Mean Plasma Aldosterone Levels Research Articles

Plasma Aldosterone Level in Metabolic Syndrome Patients Compared with Individuals without Metabolic Syndrome. A Survey on Iranian Population

Background: previous studies showed the role of aldosterone in pathogenesis of metabolic syndrome. The aim of this study was analysis the relation between plasma aldosterone (PA) and metabolic syndrome (MetS) and its components by comparison of PA in subjects with and without MetS. Methods: This cross-sectional study was designed on an Iranian sample in two groups with and without MetS (240 people in all). Aldosterone level in both groups was measured and then compared with presence of MetS and its components (waistline circumference, HDL, FBS and TG). Finally al of gathered data was analyzed using SPSS-17 software. Results: No significant differences between mean PA level in subjects with and without MetS were seen. In subjects without MetS, HDL was positively correlated with plasma aldosterone (r=0.294, p<0.001) and TG was inversely correlated with PA (r=-0.220, p=0.012). In subjects with MetS plasma aldosterone correlated positively with FBS (r=0.228, p=0.021). With increasing age and metabolic risk factors, PA level was decreased. Conclusion: This result suggests that aldosterone may contribute some roles in early stages of metabolic syndrome, not in late stage of the syndrome. These findings need to be evaluated in future studies and the positive association of aldosterone with HDL needs to be more explained.

Elevated plasma aldosterone is an independent risk factor for erectile dysfunction in men.

Erectile dysfunction (ED) and cardiovascular disease (CVD) share a great number of common risk factors. There is growing evidence that aldosterone, an independent CVD risk factor, is associated with ED. The purpose of this study was to determine the relationship between plasma aldosterone and erectile dysfunction. This study recruited 287 participants, ranging from 18 to 84years old; 217 were suffering from ED, diagnosed by the International Index of Erectile Function 5 (IIEF-5) scores. Based on IIEF-5 scores, patients were divided into one control group and three ED groups (mild ED; moderate ED; severe ED). The differences in principal characteristics, blood routine, sexual hormone, adrenal hormone, thyroid hormone, renal function, liver function and blood lipid were compared between ED and control groups. Our study demonstrated that the difference of mean plasma aldosterone levels between ED group and the control group was statistically significant (P<0.05). Stepwise logistic regression analysis of all the possible factors support the role of aldosterone as an independent risk factor for ED (OR 1.011; 95% CI 1.003-1.018; P=0.004). Similar statistical methods were applied to the comparison between moderate to severe ED group and control to mild ED group (OR 1.017; 95% CI 1.009-1.024; P<0.001). ROC curve and the area under the curve (0.718; 95% CI 0.643-0.794; P<0.001) were performed to assess the diagnostic effect and to compare the severity of risk with the known independent risk factors, such as age and cholesterol (0.704; 95% CI 0.631-0.778; P<0.001). When using a 374pg/mL cut-off value from Youden index, the OR of ED group versus controls is 3.106 (95% CI 1.458-6.617), while the OR of moderate to severe ED versus control and mild ED is 5.480 (95% CI 3.108-9.662). We determined that elevated plasma aldosterone concentration is an independent risk factor for ED. Our findings also indicate that the aldosterone, a well-recognized contributor to vascular injury, might be a potential bond between ED and CVD.

060 Plasma aldosterone levels predict long-term clinical outcome after percutaneous coronary revascularization

The renin-angiotensin-aldosterone system is a major therapeutic target in coronary artery disease (CAD). Recent data suggest that plasma aldosterone has a high prognostic value in acute coronary syndrome (ACS). We tested whether plasma aldosterone could predict clinical outcome in patients undergoing scheduled percutaneous coronary revascularization (PCR). Methods From June 2001 to September 2002, we included all consecutive patients referred to Lille's University Hospital for scheduled PCR. Blood samples were taken during the PCR. The primary endpoint was cardiac death throughout at least 12 months of follow-up. Results 807 patients were included, with a mean age of 61 years. Most were men (78%), smokers (71%). 32% were diabetics, mean LVEF was 58±15% and 93% received stents. 50% had stable angina. The mean plasma aldosterone level was 25(13-45)pg/mL. BMI (p=0.003), NYHA class>1 (p=0.0001) and elevated baseline troponine (p=0.01) were associated with increased aldosterone level. Old age (p=0.0001), normal GFR (p=0.01) and betablockers (p=0.01) were associated with decreased aldosterone level. The mean follow-up was 14.9 months and there were 40 cardiac deaths during this period. In multivariate analysis, old age (HR=1.42, p=0.04), low LVEF (HR=1.58, p=0.001), diabetes mellitus (HR=2.2, p=0.04), a recent history of ACS (HR=3.23, p=0.02), high usCRP (HR=2.59, p=0.004) and high plasma aldosterone (HR=3.48, p=0.004) were independent predictors of cardiac mortality. Conclusion Plasma aldosterone level seems to have an independent prognostic value in patients referred for PCR and could be useful in determining the individual cardiovascular risk. Whether this is the result of direct deleterious effects (promotion of endothelial dysfunction, pro-fibrotic, pro-inflammatory and pro-thrombotic effects) or the marker of a global activation of the neuroendocrine system remains to be determined. However plasma aldosterone appears to be an attractive risk marker in CAD. Download : Download full-size image

Does the captopril test improve the diagnosis of primary hyperaldosteronism?

Plasma concentrations of renin and aldosterone were measured before and 60 min after taking 25 mg captopril in 242 patients with arterial hypertension (124 men, 118 women, aged 51.9 +/- 12.7 years; unilateral aldosterone-producing adrenal adenoma in 8, idiopathic hyperaldosteronism in 16 and essential hypertension in 189). Basal plasma aldosterone levels were twice as high in those with adenoma or hyperaldosteronism (216.9 +/- 99.1 pg/ml and 256 +/- 123 pg/ml, respectively) as in those with essential hypertension (117.7 +/- 115 pg/ml). Basal renin levels in adenoma and idiopathic hyperaldosteronism (1 +/- 0.8 microU/ml and 2.6 +/- 1.9 microU/ml, respectively) were decreased compared with those in essential hypertension (13.1 +/- 14.2 microU/ml). The basal aldosterone/renin ratio was higher in adenoma (436 +/- 370 pg/microU) and idiopathic hyperaldosteronism (615 +/- 950 pg/microU) than in essential hypertension (52.9 +/- 151.3 pg/microU). The sensitivity of this ratio in combination with the aldosterone concentration was 100% for recognizing an adrenal adenoma, its specificity 92.7%. The mean plasma aldosterone level after captopril administration did not change in adenoma patients, but fell to 162 +/- 85 pg/ml (P less than 0.001) in those with idiopathic hyperaldosteronism. These data indicate that the captopril test contributes to distinguishing primary from idiopathic hyperaldosteronism.

Aldosterone Levels in Obese Women with or without Hypertension

ABSTRACTIn this study, our objective was to evaluate aldosterone levels after administration of furosemide and angiotensin-converting enzyme (ACE) inhibiting drugs in hypertensive and normotensive obese women. 40 normotensive (group I) and 40 hypertensive obese women (group II) were included in the study. Mean plasma aldosterone level changed from 9.45±2.60 ng/dl to 8.85±2.70 ng/dl after administration of furosemide in group I patients. In the same group, mean aldosterone level changed from 9.175±2.89 ng/dl to 8.75±2.70 ng/dl after administration of captoprile. In hypertensive obese women, mean plasma aldosterone level changed from 11.60±3.69 ng/dl to 9.60±2.90 ng/dl (P=0.04) after administration of furosemide. In the same group mean aldosterone level changed from 13.30±3.30 ng/dl to 12.85±3.67 ng/dl after captoprile administration. Despite normal range of aldosteron levels at baseline, hypertensive obese patients had higher plasma levels.

Aldosterone resistance in kidney transplantation is in part induced by a down-regulation of mineralocorticoid receptor expression.

After renal transplantation immunosuppressive drugs-like cyclosporin A (CsA) and FK506 induce either hypoaldosteronism or pseudo-hypoaldosteronism presenting with hyperkalemia and metabolic acidosis. We investigated the relationship between renal allograft function under CsA therapy and plasma aldosterone concentration, potassium- and water homeostasis and mineralocorticoid receptor (MR) expression level in peripheral leukocytes. We studied 21 renal transplant patients under CsA therapy and 12 healthy controls. Transplant recipients were studied before and under fludrocortisone treatment. Using quantitative reverse-phase polymerase chain reaction (RT-PCR) specific for the MR, we analyzed the level of expression of MR in peripheral leukocytes. In acidotic transplant recipients (HCO(3) 18.5 +/- 1.2 mM) renal function was only slightly impaired with 2.0 +/- 0.2 mg creatinine/dL when compared with 1.8 +/- 0.3 mg/dL (ns) in non-acidotic patients (HCO(3) 23.0 +/- 2.8 mM). Mean plasma aldosterone levels in renal transplant recipients did not differ from control levels (150 +/- 33 pg/mL vs. 148 +/- 33 pg/mL, ns). In contrast, the expression level of MR in peripheral leukocytes of renal transplant recipients treated with CsA was significantly decreased when compared with healthy controls without renal disease (120 +/- 78 vs. 423 +/- 73 RNA molecules/0.5 microg total RNA, p < 0.01). The level of expression of MR in renal transplant recipients did not differ between acidotic patients and non-acidotic patients (ns). The application of fludrocortisone reversed hyperkalemia and metabolic acidosis without significant effect on MR expression. The present data demonstrate that hyperkalemia and metabolic acidosis following CsA treatment in kidney transplantation might be associated with a down-regulation of MR expression on peripheral leukocytes. Electrolyte imbalance is reversible on application of fludrocortisone. This observation supports fludrocortisone treatment in transplant patients with severe electrolyte disturbances.

Genetic deficiency of angiotensinogen produces an impaired urine concentrating ability in mice

Angiotensinogen gene-knockout (Atg-/-) mice lacking angiotensin II exhibit chronic hypotension. The present study was designed to investigate pathophysiology of Atg-/- mice from the renal functional view. Wild-type (Atg+/+) and Atg-/- mice at 10 weeks of age were housed in metabolic cages for 24-hour urine collection. When provided free access to water, Atg-/- mice showed an increased urine output and a decreased urine osmolality compared with Atg+/+ mice. Urinary excretion and plasma levels of vasopressin were significantly higher in mutant mice than in wild-type mice. On the other hand, urinary excretion of aldosterone in mutant mice was suppressed to the levels under the detection limit of the assay system. The mean plasma aldosterone level of Atg-/- mice was suppressed to 30% of that of Atg+/+ mice. Plasma levels of creatinine, endogenous creatinine clearance, and urinary electrolyte excretion were not different between these mice. In Atg+/+ mice, urine osmolality was markedly increased from 1929 +/- 21 to 3314 +/- 402 mOsm/kg during water deprivation, whereas this parameter in Atg-/- mice did not change significantly (from 1413 +/- 121 to 1590 +/- 92 mOsm/kg). Urinary vasopressin excretion increased during water deprivation from 0.24 +/- 0.04 and 0.70 +/- 0.08 to 0.42 +/- 0.06 and 2.31 +/- 0.35 ng/mg creatinine in wild-type and mutant mice, respectively. Histologic study revealed interstitial inflammation, and atrophic changes in the tubules and papilla in Atg-/- mice. In conclusion, a genetic deficiency of angiotensinogen produced an impaired urine concentrating ability and tubulointerstitial lesions, indicating the critical role of angiotensinogen in developing normal tubular function and construction.

Invasive Pharmacodynamics of Fosinopril in Patients with Congestive Heart Failure

Five patients with NYHA Class III CHF received 5 mg of fosinopril on each of 4 days. Hemodynamics were measured with a Swan-Ganz catheter after dosing on day 1. Measurements of plasma fosinoprilat, ACE activity, renin, and aldosterone were obtained. An Emax model was used to fit the effect-site concentration and mean arterial pressure change. A linear model was used to fit the effect-site concentration and the pulmonary artery wedge pressure (PAWP) change. At steady state on day 4, AUC0-24 was 1668 +/- 476 ng.hr/mL and Cmax was 143.5 +/- 33.6 ng/mL. The mean elimination half-life of fosinoprilat was 11.3 +/- 0.7 hours, and median Tmax occurred at 3 hours, corresponding to maximum plasma ACE inhibition. Plasma renin activity was unchanged, and mean plasma aldosterone level declined. Emax modeling using fosinoprilat concentrations and mean arterial pressure showed good prediction of the pharmacodynamic effects from the effect-site concentration. A linear relationship was observed between the effect-site concentrations of fosinoprilat and PAWP. When expressed in an Emax model, the pharmacodynamic actions of fosinopril in patients with CHF are a reflection of its pharmacokinetics.

Attenuation of atrial natriuretic peptide response to sodium loading after cardiac operation

To evaluate the role of cardiac operation and the atrial appendage in secretion of atrial natriuretic peptide in response to sodium loading, we studied 44 patients who underwent heart operations with (28 patients; group I) or without (16 patients; group II) right atrial appendectomy and 16 patients who underwent lobectomy (group III). Before and after operation 1 ml/kg of 10% NaCl was infused for 15 minutes. Blood samples were taken before NaCl infusion and immediately after infusion and at 60 minutes after infusion. There were no significant changes in hemodynamics or hematocrit level throughout the study. Plasma and urine sodium levels and the fractional excretion of sodium were significantly increased by sodium loading. Before operation, plasma mean atrial natriuretic peptide levels increased markedly in response to sodium infusion in all groups. After operation, this atrial natriuretic peptide response disappeared in groups I and II, but remained present in group III. Elution profiles of plasma atrial natriuretic peptide showed that the major peak coincided with alpha-atrial natriuretic peptide before sodium loading, whereas a beta-atrial natriuretic peptide peak appeared 60 minutes after sodium loading in all groups both before and after operation. The mean plasma arginine vasopressin levels were significantly increased by sodium loading both before and after operation in all groups. Sodium loading decreased the mean plasma aldosterone levels in all groups before operation, but did not after operation in groups I and II. Plasma renin activity and angiotensin II concentrations were not changed by sodium loading. We conclude that atrial natriuretic peptide response to sodium loading is attenuated by cardiac operation irrespective of right appendectomy, but not by lobectomy. Sodium loading augments secretion of beta-atrial natriuretic peptide even in reduced atrial natriuretic peptide response states after heart operations.

Evidence for Cholinergic Modulation of Aldosterone Secretion in Man

Acetylcholine stimulates aldosterone secretion in bovine glomerulosa cells in vitro via specific cholinergic receptors. In this study we examined the effect of peripheral muscarinic blockade with atropine on metoclopramide-, angiotensin-II-, and ACTH-stimulated aldosterone secretion in man. Atropine (0.6 mg, iv) administered 10 min before MCP delayed the onset of the plasma aldosterone response and attenuated the mean peak response from 502 +/- 103 (+/- SE) to 322 +/- 72 pmol/L (P less than 0.05) without affecting zero time mean plasma aldosterone levels (144 +/- 28 vs. 136 +/- 36 pmol/L for control and atropine, respectively). This inhibitory effect was not mediated by changes in PRA or plasma potassium or ACTH (as reflected by cortisol) concentrations. Atropine also attenuated the plasma aldosterone response to a low dose angiotensin II infusion (2 ng/kg.min; control, 449 +/- 99 pmol/L; atropine, 297 +/- 78 pmol/L; P less than 0.05). In contrast, atropine had no effect on the plasma aldosterone response to a bolus dose (250 micrograms) of ACTH. Neither atropine (0.6 mg, iv) nor the cholinergic muscarinic agonist bethanechol (5 mg, sc) alone elicited a change in plasma aldosterone. Collectively, these data provide evidence for cholinergic modulation of aldosterone secretion in man. We conclude that cholinergic mechanisms may facilitate the aldosterone responses to angiotensin-II and metoclopramide, but not to ACTH.

Diminished Aldosterone Responses to Angiotensin II and Adrenocorticotropin in Hypocalcemic Subjects: Restoration of Responsiveness with Normocalcemia

ACTH-, angiotensin II (AII)-, and K+-mediated aldosterone responses in vitro are dependent on extracellular and intracellular Ca concentrations. This study examined in vivo the relationship of changes in ambient serum calcium (serum Ca) to ACTH- and AII-mediated aldosterone release in hypoparathyroid subjects. Plasma aldosterone (PA) responses to graded dose infusions of ACTH and AII were examined in hypoparathyroid (HypoPTH) patients before (n = 8) and after correction of hypocalcemia (n = 6) and compared to responses in 20 normotensive normocalcemic subjects. ACTH and AII were infused for 90 min at rates increasing from 12.5 to 50 mIU/30 min and 0.5 to 2.0 ng/kg X min, respectively. Pretreatment mean serum Ca was 6.8 +/- 0.2 (+/- SEM) mg/dl, and it rose to 9.3 +/- 0.2 mg/dl after 3-8 weeks of vitamin D administration. In the untreated HypoPTH patients, basal mean PA (5.4 +/- 1.3 ng/dl) was lower (P less than 0.01) than in the normal subjects (10.6 +/- 0.6 ng/dl) or treated HypoPTH patients (9.5 +/- 1.8 ng/dl). There was a marked reduction in PA responses to ACTH at all doses in the untreated HypoPTH patients compared to the normal subjects. With normalization of serum Ca in four patients, the mean peak PA response to ACTH (25.1 +/- 6.0 ng/dl) was not significantly different from normal (28.9 +/- 1.7 ng/dl). During graded dose AII infusion in five untreated HypoPTH patients, mean PA levels increased from 6.9 +/- 1.2 to 11.6 +/- 2.2 ng/dl; when the serum Ca was normal, the corresponding values were 8.7 +/- 1.8 and 20.2 +/- 3.61 ng/dl. There was a positive correlation (r = 0.475; P less than 0.05) between basal PA and serum Ca levels. In addition, maximum changes in mean arterial pressure in response to AII infusions were significantly greater after correction of hypocalcemia. These observations indicate that in HypoPTH patients, extracellular Ca concentrations can influence humoral aldosterone response to ACTH and AII and pressor responses to AII.

Circadian rhythm of plasma renin activity in older normal and essential hypertensive men: relation with inactive renin, aldosterone, cortisol and REM sleep.

The 24-h pattern of plasma renin activity (PRA), inactive renin (IR), plasma aldosterone (PA) and cortisol was studied in 13 normal men and 12 male patients with essential hypertension, all of whom were older than 55 years. Following gradual habituation over 4 days to the sleep laboratory and intravenous lines, blood samples were obtained every 2 h between 0900-2100 h and every 30 min between 2100-0900 h, during which sleep was also monitored. Plasma renin activity showed a circadian rhythm in both groups, but mean levels were lower in the hypertensive subjects (0.92 +/- 0.03 versus 1.41 +/- 0.06 ng/ml per h). The circadian rhythm of PRA in older men appeared to follow the same pattern described in younger individuals. Rapid eye movement (REM) sleep was associated with a small decrease in PRA, but this link was only evident in the normotensive group. Mean 24-h IR levels were also lower in the hypertensive group (7.26 +/- 0.18 versus 15.10 +/- 0.47 ng/ml per h) but were not affected by clock-time and generally showed no association with the 24-h PRA cycle. Mean 24-h PA was closely related to cortisol but not to PRA in both groups. Mean PA levels of the two groups were similar. Thus, the PA:PRA ratio was higher in the hypertensive group. The higher basal PA:PRA ratio in older hypertensives that emerged over the 24-h study period may reflect increased sensitivity of the adrenal gland to angiotensin II (ANG II) in hypertension of the elderly.

Plasma adrenocorticotropin, cortisol, and aldosterone responses to corticotropin-releasing factor: modulatory effect of basal cortisol levels.

Two hundred micrograms of corticotropin-releasing factor (CRF) were administered as an iv bolus injection to 10 normal subjects (5 men and 5 women). Mean plasma ACTH levels rose significantly (P less than 0.0005, by Friedman's nonparametric analysis of variance) from a basal value of 27 +/- 5 pg/ml (mean +/- SEM) to a peak value of 63 +/- 8 pg/ml 30 min after CRF administration. This ACTH response was followed by a rise in plasma mean cortisol levels (P less than 0.0005, by Friedman's test) from a baseline value of 12.3 +/- 1.4 micrograms/100 ml to a peak value of 21.0 +/- 0.7 micrograms/100 ml 60 min after CRF and a rise in mean plasma aldosterone levels from a basal value of 13 +/- 2 ng/100 ml to a peak value of 23 +/- 2 ng/100 ml. There was no significant difference between men and women in the responsiveness of ACTH, cortisol, and aldosterone to CRF administration. The individual basal cortisol levels were highly significantly and negatively correlated with the areas under the individual ACTH curves (r = -0.76; P less than 0.005, by Pearson's correlation test) and cortisol curves (r = -0.91; P less than 0.001, by Pearson's test). These data suggest a modulatory effect of physiological cortisol levels on the response of the pituitary-adrenal axis to CRF.

Plasma renin substrate, renin activity, and aldosterone levels in a sample of oral contraceptive users from a community survey

Fasting plasma renin substrate (PRS), plasma renin activity (PRA), plasma aldosterone (PA), and blood pressure (BP) levels were measured from 212 apparently healthy normotensive nonpregnant white women aged 21 to 39 years, selected on the basis of oral contraceptive (OC) use or nonuse in 1976 following a community survey in East Boston. The mean PRS level was 7118 ng/dl among OC users and 1935 ng/dl among nonusers ( p < 0.0001). In contrast, mean PRA was 2.9 ng of angiotensin I per milliter per hour among users and 3.0 ng of angiotensin l/ml/hr among nonusers ( p = NS); mean PA levels were 26.2 ng/dl and 25.4 ng/dl, respectively ( p = NS). Mean systolic BPs were 113.8 mm Hg among current OC users and 111.2 mm Hg among nonusers ( p = 0.078); diastolic BPs were 68.5 and 68.9, respectively ( p = NS). These data indicate a greater than three-fold increase in PRS among current OC users compared to nonusers, with virtually identical PRA and PA levels. The data indicate that normotensive women using OCs maintain normal PRA and PA levels despite marked elevations in PRS.