients with IAH (n=1). Mean basal PA and mean urinary excretion rate of aldosterone-18-glucuronide were higher though not significantly different in patients with APA or CA than in those with IAH. A substantial number of the patients with APA (n=5) and with IAH (n=3) showed urinary excretion rates of aldosterone-18-glucuronide less than 13 microgram/24 h. Mean PA and PRA significantly increased (P less than 0.025) in patients with IAH in response to posture. However, these changes also occurred at times in some patients with APA. Both fludrocortisone and high sodium intake produced a variable and no group-specific effect on basal PA. Night-day variations in PA were positively correlated with those in PC in all patients with APA (n=12) and in 5 of 8 patients with IAH. A dissociation of PA and PC, however, was only observed in patients with IAH. Finally, the effect of dexamethasone on plasma aldosterone curves was variable in both groups of patients. Our results indicate that under the described conditions analysis of routine clinical and laboratory data and of peripheral PA, PRA and PC are of limited value in differentiating patients with APA or CA from those with IAH.

Adenoma↗
PubMed1986

Plasma aldosterone-plasma renin activity ratio. A simple test to identify patients with primary aldosteronism.

Thirty-two patients with hypertension and recurrent hypokalaemia were investigated on the suspicion of primary aldosteronism. On the basis of unsuppressible aldosterone secretion upon oral mineralocorticoid administration in 16 patients, a surgical exploration was made revealing a typical aldosteronoma in 12 of them, macronodular hyperplasia in two, micronodular hyperplasia in one, and micronodular hyperplasia together with a phaeochromocytoma in one patient. The remaining 16 patients with normal aldosterone suppressibility were considered to have primary hypertension. The discriminatory power of various biochemical tests related to the renin-angiotensin-aldosterone axis was analyzed in retrospect. The only parameter allowing a separation of patients with biochemically and surgically confirmed primary aldosteronism from the other group was the plasma aldosterone-plasma renin activity ratio. The present study therefore confirms the diagnostic value of this ratio for identifying patients with primary aldosteronism.

Adult↗
PubMed1983

Unilateral hypersecretion of aldosterone associated with adrenal hyperplasia as a cause of primary aldosteronism.

In 3 patients with longstanding hypertension and spontaneous or diuretic-induced hypokalemia, the diagnosis of primary aldosteronism was established by the dual criteria of non-suppressible plasma aldosterone level and suppressed plasma renin activity. Preoperative studies of the etiology for the hyperaldosteronism using the postural plasma aldosterone test and adrenal venous steroid measurements gave conflicting results. On the basis of the differential adrenal venous steroid content, which suggested an unilateral adrenal source for the aldosterone hypersecretion, presumed to be adrenal adenoma, each patient was operated upon. In each case the excised adrenal revealed adenomatous or macronodular hyperplasia. Reinvestigation of the patients 3 to 12 months after the adrenalectomy showed that the dynamics of the renin-aldosterone axis was now restored to the normal state even though the patients remained hypertensive. These findings indicate that unilateral hypersecretion of aldosterone associated with adrenal hyperplasia can occur in some patients with primary aldosteronism simulating that due to an aldosteronoma. Such observations also raise questions about the pathogenesis of the adrenal hyperplasia and seem to add further complexity to the evaluation of patients with hyperaldosteronism.

Adrenal Cortex↗
PubMed1975

Vasodilating antihypertensive drug-induced aldosterone release--a study of endogenous angiotensin-mediated aldosterone release in the rat.

The vasodilatory drugs, minoxidil and hydralazine, induce renin release in the rat, man and the dog. Previous reports suggest that the rat adrenal cortex was insensitive to angiotensin stimulation. As a result these studies were designed to obtain evidence for or against the hypothesis that the control of aldosterone release in the rat is unique among mammalian species. Minoxidil and hydralazine induced a time-related increase in both serum renin activity and serum aldosterone. Minoxidil caused a dose-related, proportional increase in serum renin and aldosterone. This response was blocked by prior bilateral nephrectomy but was not affected by hypophysectomy. A competitive angiotensin antagonist, saralasin (1-Sar-8-Ala angiotensin II), impaired minoxidil-induced aldosterone release in a dose-related manner while potentiating minoxidil-induced renin release. Pretreatment with propranolol, a beta adrenergic blocking drug, impaired minoxidil-induced renin and aldosterone release. Only small changes in serum corticosterone occurred after minoxidil or hydralazine administration. These results indicate that minoxidil-induced aldosterone release was mediated by the endogenous angiotensin II formed from renin release. They also support the unanesthetized rat as an appropriate animal model for study of the renin-angiotensin-aldosterone axis and its modification by drugs.

Aldosterone↗
PubMedDate not supplied

[The circadian rhythm of serum aldosterone in the diagnostics of primary aldosteronism].

Diagnosis of primary aldosteronism should be easy in patients with unprovoked hypokaliemia and hypertension. However, it is more difficult to differentiate patients with primary normokaliemic aldosteronism from those with essential hypertension with low plasma renin activity. The aim of this study was to evaluate the appropriate testing of diagnosis and differential diagnosis of primary aldosteronism. The study group consisted of 17 patients with primary aldosteronism (12 with aldosteronoma and 5 with bilateral hyperplasia) and 20 patients with essential hypertension. The finding of increased serum aldosterone level using a single measurement, without anti-hypertensive therapy and on normal sodium intake is sufficient to confirm the diagnosis of primary aldosteronism with specificity of 95% and sensitivity of 94%. Upright posture test is shown to be fairly good tool in differentiation aldosteronoma and bilateral adrenal hyperplasia. Specificity of this test is 100% and sensitivity 88%. Although primary aldosteronism is not a common cause of hypertension it is reasonable to screen for this disorder because complete cure can be provided in a large percentage of patients.

Aldosterone↗
PubMed1980

Effects of propranolol on aldosterone plasma concentration and aldosterone metabolic clearance in hypertensive patients.

Although propranolol administration produces a lowering of PRA, PAC does not decrease in a similar fashion. In the present study the effects of propranolol on the aldosterone MCR were examined. Eight patients with essential hypertension were studied while receiving treatment with a diuretic and again after propranolol (160 to 320 mg/day) was added to the therapeutic regimen. Propranolol therapy was associated with a 25% decrease in PRA (p less than 0.05) and changes in PACs that were variable but not significantly different from diuretic therapy alone. The aldosterone MCR decreased from 1420 +/- 120 to 1120 +/- 90 L/24 hr in response to propranolol (p less than 0.01). The average production rate of aldosterone (MCR X PAC) did not change after propranolol treatment despite a decrease in PRA. There were no changes in plasma concentrations of potassium or in ACTH secretion (as reflected by levels of cortisol) to explain a role for propranolol to sustain aldosterone secretion. Thus propranolol administered to hypertensive patients pretreated with a diuretic can affect circulating levels of aldosterone apart from changes in PRA. Propranolol therapy produces a moderate reduction in aldosterone MCR and appears to augment aldosterone production by a mechanism exclusive of known stimuli.

Adult↗
PubMed1987

Effect of verapamil on aldosterone secretion in primary aldosteronism.

Intracytoplasmic calcium seems to act as second messenger for aldosterone secretion. Both in vitro and in vivo studies demonstrate that drugs which block calcium entry cause a decreased responsiveness of glomerulosa cells to Angiotensin II and potassium. In order to evaluate the effect of a calcium channel blocking agent (Verapamil) in conditions of abnormal aldosterone secretion, we have studied 11 patients with primary aldosteronism, 5 with idiopathic hyperaldosteronism (IHA) and 6 with aldosterone producing adenoma (APA). In our study plasma aldosterone levels decreased after Verapamil infusion in IHA whereas no significant variations were observed in APA patients. These results suggest that calcium blockade can interfere with a possible regulatory system which plays a greater role in idiopathic aldosteronism.

Aldosterone↗
PubMed2003

Aldosterone and specific aldosterone receptor antagonists in hypertension and cardiovascular disease.

Recent preclinical and clinical studies indicate that aldosterone, independent of angiotensin II and elevated blood pressure, may play a role in health and disease. In addition to its role in fluid and electrolyte balance and circulatory homeostasis, more recent studies have identified aldosterone as a critical mediator of vascular damage. In animal studies, aldosterone is implicated in cardiac and vascular fibrosis, renal disease, and cerebrovascular damage. These lesions are prevented by specific aldosterone receptor blockade. In clinical studies, aldosterone receptor antagonism is associated with decreased hospitalization, symptomatology, and mortality, and improvement of endothelial dysfunction in patients with chronic heart failure. A better understanding of aldosterone's actions in nonepithelial tissues should pave the way to better protection of organs at risk such as the kidneys, heart, and brain.

Aldosterone↗
PubMed1985

A study of [3H]aldosterone binding by nuclear and cytoplasmic receptors of the rat kidney with different content of aldosterone in the organism.

The distribution of specific mineralocorticoid receptors in rat kidney cells was found to depend on aldosterone concentration. With increasing aldosterone concentrations the number of specific receptors for aldosterone in the cytoplasm decreased and their quantity in the nuclei increased. This was evidently due to their enhanced transport from the cytoplasm to the nuclei. It was found that aldosterone (its complex with the receptor) attached to non-histone proteins of chromatin and that the structural integrity of DNA is needed to provide the binding of this complex to the cell nuclei. The quantity of aldosterone acceptor sites in the kidney cell nuclei remained constant when aldosterone concentrations in the organism changed, and, hence, the functional states of the target organ changed too.

Aldosterone↗
PubMed1985

Absent aldosterone response to metoclopramide in patients with high spinal cord transection: evidence that metoclopramide stimulates aldosterone secretion through central pathways.

This study evaluates dopaminergic regulation of aldosterone secretion in 6 patients with high spinal cord transections. Administration of the dopamine antagonist metoclopramide resulted in a marked rise in plasma aldosterone and 18-hydroxycorticosterone levels in 12 normal individuals, but no change in plasma levels of these zona glomerulosa corticosteroid products in spinal cord patients. Spinal cord transected patients also did not have the rise in plasma renin activity that was observed in normals following metoclopramide administration. Basal levels of aldosterone, 18 hydroxycorticosterone, corticosterone and renin activity as well as the aldosterone responses to graded dose infusion of adrenocorticotropin were similar in the spinal cord patients and the normals. These data suggest that dopaminergic regulation of adrenal zona glomerulosa corticosteroid and renal renin secretion is absent in patients with high spinal cord transections, suggesting that intact neural pathways from the central nervous system are necessary for metoclopramide stimulation of aldosterone and renin secretion in men. Since basal plasma aldosterone levels were normal in spinal cord transected patients, it appears that the absence of dopaminergic control does not result in elevated secretion.

18-Hydroxycorticosterone↗
PubMed2005

Aldosterone-to-renin ratio, arterial stiffness, and the response to aldosterone antagonism in essential hypertension.

BACKGROUND: Some 10% to 15% of hypertensive patients have hyperaldosteronism, an increased ambulant aldosterone-to-renin ratio. As aldosterone reduces arterial compliance, we examined the relationship between aldosterone-to-renin ratio, aortic blood pressure (BP), arterial stiffness, and the effect of spironolactone in a hypertensive population. METHODS: In 24 untreated patients (mean age 51 +/- 2 years, 10 women), we assessed arterial stiffness by augmentation index-height of the late systolic peak in the aorta, pulse pressure (Sphygmocor), and aortic pulse wave velocity (Complior). RESULTS: There were significant positive correlations between the aldosterone-to-renin ratio and aortic systolic pressure, aortic pulse pressure, and augmentation index and negative correlations with pulse pressure amplification, but none with brachial BP or pulse wave velocity. After randomization in a cross-over design to 50 mg of spironolactone or 2.5 mg of bendroflumetazide for 4 weeks with washout period of 1 month, both drugs significantly reduced brachial BP, but only spironolactone reduced (P < .001) pulse wave velocity and augmentation index, which remained significant when corrected for its greater reduction in mean BP. There were significant (P < .001) positive correlations between the ratio and decrease in aortic systolic (r = 0.78), mean (r = 0.75), diastolic BP (r = 0.66), aortic pulse pressure (r = 0.69, augmentation index (r = 0.64) and with, brachial systolic pressure (r = 0.66), brachial pulse pressure (r = 0.44, P < .05) and pulse pressure amplification (r = 0.46, P < .05). Such relationships were not found with pulse wave velocity. CONCLUSIONS: The aldosterone-to-renin ratio may have an important role in determining arterial stiffness, particularly wave reflection and aortic systolic pressure and is of predictive value for the responsiveness to spironolactone. Aldosterone antagonism has BP-independent effects on arterial stiffness.

Aldosterone↗
PubMed1975

Location of aldosterone-producing adenomas by the determination of plasma aldosterone in adrenal vein or renal vein blood.

1. Aldosterone-producing adenomas were located before operation in eighteen patients by comparison of aldosterone concentrations in blood obtained by percutaneous catheterization of the adrenal vein or renal vein. The concentration of aldosterone in the venous effluent from the adrenal glands containing adenomas was significantly greater than in the venous effluent from contralateral glands. 2. Cathetherization of the adrenal vein is, however, technically difficult. The location of adrenal adenomas was also possible by analysis of blood from the renal vein. 3. If the concentrations of aldosterone in blood from the left renal vein were higher than those from the right, the existence of a left adrenal adenoma was suggested. A high value in plasma, obtained from the inferior vena cava above the entry of the right adrenal vein, showed a right adrenal adenoma. This procedure identified very small functional adenomas which could not be demonstrated radiographically, or seen or palpated at surgery. 4. It was concluded that differential aldosterone measurement after percutaneous bilateral adrenal vein or renal vein catheterization can be used as a definitive test for the location of an aldosterone-producing adenoma, where this is uncertain.

Adenoma↗
PubMed1981

Effect of angiotensin II and converting enzyme inhibitor (captopril) on blood pressure, plasma renin activity and aldosterone in primary aldosteronism.

1. Patients with idiopathic hyperaldosteronism (IHA) show a response of aldosterone to posture which is not present in patients with aldosterone-producing adenoma (APA). We have determined whether this could be explained by a different sensitivity to angiotensin II. 2. Angiotensin II was infused in gradually increasing doses in six patients with APA and in seven patients with IHA. No changes in aldosterone concentration were found at the end of each period in APA, whereas there was a significant increase in IHA; blood pressure rose by a similar extent in both groups. 3. In order to evaluate the role of endogenous angiotensin II, captopril, a converting enzyme inhibitor, was administered to six patients with APA and five patients with IHA at a dose of 75 mg/day for 1 week. There was a significant fall of mean blood pressure in IHA and only minimal changes in APA. Plasma renin activity and plasma in urinary aldosterone were unchanged in APA. In IHA there was a small increase in upright plasma renin activity and a slight decrease in both plasma and urinary aldosterone, but these changes were not significant. 4. These findings further support the idea that idiopathic hyperaldosteronism is a clinical state different from that occurring in primary aldosteronism due to adenoma, and may be more closely related to essential hypertension.

Aldosterone↗
PubMed2005

Dual blockade of the renin-angiotensin-aldosterone system in diabetic nephropathy: the role of aldosterone.

Dual blockade of the renin-angiotensin-aldosterone system (RAAS) with both ACE inhibitors and angiotensin II receptor-blockers has been shown to reduce both albuminuria and blood pressure compared to either monotherapy. The mechanisms behind these beneficial effects are not known, and we hypothesized that the effect of dual RAAS blockade may be due to a more complete suppression of circulating aldosterone. We performed a combined analysis on three randomized, double-masked, cross-over trials where 51 type 1 diabetic patients suffering from diabetic nephropathy received 8 weeks of dual RAAS blockade using an angiotensin II receptor blocker in combination with an ACE inhibitor and 8 weeks of monotherapy with the same ACE inhibitor. Albuminuria, 24 h blood pressure, GFR, and plasma aldosterone were determined at the end of each treatment period. Compared to ACE inhibition alone, dual RAAS blockade lowered blood pressure by 7/5 mm Hg from 137/76 mm Hg, decreased albuminuria by 37% from 558 mg/24 hour, and reduced plasma aldosterone by 28% from 59 pg/ml and caused a reversible decline in GFR of 4 ml/min/1.73 m2 (p < or = 0.01 for all comparisons). There was and a significant correlation between changes in 24-hour diastolic blood pressure and changes in albuminuria. Furthermore, the antialbuminuric response to dual blockade was influenced by the ACE/ID polymorphism, that is, patients carrying the D-allele had a significantly lower reduction of 31% compared to the 55% in patients with the II genotype (p = 0.021). Multiple linear regression analysis revealed that ACE/ID genotypes and reduction in plasma aldosterone, diastolic blood pressure and GFR is associated with changes in albuminuria on dual blockade treatment (R2 (adjusted) = 0.57, p < 0.001). Dual RAAS blockade is a new treatment concept that may offer additional cardiovascular and renal protection in type 1 diabetic patients with diabetic nephropathy. The beneficial response may be influenced by genetic factors and reductions in blood pressure and plasma aldosterone concentrations.

Adult↗
PubMed2004

Aldosterone synthase gene (CYP11B2) C-344T polymorphism, plasma aldosterone, renin activity and blood pressure in a multi-ethnic population.

BACKGROUND: The aldosterone synthase gene (CYP1B2) locus is a candidate region involved in the development of hypertension. OBJECTIVE: To study the relationship between the C-344T CYP1B2 polymorphism, plasma aldosterone, renin activity and blood pressure in a multi-ethnic population. DESIGN: Population-based, cross-sectional study of 1313 middle-aged men and women (456 white, 441 of African origin and 416 South Asian). Anthropometry, blood pressure, biochemistry, questionnaire data and timed urine collections were taken with standardized techniques. All were genotyped for the C-344T CYP11B2 polymorphism. RESULTS: The frequency of the C allele was significantly lower in people of African origin (0.21) than in white (0.46) and South Asian (0.43) (P < 0.001). After adjustment for age, sex and ethnicity the TT genotype was associated with 14% higher plasma aldosterone levels, 3.7 mmHg higher systolic and 2.1 mmHg higher diastolic blood pressure than CC (P for linear trend < 0.05). No significant interactions with age, sex, ethnicity, body mass index (BMI) and fractional excretion of sodium were found in the associations between genotype and both blood pressure and aldosterone levels. In a sub-sample of participants in which plasma renin activity was measured (n = 457), a significant excess of T alleles was found in those with a raised (>/= 750) aldosterone-to-renin ratio (ARR). CONCLUSION: In this multi-ethnic population, the C-344T CYP1B2 polymorphism is associated with blood pressure, plasma aldosterone levels and ARR. Although significant differences in allele frequencies were found between groups, ethnicity does not explain the results.

Adult↗
PubMedDate not supplied

Aldosterone and aldosterone antagonism in cardiovascular disease: focus on eplerenone (Inspra).

Aldosterone has long been known to mediate water and electrolyte balance by acting on mineralocorticoid receptors in the kidneys. However, recent studies have demonstrated the presence of these receptors in nonclassical locations, including the brain, blood vessels, and the heart. This finding suggests that aldosterone may play a larger role than once appreciated in normal physiologic function and cardiovascular disease. Some of the adverse cardiovascular effects that have been described include cardiac and vascular fibrosis, left ventricular hypertrophy, congestive heart failure, hypertension, endothelial dysfunction, reduced fibrinolysis, and cardiac arrhythmias. In light of these findings, aldosterone receptor blockers have become increasingly more important. This is especially true considering the fact that traditional therapies, such as angiotensin-converting enzyme inhibitors and angiotensin II-receptor blockers, may not be effective in maintaining long-term suppression of aldosterone. Therefore, a great deal of focus has been placed on spironolactone, which has proven to be an effective, albeit nonselective, aldosterone receptor blocker. The Randomized Aldactone Evaluation Study has shown that spironolactone results in a 30% reduction in mortality among patients with severe congestive heart failure. Other studies have shown spironolactone to lower high blood pressure, improve endothelial dysfunction, reduce left ventricular hypertrophy, and lower the incidence of fatal arrhythmias. However, spironolactone, because of its interaction with other steroid receptors, is not without its limitations, which include gynecomastia, breast tenderness, menstrual irregularities, and impotence. As a result, eplerenone (INSPRA), a selective aldosterone blocker, is currently being investigated for its efficacy and side-effect profile compared with spironolactone. Eplerenone has already been approved for the treatment of systemic hypertension, and several clinical trials are currently underway to identify other therapeutic uses for this agent in cardiovascular disease management.

Aldosterone↗