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PubMed1999

Aldosterone excretion rate and blood pressure in essential hypertension are related to polymorphic differences in the aldosterone synthase gene CYP11B2.

Significant correlation of body sodium and potassium with blood pressure (BP) may suggest a role for aldosterone in essential hypertension. In patients with this disease, the ratio of plasma renin to plasma aldosterone may be lower than in control subjects and plasma aldosterone levels may be more sensitive to angiotensin II (Ang II) infusion. Because essential hypertension is partly genetic, it is possible that altered control of aldosterone synthase gene expression or translation may be responsible. We compared the frequency of 2 linked polymorphisms, one in the steroidogenic factor-1 (SF-1) binding site and the other an intronic conversion (IC), in groups of hypertensive and normotensive subjects. In a larger population, the relationship of aldosterone excretion rate to these polymorphisms was also evaluated. In 138 hypertensive subjects, there was a highly significant excess of TT homozygosity (SF-1) over CC homozygosity compared with a group of individually matched normotensive control subjects. The T allele was significantly more frequent than the C allele in the hypertensive group compared with the control group. Similarly, there was a highly significant relative excess of the conversion allele over the "wild-type" allele and of conversion homozygosity over wild-type homozygosity in the hypertensive group compared with the control group. In 486 subjects sampled from the North Glasgow Monitoring of Trends and Determinants in Cardiovascular Disease (MONICA) population, SF-1 and IC genotypes were compared with tetrahydroaldosterone excretion rate. Subjects with the SF-1 genotypes TT or TC had significantly higher excretion rates than those with the CC genotype. The T allele was associated with higher excretion rates than the C allele. However, no significant differences were found in excretion rate between subjects of different IC genotype. Urinary aldosterone excretion rate may be a useful intermediate phenotype linking these genotypes to raised BP. However, no causal relationship has yet been established, and it is possible that the polymorphisms may be in linkage with other causative mutations.

Adult↗
PubMed1999

Angiotensin AT1 receptor subtype as a cardiac target of aldosterone: role in aldosterone-salt-induced fibrosis.

This study tests the hypothesis that aldosterone induces cardiac fibrosis through an increase of cardiac angiotensin II (Ang II) AT1 receptor levels, thereby potentiating the fibrotic effect of Ang II by determining the effects of spironolactone and losartan on cardiac fibrosis, AT1 density, and gene expression in aldosterone-salt-treated rats. Fibrosis was quantified by slot blots of collagen I and III mRNA levels and videomorphometry of Sirius red-stained collagen. AT1 receptor density was determined by (125I-Sar1-Ile8)-Ang II competition binding, and AT1 mRNA levels were analyzed by quantitative reverse transcriptase polymerase chain reaction. One month of aldosterone-salt treatment induced a decrease in plasma Ang II and an increase in blood pressure, left ventricular hypertrophy, and ventricular fibrosis. Spironolactone (20 mg/kg per day) and losartan spironolactone (10 mg/kg per day) had no effect on the first 3 parameters. Losartan was as effective as spironolactone in preventing ventricular collagen mRNA increase and fibrosis. Ventricular density of AT1 receptors increased 2-fold and was accompanied by a 3-fold increase in the corresponding mRNA in aldosterone-salt compared with sham-operated rats. Both spironolactone and losartan prevented the elevation of ventricular AT1 density and that of right ventricular AT1 mRNA levels. These results demonstrate that the mechanism by which aldosterone-salt induces cardiac fibrosis involves Ang II acting through AT1 receptors. They also suggest that the cardiac AT1 receptor is a target for aldosterone.

Aldosterone↗
PubMed1986

Evaluation of an aldosterone radioimmunoassay: the renin-angiotensin-aldosterone axis as a function of sex and age.

A highly specific radioimmunoassay for aldosterone in plasma has been developed utilising extraction from plasma into dichloromethane, an antiserum raised to aldosterone-3-carboxy-methyloxime-BSA and a radio-iodinated derivative of aldosterone. The plasma values obtained after only extraction correlated very well with the results following chromatography over celite. The within- and between-batch variations for plasma pools ranged between 5 and 15%. The range obtained, 100-1806 pmol/L for 96 random upright subjects, was comparable to others reported. Measurement of plasma aldosterone and plasma renin activity in these subjects showed that both these parameters are higher in subjects under 40 years of age than in those over 40. In addition, plasma aldosterone levels are higher in women than in men even though their plasma renin activity levels are similar. The plasma aldosterone/renin activity ratios which provide an index of adrenal sensitivity to stimulation, are lower in men than in women. The findings in this study suggest that higher aldosterone levels in younger subjects are associated with greater stimulation of the adrenals than in older subjects and that the adrenal is more sensitive in women than in men.

Age Factors↗
PubMed1980

Angiotensin II receptors and in vitro aldosterone responses of aldosterone-producing adenomas, adjacent nontumorous tissue, and normal human adrenal glomerulosa.

Angiotensin II (angio II) receptors have been compared using tissues from aldosterone-producing adenomas (APAs), adjacent nontumorus tissue, and normal human adrenal glomerulosa. Plasma membrane-rich subcellular fractions were employed in a radioreceptor assay with [125I]angio II. In vitro aldosterone secretory response to angio II were determined using isolated cells obtained by collagenase digestion. Results are reported as the mean +/- SE. Normal glands have high and low affinity receptor sites for angio II. The Ka values for a normal adrenal obtained at surgery were 2.5 and 0.4 nM-1, while autopsy adrenals were 1.1 +/- 0.4 and 0.3 +/- 0.15 nM-1 (n = 3). APAs and adjacent nontumorous tissue possessed only low affinity receptor sites (0.22 +/- 0.05 nM--1; n = 11). The receptor concentration for a surgically obtained adrenal was 1562 fmol/mg protein, contrasted with 466 +/- 135 from autopsy adrenals. APA and adjacent tissue bound 462 +/- 112 fmol/mg protein. Cells from seven of eight APAs produced aldosterone when stimulated by angio II (3 x 10(-10)-10(-6) m). The increments were 16-105% above basal levels. The response were similar to but less senstive than cells from normal adrenals. The only tumor that failed to respond had 1/50th of the receptors of the other APAs. In contrast, only three of seven adjacent tissues responded, and then only negligibly. ACTH (10(-8) M) increased aldosterone production by APAs 10-158%, by normal cells 283% and by three of six adjacent nontumorous tissues 170-400%. The observations that APAs have angio II receptors and aldosterone responses to angio II is consistent with the fact that some patients with APA have postural increments of plasma posture. The presence of receptors of adjacent tissue and no in vitro response suggest a defect in the aldosterone biosynthetic pathway as a cause of the prolonged absence of response to angio II after removal of APAs.

Adenoma↗
PubMed1985

Effect of synthetic human atrial natriuretic peptide on aldosterone secretion by dispersed aldosterone-producing adenoma cells in vitro.

The effect of synthetic alpha-human atrial natriuretic peptide (alpha hANP), a potent natriuretic and vasorelaxant polypeptide recently isolated from human atria, on aldosterone secretion was studied in vitro in collagenase-dispersed adrenal adenoma cells from a patient with primary aldosteronism. alpha hANP (3.2 X 10(-7) M) significantly inhibited both basal and potassium (16 mM)-stimulated aldosterone secretion, whereas it had little or no effect on aldosterone secretion submaximally or maximally stimulated by ACTH (3.4 X 10(-10)-3.4 X 10(-9) M) or angiotensin II (10(-8)-10(-9) M). The less potent effect of alpha hANP on aldosterone secretion by dispersed human adrenal tumor cells compared to that in in vitro animal studies may reflect decreased affinity and/or number of specific receptors for ANP on the tumor cells. Whether ANP plays a physiological role in regulation of aldosterone secretion in humans in vivo remains to be determined.

Adenoma↗
PubMed1994

Abnormality of aldosterone and cortisol late pathways in glucocorticoid-remediable aldosteronism.

Patients with glucocorticoid-remediable aldosteronism (GRA) possess a chimeric gene resulting from fusion of the genes encoding steroid aldosterone synthase and 11 beta-hydroxylase. In the adrenal zona fasciculata, this may lead to ectopic expression under ACTH control of aldosterone synthase activity and increased formation of cortisol C18 oxidation products. We assessed mineralocorticoid and glucocorticoid pathways in three patients with GRA. Baseline plasma progesterone, 17 alpha-hydroxyprogesterone, corticosterone, and cortisol were normal in all patients, whereas 11-deoxycorticosterone, aldosterone, and 11-deoxycortisol were above normal. The ratios of both corticosterone/11-deoxycorticosterone and cortisol/11-deoxycortisol were abnormally low, and decreased further 60 min after administration of ACTH-(1-24) (250 micrograms) as an i.v. bolus. A low corticosterone/11-deoxycorticosterone ratio is consistent with an increased aldosterone synthase activity forming aldosterone by corticosterone. Similarly, a decreased cortisol/11-deoxycortisol ratio could reflect enhanced cortisol C18 oxidation. Our findings are in agreement with a hyperfunction of the 11 beta-hydroxylase/aldosterone synthase complex in the adrenal zona fasciculata of GRA induced by the new chimeric gene.

Adrenocorticotropic Hormone↗
PubMed1989

Study on clinical and endocrine characteristics of dexamethasone-suppressible hyperaldosteronism compared with those in primary aldosteronism owing to aldosterone-producing adenoma.

The clinical and endocrine characteristics of 12 Japanese patients with dexamethasone-suppressible hyperaldosteronism were compared with those in 49 Japanese patients with primary aldosteronism due to aldosteronoma. The results were as follows: 1. Most of the laboratory data in the two groups were almost the same. 2. The grade of vascular damage in both uncontrolled (3) and well-controlled (9) patients with dexamethasone-suppressible hyperaldosteronism did not correlate with blood pressure response. 3. The responsiveness of plasma aldosterone to exogenous ACTH in 6 patients with dexamethasone-suppressible hyperaldosteronism was not different from that in 9 patients with aldosteronoma. Even in 3 well-controlled patients in the former group, the plasma aldosterone response was as low as in all the 3 patients with small aldosteronomas. 4. In 4 patients with small aldosteronomas, plasma aldosterone was continuously suppressed with daily dexamethasone to the same degree as in dexamethasone-suppressible hyperaldosteronism. 5. The blood pressure, however, did not improve even in the patients with small aldosteronomas. The possible indistinguishable mechanism in dexamethasone-suppressible hyperaldosteronism and primary aldosteronism with small adenomas and the role of unknown hypertensinogenic steroid(s) other than aldosterone in inducing hypertension in dexamethasone-suppressible hyperaldosteronism are discussed.

Adenoma↗
PubMed1990

Effects of dietary sodium restriction and posture on plasma levels of atrial natriuretic peptide, aldosterone and free aldosterone in normal human pregnancy.

The effects of dietary sodium restriction and posture on plasma concentrations of atrial natriuretic peptide (ANP), aldosterone and free aldosterone were investigated in ten women between weeks 29 and 33 of normal pregnancy. Hormone levels were studied during unrestricted sodium intake and on day 6 of a low sodium diet. On both occasions venous blood was obtained in the sitting as well as in the left lateral tilt position. Plasma concentrations of ANP during the unrestricted sodium intake were not raised compared with control values in healthy non-pregnant females. Recovery experiments showed no differences in the degradation of ANP in blood from pregnant and non-pregnant women. Plasma concentrations of ANP significantly decreased (by 32%) in response to the low sodium regime in both positions. Concentrations of aldosterone and free aldosterone (in women in the sitting position) increased twofold after sodium restriction. Mean values of ANP were higher in women in the left lateral tilt position that in those in the sitting position, but the difference was not significant. Concentrations of aldosterone and free aldosterone were significantly lower (by around 30%) in women in the left lateral tilt position compared with those in the sitting posture.

Adult↗
PubMed2001

Basolateral translocation by vasopressin of the aldosterone-induced pool of latent Na-K-ATPases is accompanied by alpha1 subunit dephosphorylation: study in a new aldosterone-sensitive rat cortical collecting duct cell line.

The regulation of plasma membrane Na(+)-K(+)-ATPases (NKA) expression by aldosterone and arginin vasopressin (AVP) in the cortical collecting duct (CCD) has been examined in a new rat CCD cell line, designated as RCCD(2). This cell line has maintained many characteristics of the CCD-in particular, the expression of the mineralocorticoid receptor. Mineralocorticoid receptor is expressed at the protein level and binds (3)H-aldosterone (approximately 15 to 20 fmol/mg protein). Short-circuit current (Isc) experiments showed approximately a twofold increase in Isc associated with a decrease in transepithelial resistance when cells were treated with aldosterone concentrations as low as 10(-9) M. This effect on Isc was significant 2 h after aldosterone addition and was still present after 24 h. It was accompanied by an increase in the amount of mRNA encoding for the alpha subunit of the epithelial sodium channel (sixfold) and the alpha1 subunit of NKA (fourfold) after 24 h of hormone treatment. In addition, mRNA expression of the serum- and glucocorticoid-induced kinase (Sgk) was increased by 10(-9) M aldosterone treatment as early as 45 min after hormone addition. As had already been documented in native CCD obtained by microdissection, incubation of RCCD(2) cells for 24 h with aldosterone resulted in the constitution of a latent pool of NKA that could be rapidly recruited by AVP (15 min). NKA biotinylation experiments and preparation of membrane fractions show that this latent pool of NKA is present in the intracellular compartment of the cells and is recruited by AVP in the basolateral membrane through a translocation process. This mechanism is accompanied by dephosphorylation of the alpha(1) catalytic subunit of NKA.

Aldosterone↗
PubMed1994

[A case of normotensive primary aldosteronism in association with non-functioning adenoma and aldosterone producing adenoma in ipsilateral adrenal gland].

A case of normotensive primary aldosteronism in association with non-functioning adenoma and aldosterone producing adenoma in ipsilateral adrenal gland is reported. Fourteen cases of normotensive primary aldosteronism were previously reported and our case was considered as the fifteenth case. Furthermore, its association with non-functioning adenoma and aldosterone producing adenoma is very rare. Only four cases of such association were reported, and in these four cases non-functioning adenoma existed in contralateral side of aldosterone producing adenoma. In our case, its association with non-functioning adenoma and aldosterone producing adenoma was seen in the ipsilateral adrenal gland. The report of this kind of association has not been seen in the literature so far.

Adenoma↗
PubMed2006

[Aldosterone-to-renin ratio threshold for screening primary aldosteronism in Chinese hypertensive patients].

OBJECTIVE: In recent years, the assessment of the plasma aldosterone-to-renin ratio (ARR) has become a most effectively and commonly used method for screening primary aldosteronism from hypertensive patients. It is known that there is a large variance in ARR value between races and ARR is affected by many factors, such as drugs, posture and serum potassium etc. The objective of this study is to establish the threshold of ARR for screening primary aldosteronism in Chinese hypertensive patients. METHODS: A total of 110 hypertensive patients were recruited and divided into essential hypertension group (n=65) and adenoma/hyperplasia group (n=45) according to the adrenal contrast CT scan. Antihypertensive drugs which can affect ARR such as beta-blockers, dihydropyridine calcium channel blockers (CCBs), ACE inhibitors (ACEIs), angiotensin II receptor blockers (ARBs) and clonidine, were withdrawn for at least 2 weeks. Washout period for diuretics including spironolactone were 4 weeks. Non-dihydropyridine calcium channel blockers (slow released verapamil) and/or alpha-blocker (terazosin) are allowed for controlling blood pressure when needed. If the serum potassium value<3.6 mmol/L, an oral potassium supplement was prescribed. After keeping upright position for 2 hours, blood samples were drawn for PRA and PAC measurement between 9:00AM-10:00AM. RESULTS: ARR was 100.00+/-48.65 (14.19-285.16) pg/ml vs ngxml-1xh-1 in patients with essential hypertension and 699.33+/-213.33 (185.8-2150) pg/ml vs ngxml-1xh-1 in patients with adenoma/hyperplasia. ARR value was greater than 240 in 42 out of 45 patients (93.3%) with adenoma/hyperplasia and was less than 240 in 59 out of 65 (90.7%) patients with essential hypertension. We used ARR 240 as the cut-off threshold for screening primary aldosteronism in another 178 hypertensive patients and ARR was greater than 240 in all 15 patients with confirmed primary aldosteronism. CONCLUSION: It is suitable to use upright ARR 240 as a cut-off threshold for screening primary aldosteronism in Chinese hypertensive patients.

Adult↗
PubMed1994

[The importance of studying the renin-angiotensin-aldosterone system in essential arterial hypertension in clinical practice. Activity of the renin-angiotensin-aldosterone system during treatment of hypertension with ACE-inhibitors and beta blockers].

The authors assessed in 20 subjects with mild or medium severe arterial hypertension basal and stimulated values of plasma renin activity (PRA) and aldosterone before onset of treatment and after 6-week therapy with enalapril (ENAP KRKA) or metoprolol (Vasocardin Slovakofarma). PRA and aldosterone secretion was stimulated by a vertical position and by administration of 40 mg furosemide by the i.v. This test proved suitable for assessment of secondary arterial hypertension in different forms of primary hyperaldosteronism and for expressing suspicion of renovascular hypertension and hypertension with affection of the renal arteries resp. Based on PRA levels, arterial hypertension can be divided into normorenin, high-renin and low-renin hypertension. This classification is, however, of no value for selection of treatment and the prognosis of hypertension. Each level of PRA can be associated with three different aldosterone levels. PRA and aldosterone did not correlate with urinary K, Na excretion nor with blood pressure. During treatment with ACE inhibitor PRA rose while basal as well as stimulated aldosterone levels declined. After administration of betablockers basal as well as stimulated PRA and aldosterone levels declined.

Adult↗
PubMed1988

[Lateralisation of aldosterone-producing adenoma in primary aldosteronism].

Four lateralizing methods were carried out in 14 patients with primary aldosteronism (PA): ultrasonography, CT scan, adrenal scintiscan and determination of adrenal venous aldosterone levels. In all cases, unilateral aldosterone-producing adenomas were verified by surgery. Of four lateralizing methods, determination of adrenal venous aldosterone, in spite of high diagnostic value, has two big problems: difficulty in selective catheterization of right adrenal vein and dilution of adrenal vein efflux from non-adrenal sources. To solve these problems, cortisol (C, micrograms/dl) levels along with aldosterone (A, ng/dl) were determined in samples from the left adrenal vein (LAV) and the inferior vena cava (IVC) in 8 patients with PA, and the (LAV A/C)/(IVC A/C) ratio was calculated. That ratio was also obtained in 7 patients with other types of hypertension for comparison. Accuracy of lateralisation by ultrasonography, CT scan and adrenal scintiscan was 23%, 64% and 69% respectively, in the first studies. Those rates changed to 23%, 93% and 85% when the second studies were performed. Venous blood was obtained from both adrenal veins in 46% (6/13), while lateralisation of adenoma was also predicted in 46% (6/13) by the measurement of aldosterone concentrations alone. On the other hand, (LAV A/C)/(IVC A/C) ratios were 3.54-6.98 in the cases of left APA, 0.15-0.98 in those of right APA and 1.10-2.86 in cases of other types of hypertension. There was no overlap of ratios among the three groups, resulting in correct prediction of lateralisation in all cases (8/8) of APA.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗
PubMed1994

Association of restriction fragment length polymorphism at the atrial natriuretic peptide gene locus with aldosterone responsiveness to angiotensin in aldosterone-producing adenoma.

Primary aldosteronism is an important, potentially curable, form of hypertension. We examined the possible association between restriction fragment length polymorphisms in the atrial natriuretic peptide (ANP) gene and responsiveness of aldosterone to angiotensin II in 59 patients with primary aldosteronism due to aldosterone-producing adenoma (APA). Significant differences in the allelic frequencies of the BglI, TaqI and XhoI polymorphic sites at the ANP gene locus (chromosome 1; 1p36) between angiotensin II-unresponsive and angiotensin II-responsive tumors were observed. Variation in the ANP gene between the two groups may result in altered expression of ANP within the adrenal gland, and may contribute to the biochemical regulation of aldosterone production of these two subgroups of patients with APA.

Adenoma↗
PubMed1995

Inhibition of angiotensin II- and potassium-mediated aldosterone secretion by KN-62 suggests involvement of Ca(2+)-calmodulin dependent protein kinase II in aldosterone secretion.

Calcium is now acknowledged to play a major role as a cellular mediator of aldosterone secretion. However, the intricacies of the involvement of calcium in aldosterone secretion have not been clearly defined. We have shown here that calmodulin-dependent kinase II is involved in angiotensin II- and potassium-evoked aldosterone secretion as judged by the marked inhibitory effect of KN-62, a specific inhibitor of such a kinase, on aldosterone secretion and this inhibition was similar to that produced by calmodulin inhibitor, W-7. These results further strengthen the case for the participatory role of calcium-calmodulin system in aldosterone secretion.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed2005

Idiopathic primary hyperaldosteronism: normalization of plasma aldosterone after one month withdrawal of long-term therapy with aldosterone-receptor antagonist potassium canrenoate.

We have re-evaluated 15 patients with idiopathic primary aldosteronism one month after withdrawal of therapy with aldosterone-receptor antagonist potassium canrenoate. Therapy had lasted for 3 to 24 yr. Median blood pressure (BP) in the sitting position at the time of diagnosis was 160/100 (ranges 150-200/95-110 mmHg); while 1 month after withdrawal of therapy median BP was 145/90 (ranges 125-160/80-100 mmHg). One month after withdrawal, the ratio aldosterone (ng/dl)/plasma renin activity (ng/ml/h) in the upright position was increased only in 3 cases (median 18, range 6.1-125). We found a significant inverse correlation between the upright aldosterone/plasma renin activity (aldo/PRA) ratio, 1 month after withdrawal, and the number of years of therapy with potassium canrenoate. We conclude that long-term therapy with the aldosterone-receptor blocker, potassium canrenoate, can normalize the aldo/PRA ratio in many cases of idiopathic primary hyperaldosteronism after one-month withdrawal of the drug. These data are consistent with possible regression of idiopathic primary hyperaldosteronism after long-term therapy with potassium canrenoate, or in alternative to a persistent effect of potassium canrenoate, on aldosterone synthesis.

Adult↗
PubMed1989

Lack of aldosterone inhibition by atrial natriuretic factor in primary aldosteronism: in vitro studies.

Several studies demonstrated that aldosterone secretion, by bovine, rat and human glomerulosa cells, is inhibited in vitro by atrial natriuretic factor (ANF). This effect has also been investigated with conflicting results in cells taken from aldosterone-producing tumors. In the present study, atrial natriuretic factor has been tested on aldosteronoma cells obtained from 4 patients with primary aldosteronism. The cells were studied both with perfusion and incubation systems. Aldosterone secretion was stimulated by ACTH, angiotensin II and potassium with or without ANF 10 microM. In this study ANF lacked to inhibit either basal and stimulated aldosterone secretion, indicating some alterations of ANF-adrenal interaction in this syndrome.

Adenoma↗