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At least 73 records · Page 4Linked to original sources
PubMed2005

Screening for primary aldosteronism in essential hypertension: diagnostic accuracy of the ratio of plasma aldosterone concentration to plasma renin activity.

BACKGROUND: The ratio of plasma aldosterone concentration to plasma renin activity (PRA) is considered the screening test of choice for primary aldosteronism. Uncertainty exists, however, regarding its diagnostic accuracy and the effects of antihypertensive drugs and dietary sodium balance on test characteristics. METHODS: We measured PRA and aldosterone in 118 white adults [71 men and 47 women; mean (SD) age, 51 (7) years] with previously diagnosed essential hypertension. Measurements were made while individuals were on antihypertensive drug therapy, after a 2-week drug-free period, after 4 days of dietary sodium loading, and after acute furosemide diuresis. We measured 24-h urine aldosterone excretion and PRA on the 4th day of dietary sodium loading to establish the diagnosis of primary aldosteronism. ROC curves were constructed for ratios measured under each clinical condition, and likelihood ratios were determined for individuals on or off antihypertensive drug therapy. RESULTS: Fifteen patients [13%; 95% confidence interval (CI), 7-20%] met the reference standard for primary aldosteronism. The mean (SD) areas under the ROC curves did not differ significantly across conditions of measurement [range, 0.80 (0.10) to 0.85 (0.04); P = 0.72]. When measured on and off antihypertensive drug therapy, the 95% CIs for the optimum cutpoint for the ratio overlapped. Point estimates of sensitivity on and off therapy were 73% (95% CI, 50-96%) and 87% (70-100%), respectively, and specificities were 74% (65-83%) and 75% (66-84%). Under either condition, increased ratios were associated with 2.4- to 13-fold increases of posttest odds above pretest odds. CONCLUSIONS: The aldosterone:PRA ratio provides only fair diagnostic accuracy in screening for primary aldosteronism, but concomitant antihypertensive drug therapy or acute variation in dietary sodium balance does not adversely affect test accuracy. Reporting of likelihood ratios associated with ranges of values of the aldosterone:PRA ratio, rather than use of a single "optimum" cutpoint, may enhance the usefulness of the test.

Adult↗
PubMed1977

[A simplified radioimmunoassay for serum aldosterone--non-extraction method with 125I-labeled aldosterone (author's transl)].

A simplified direct radioimmunoassay system for serum aldosterone measurement was developed by using radio iodine-labeled aldosterone and highly specific antiserum to aldosterone. 8-anilino-1-naphthalene sulfonic acid(ANS) was used to prevent the binding of aldosterone to serum proteins. Polyethylene glycol was used to separate the antibody-bound aldosterone from the free aldosterone as the precipitant. The minimum measurable concentration of aldosterone is 30pg/ml of serum by short incubation method (at 25 degrees C for 3hr incubation) and 15pg/ml of serum by long incubation method (at 4 degrees C for 20 hr incubation) respectively. Present radioimmunoassay eliminates extraction of the aldosterone from serum and chromatographic separation procedures, and requires only 0.1ml of serum sample for assay. The intra-assay precision was C. V. 6.9% (average of 4 samples) and the inter-assay precision was C. V. 10.7% (average of 4 samples). There is an excellent correlation between the extraction method and this direct method in serum aldosterone value obtained (correlation coefficient, 0.96). The normal value was 36.8+/-25.9pg/ml (recumbent) and 113.6+/-6.15pg/ml (upright).

Aldosterone↗
PubMed1985

[The effects of metoclopramide and dopamine on aldosterone secretion in cultured adrenocortical adenoma cells and adjacent non-adenoma cells from patients with primary aldosteronism].

Several authors have reported that metoclopramide (MCP), a dopaminergic antagonist, stimulates aldosterone secretion and that dopamine (DA) inhibits the MCP-mediated aldosterone secretion in man. However, many controversial results have been reported relating to the direct effect of MCP and DA on the secretion of aldosterone by adrenocortical cells in in vitro experiments. The present studies were designed to determine whether or not MCP and DA exerts its effect directly on the cultured human adrenocortical adenoma cells and adjacent non-adenoma cells obtained from patients with primary aldosteronism. A bolus intravenous injection of 10 mg MCP significantly increased the plasma aldosterone concentration (PAC) from 255 +/- 57 pg/ml (mean +/- SD) to 386 +/- 98 pg/ml after 15 min in patients with primary aldosteronism. But MCP (10(10)-10(-6) M) failed to increase aldosterone secretion from both adenoma cells and non-adenoma cells in culture. DA (10(-9) and 10(-6) M) did not suppress the basal secretion and the enhanced secretion of aldosterone by A II or ACTH in cells of either culture. The analysis by HPLC showed that 57% of dopamine hydrochloride added in the medium was preserved after 60 min incubation. These results suggest that MCP and DA do not act directly on the human adrenal glomerulosa cells in the regulation of aldosterone secretion.

Adenoma↗
PubMed1994

Aldosterone response to adrenocorticotrophin and furosemide in primary aldosteronism after prolonged spironolactone treatment.

We evaluated the effects of prolonged spironolactone treatment on aldosterone secretion in patients with primary aldosteronism. The patients were hospitalized and underwent a furosemide test with or without dexamethasone, as well as an adrenocorticotrophin (ACTH) test. In untreated patients, neither plasma renin activity (PRA) nor plasma aldosterone showed a response in the furosemide test. In patients receiving spironolactone, furosemide increased significantly both the PRA and the plasma aldosterone concentration (from 2.6 +/- 0.8 to 7.0 +/- 2.0 micrograms.l-1.h-1 (p < 0.05) and from 345.6 +/- 55.8 to 492.7 +/- 76.8 ng/l (p < 0.05), mean +/- SEM, respectively). Dexamethasone administration had no effect on the results of the furosemide test (p > 0.1). However, dexamethasone tended to decrease the basal plasma aldosterone concentration in the untreated patients, but not in the patients receiving spironolactone. In the ACTH test, the plasma aldosterone concentration increased significantly in the untreated patients (from 549.0 +/- 69.8 to 1169.3 +/- 165.5 ng/l, p < 0.01), but there was no significant aldosterone response in the spironolactone-treated patients (from 885.5 +/- 204.9 to 1260.3 +/- 289.2 ng/l, p > 0.1). We conclude that aldosterone secretion is mainly dependent on ACTH in the untreated patients with primary aldosteronism and is more strongly regulated by the renin-angiotensin system during spironolactone treatment.

Adrenocorticotropic Hormone↗
PubMed1982

Increased steroidogenesis by rat zona glomerulosa cells with increased cell concentration in vitro: evidence for a novel aldosterone-stimulating factor and implications regarding aldosterone biosynthesis.

A fourfold increase in the concentration of rat zona glomerulosa cells incubated in Krebs-Ringer bicarbonate buffer (KRBGA) increased aldosterone production per cell twofold. This cell concentration associated (CCA) increase in aldosterone production showed a dose-response relationship with the number of cells per incubation and was further increased in modified Medium 199, compared with KRBGA. The combination of a fourfold increase in cell concentration with each of maximally steroidogenic concentrations of K+, angiotensin II, ACTH, 5-hydroxytryptamine or cyclic AMP produced an increase in aldosterone production greater than that predicted from the algebraic sum of the steroidogenic effects of the factors acting separately. The CCA increase in basal aldosterone production maximal during the first 30 min of incubation, could not be accounted for by accumulation of corticosterone in the incubation medium and was largely or completely abolished by the addition of pregnenolone, progesterone, deoxycorticosterone or corticosterone to the incubation medium. Together, these data support the proposal that the CCA effect was due to a novel aldosterone-stimulating factor which increased aldosterone production by stimulating pregnenolone formation. The aldosterone and corticosterone responses to exogenous pregnenolone, progesterone, deoxycorticosterone and corticosterone demonstrated that aldosterone and corticosterone production by zona glomerulosa cells in vitro may represent separate biosynthetic pathways. Furthermore, these studies provided evidence for a mechanism by which increased levels of exogenous pregnenolone, progesterone and deoxycorticosterone were able to increase their per cent conversion to aldosterone, but not to corticosterone.

Adrenal Cortex↗
PubMed1979

The effect of extremely high sodium intake on plasma renin activity, plasma aldosterone concentration, and urinary excretion of aldosterone metabolites.

The effect of sodium intake on aldosterone production was examined in eight healthy men whose urinary sodium excretion approached their dietary sodium intake at levels of 10, 300, 800 and 1500 mEq sodium/day. Aldosterone secretion was estimated from the excretion rate of two aldosterone metabolites: Thaldo and aldosterone-18-glucuronide. Maximal suppression of aldosterone secretion appeared to have been reached when sodium intake was 800 mEq/day, since no further decrease in aldosteron metabolite excretion rates was observed at 1500 mEq/day dietary sodium. Both plasma renin activity and plasma aldosterone concentration were suppressed and approached or were below the detection limits of the respective radioimmunoassays when sodium intake reached 800 and 1500 mEq/day. Body weight and blood pressure significantly increased at each increment of sodium intake. Our findings show that when sodium intake is extremely high, aldosterone secretion does not decrease to zero but continues at a rate we estimate to be 10 to 30 microgram/day. We suggest that this nonsuppressible secretion of aldosterone may have contributed to the observed increases in weight and blood pressure.

Adult↗
PubMed1995

Neointimal thickening after balloon denudation is enhanced by aldosterone and inhibited by spironolactone, and aldosterone antagonist.

OBJECTIVE: The aim was to examine the effects of aldosterone and of an aldosterone antagonist, spironolactone, on neointimal thickening in a rabbit model of balloon injury. METHODS: Eighteen rabbits underwent aortic and iliac balloon injury and were randomised to subcutaneous infusion of aldosterone (70 micrograms.kg-1.d-1) or vehicle solution for 28 d. Eighteen other rabbits were randomised to receive daily subcutaneous injections of spironolactone (50 mg.kg-1.d-1) or of vehicle for 7 d before injury and for 28 d after the procedure. All animals were then killed just after measurement of plasma renin activity and of arterial pressure. Vessels were fixed and five cross sections were analysed per rabbit (three aortic; two from iliac artery). Mean values of neointimal area and of the neointimal area/medial area ratio were calculated. RESULTS: Aldosterone treatment was associated with a decrease in renin activity and a non-significant increase in mean arterial pressure. Aldosterone significantly augmented the neointimal thickening in the iliac artery [0.42(SEM 0.07) v 0.24(0.03) mm2, P < 0.05] but not in the aorta [0.63(0.08) v 0.59(0.12) mm2, NS]. Spironolactone significantly inhibited intimal thickening, both in the iliac artery [0.09(0.02) v 0.29(0.01) mm2, P < 0.001] and in the aorta [0.31(0.03) v 0.59(0.06) mm2, P < 0.001]. Spironolactone administration was associated with an increase in renin activity and a decrease in mean arterial blood pressure. CONCLUSIONS: Aldosterone administration enhances neointimal thickening after injury and spironolactone, an aldosterone antagonist, is a potent inhibitor of neointimal thickening in the same model. This suggests a role for aldosterone in the pathophysiology of neointimal proliferation after balloon injury and for aldosterone antagonists in its prevention.

Aldosterone↗
PubMed1993

Imaging of aldosterone-secreting adenomas: a prospective comparison of computed tomography and magnetic resonance imaging in 27 patients with suspected primary aldosteronism.

We have compared prospectively the sensitivity, specificity and accuracy of CT and MRI in a series of 27 consecutive patients (age 23-76 yrs, 17 females, 10 males) with clinically suspected primary aldosteronism. We found 13 patients with a unilateral aldosterone-producing adenoma (11 on the left and 2 on the right side), 6 with idiopathic hyper-aldosteronism and 8 with primary hypertension, which in two cases was associated with a nonfunctioning adrenal adenoma. The diagnosis of aldosterone-producing adenoma was confirmed at surgery and pathology in all cases. Idiopathic hyper-aldosteronism was diagnosed on the basis of the results of dexamethasone-suppressed adrenal scintigraphy and/or selective adrenal vein sampling. MRI correctly identified all cases of aldosterone-producing adenoma, but gave false positive results in five cases: one had idiopathic hyper-aldosteronism with bilateral nodular hyperplasia and four primary hypertension, which in two patients was associated with a nonfunctioning adrenal adenoma. Therefore, the sensitivity of MRI was 100%, its specificity 64% and overall diagnostic accuracy 81%. In comparison, CT correctly recognized only eight of the 13 patients with aldosterone-producing adenoma and gave false positive results in three primary hypertensives, including the two patients with a nonfunctioning adrenal adenoma. Therefore, its sensitivity, specificity and accuracy were 62, 77 and 69%, respectively. Based on these results, it could be anticipated that about four of every ten patients with aldosterone-producing adenoma would not be correctly diagnosed by CT.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenoma↗
PubMed1991

Aldosterone synthase cytochrome P-450 expressed in the adrenals of patients with primary aldosteronism.

A human cytochrome P-450 with aldosterone synthase activity was purified from the mitochondria of an aldosterone-producing adenoma. It was recognized by an anti-bovine cytochrome P-450(11 beta) IgG and by a specific antibody raised against a portion of the CYP11B2 gene product, one of the two putative proteins encoded by human cytochrome P-450(11 beta)-related genes (Mornet, E., Dupont, J., Vitek, A., and White, P. C. (1989) J. Biol. Chem. 264, 20961-20967). A similar and probably the same aldosterone synthase cytochrome P-450 was detected in the adrenal of a patient with idiopathic hyperaldosteronism. These aldosterone synthases were distinguishable from cytochrome P-450(11 beta), the product of another cytochrome P-450(11 beta)-related gene, i.e. CYP11B1, by their catalytic, molecular, and immunological properties and also by their localization. The latter enzyme was unable to produce aldosterone and did not react with the specific antibody against the CYP11B2 gene product. It was present both in tumor and non-tumor portions of the adrenals carrying the adenoma and in normal adrenal cortex. On the other hand, aldosterone synthase cytochrome P-450 localized in the tumor portions of the adrenals or in the adrenal of a patient with idiopathic hyperaldosteronism. Thus aldosterone synthase cytochrome P-450, a distinct species from cytochrome P-450(11 beta), is responsible for the biosynthesis of aldosterone in the human, at least in patients suffering from primary aldosteronism.

Adenoma↗