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Background In primary aldosteronism (PA), excessive, autonomous secretion of aldosterone is not suppressed by salt loading or fludrocortisone. For seated saline suppression testing (SSST), the recommended diagnostic cutoff 4-hour plasma aldosterone concentration (PAC) measured by high-performance liquid chromatography–mass spectrometry (HPLC-MS/MS is 162 pmol/L. Most diagnostic laboratories, however, use immunoassays to measure PAC. The cutoff for SSST using immunoassay is not known. We hypothesized that the cutoff is different between the assays. Methods We analyzed 80 of the 87 SSST tests that were performed during our recent study defining the HPLC-MS/MS cutoff. PA was confirmed in 65 by positive fludrocortisone suppression testing (FST) and/or lateralization on adrenal venous sampling and excluded in 15 by negative FST. PAC was measured by a chemiluminescence immunoassay (PACIA) in the SSST samples using the DiaSorin Liaison XL analyzer, and receiver operating characteristics (ROC) analysis was performed to identify the PACIA cutoff. Results ROC revealed good performance (area under the curve = 0.893; P < .001) of 4-hour postsaline PACIA for diagnosis of PA and an optimal diagnostic cutoff of 171 pmol/L, with sensitivity and specificity of 95.4% and 80.0%, respectively. A higher cutoff of 217 pmol/L improved specificity (86.7%) with lower sensitivity (86.2%). PACIA measurements strongly correlated with PAC measured by HPLC-MS (r = 0.94, P < .001). Conclusions A higher diagnostic cutoff for SSST should be employed when PAC is measured by immunoassay rather than HPLC-MS/MS. The results suggest that (i) PA can be excluded if 4-hour PACIA is less than 171 pmol/L, and (ii) PA is highly likely if the PACIA is greater than 217 pmol/L by chemiluminescence immunoassay. A gray zone exists between the cutoffs of 171 and 217 pmol/L, likely reflecting a lower specificity of immunoassay.

Context Current threshold values for primary aldosteronism (PA) diagnostic testing are based on measuring aldosterone (PAC) using immunoassays. Quantification of PAC by liquid chromatography-tandem mass spectrometry (LC-MS/MS) yields lower values. Objective To compare aldosterone measurement by radioimmunoassay (RIA) with LC-MS/MS and evaluate performances of proposed LC-MS/MS–specific cutoffs for PA screening and confirmatory testing. Patients and Intervention Forty-one patients underwent aldosterone/renin ratio (ARR) testing to screen for, and fludrocortisone suppression testing (FST) to confirm or exclude, PA. Renin (DRC) was measured by chemiluminescent immunoassay. Results Median serum PACLC-MS/MS was 27.8% lower (P < 0.05) than plasma PACRIA in 164 pairs of FST samples. A positive correlation (Spearman coefficient, 0.894, P < 0.01; Pearson r coefficient, 0.861, P < 0.01) was observed between the two assays. Thirty-seven patients showed consistent FST diagnoses (29 positive, 8 negative), whereas four showed inconsistent FSTs by the two assays. Good agreement (κ coefficient, 0.736; P < 0.01) was observed between the current FST diagnostic PACRIA cutoff of 165 pmol/L and the proposed PACLC-MS/MS cutoff of 133 pmol/L. Among 37 patients with consistent FST results, no differences were observed in sensitivity (89.7% vs 93.1%) or specificity (87.5% vs 87.5%) for PA screening between the current ARR cutoff of 70 pmol/mU (PACRIA/DRC) and the proposed cutoff of 55 pmol/mU (PACLC-MS/MS/DRC). Conclusions Adjustment of the current cutoffs for PA diagnostic testing is necessary if PAC is measured by LC-MS/MS. Our preliminary results suggest that the proposed LC-MS/MS cutoffs for ARR and FST perform as well as current RIA cutoffs.

Background: Plasma aldosterone/renin ratio (ARR) is the most popular screening test for primary aldosteronism (PA). Because both estrogen and progesterone (including in oral contraceptive agents) affect aldosterone and renin levels, we studied the effects of combined hormonal replacement therapy (HRT) on ARR; renin was measured as both direct renin concentration (DRC) and plasma renin activity (PRA). Methods: Fifteen normotensive, healthy postmenopausal women underwent measurement (seated, midmorning) of plasma aldosterone, DRC, PRA, electrolytes, and creatinine and urinary aldosterone, cortisol, electrolytes, and creatinine at baseline and after 2 weeks and 6 weeks of treatment with combined HRT (conjugated estrogens 0.625 mg and medroxyprogesterone 2.5 mg daily). Results: Combined HRT was associated with statistically significant increases in aldosterone [median (range): baseline, 150 (85 to 600); 2 weeks, 230 (129 to 790); 6 weeks, 434 (200 to 1200) pmol/L; P < 0.001 (Friedman test)] and PRA [2.3 (1.2 to 4.3), 3.8 (1.4 to 7.0), 5.1 (1.4 to 10.8) ng/mL/h, respectively; P < 0.001] but decreases in DRC [21 (10 to 31), 21 (10 to 39), and 14 (8.0 to 30) mU/L, respectively; P < 0.01], leading to increases in ARR calculated by DRC [7.8 (3.6 to 34.8), 11.4 (5.4 to 48.5), and 30.4 (10.5 to 90.2), respectively; P < 0.001]. The ARR calculated by DRC exceeded the cutoff value (70) in three patients after 6 weeks. There were no significant changes in ARR calculated by PRA [79 (26 to 184), 91 (23 to 166), and 88 (50 to 230), respectively; P = 0.282], plasma electrolytes and creatinine, or any urinary measurements. Conclusion: The combined oral HRT used in this study is capable of significantly increasing ARR with a risk of false-positive results during screening for PA but only if DRC (and not PRA) is used to calculate the ratio.

Background: The most popular screening test for primary aldosteronism is the plasma aldosterone/ renin ratio (ARR). Medications, dietary sodium, posture, and time of day all affect renin and aldosterone levels and can result in false-negative or false-positive ARRs if not controlled. Most antihypertensive medications affect the ARR and can interfere with interpretation of results. To our knowledge, no study has been undertaken to evaluate the effects of moxonidine on the ARR. Methods: Normotensive, nonmedicated male volunteers (n = 20) underwent measurement (seated, midmorning) of plasma aldosterone (by high-performance liquid chromatography-tandem mass spectrometry), direct renin concentration (DRC), plasma renin activity (PRA), cortisol, electrolytes and creatinine; and urinary aldosterone, cortisol, electrolytes and creatinine at baseline and after 1 week of moxonidine at 0.2 mg/d and a further 5 weeks at 0.4 mg/d. Results: Compared with baseline, despite the expected significant falls in both systolic and diastolic blood pressure, levels of plasma aldosterone [median, 134 (range, 90 to 535) pmol/L], DRC [20 (10 to 37) mU/L], PRA [2.2 (1.0-3.8) ng/mL/h], and ARR using either DRC [8.0 (4.4 to 14.4)] or PRA [73 (36 to 218)] were not significantly changed after either 1 [135 (98-550) pmol/L, 20 (11-35) mU/L, 2.0 (1.2-4.1) ng/mL/h, 8.8 (4.2 to 15.9), and 73 (32-194), respectively] or 6 weeks [130 (90-500) pmol/L, 22 (8 to 40) mU/L, 2.1 (1.0 to 3.2) ng/mL/h, 7.7 (4.3 to 22.4), and 84 (32 to 192), respectively] of moxonidine. There were no changes in any urinary measurements. Conclusion: Moxonidine was associated with no significant change in the ARR and may therefore be a good option for maintaining control of hypertension when screening for primary aldosteronism.

Context:In primary aldosteronism (PA), adrenal vein sampling (AVS) distinguishes unilateral and bilateral disease by comparison of aldosterone/cortisol (A/F) ratios. There is controversy about the criteria for interpretation, however, and in particular it is not clear whether contralateral suppression (CS) (defined as A/Fadrenal ≤ A/Fperipheral on the unaffected side) is important. We therefore performed a retrospective study to determine whether CS in surgically treated unilateral PA was associated with blood pressure (BP) and biochemical outcomes.Setting and Design:Patients who underwent unilateral adrenalectomy for PA after successful AVS were included if the lateralization index (A/Fdominant:A/Fnondominant) was ≥2. Cases were reviewed at 6 to 24 months follow-up for outcomes with respect to the presence and degree of CS.Results:Sixty-six of 80 patients had CS. Baseline characteristics were similar. At postoperative follow-up, those with CS had lower systolic BP (SBP) (128 mm Hg vs 144 mm Hg, P = .001), a greater proportion with cure or improvement of hypertension (96% vs 64%, P = .0034), a greater proportion with biochemical cure of PA on fludrocortisone suppression testing (43 of 49 [88%] vs 4 of 9 [44%], P = .002) and were taking a lower median number of antihypertensive medications (0 vs 1.5, P = .0032). In a multivariate model, the degree of CS and preoperative SBP were both significantly correlated with postoperative SBP, but the lateralization index, sex, and age were not.Conclusion:In this study, the presence of CS correlated with good BP and biochemical outcomes from surgery. This finding suggests that CS should be a factor in deciding whether to offer surgery for treatment of PA.

Measurement of quality of life (QOL) allows assessment of the impact of a disease or treatment from the patient's perspective, including need for social, emotional, or physical support. We are not aware of any published QOL assessment in patients with bilateral primary aldosteronism (BPA), before or after commencing medical treatment (MT) with spironolactone and/or amiloride.Using the internationally validated Medical Outcomes Study Short Form 36 General Health Survey (SF-36), QOL was assessed in 21 patients with BPA at baseline (time of diagnosis), and at 3 and 6 months after commencing MT. QOL scores at baseline were compared with published normative values for the Australian population. The results of the current study were compared with those from our previous study showing reduced QOL in patients with unilateral primary aldosteronism (UPA) with normalization by 3 months after unilateral laparoscopic adrenalectomy.Compared with the general population, patients with BPA showed significant reduction (P0.01) in four QOL domains--physical functioning, role limitations due to physical health problems, general health perceptions, and vitality. After 6 months (but not 3 months) of MT, statistically significant (P0.05) improvements were detected in all these domains of QOL. When compared with patients with UPA treated surgically, scores were significantly (P0.05) lower at 3 months for five domains (role limitations due to physical health, general health, role limitations due to emotional health, mental health, and vitality) but at 6 months for only one domain (role limitations due to emotional problems).Subnormal QOL scores were improved after 6 months of MT in 21 patients with BPA, but more slowly and to a lesser degree than surgical treatment had previously been shown to improve QOL scores in 22 patients with UPA.

The most popular screening test for primary aldosteronism is plasma aldosterone/renin ratio (ARR). Because both estrogen and progesterone affect aldosterone and renin levels, we studied effects of two contraceptives commonly used in our population, one oral and one subdermal, on ARR, measuring renin as both direct renin concentration (DRC) and plasma renin activity (PRA).Normotensive, healthy women underwent measurement (seated, midmorning) of plasma aldosterone, DRC, PRA, electrolytes, and creatinine and urinary aldosterone, cortisol, electrolytes, and creatinine at baseline (menses) and after either 1) 3 wk treatment with oral ethinylestradiol plus drospirenone (n = 17) or 2) 1 wk and 6 wk treatment with subdermal etonogestrel (n = 15), a third-generation progestin.Treatment with oral ethinylestradiol plus drospirenone was associated with significant increases in aldosterone [median (range) at baseline = 131 (85-590) pmol/liter; at 1 wk, 200 (130-784) pmol/liter; and at 3 wk, 412 (199-1010) pmol/liter (P0.001, Friedman test)] and PRA [2.1 (1.2-4.7), 3.6 (1.5-7.1), and 4.9 (1.5-10.8) ng/ml · h, P0.001] but decreases in DRC [22 (11-36), 21 (8.7-41), and 14 (8.5-39) mU/liter, P0.01] leading to increases in ARR calculated by DRC [6.6 (3.3-31.3), 10.9 (5.2-58.9), and 29.8 (5.1-88.5), P0.001]. There were no significant changes in ARR calculated by PRA, plasma electrolytes and creatinine, and all urinary measurements. In contrast, treatment with subdermal etonogestrel was associated with no significant changes in PRA, DRC, aldosterone, or ARR at either 1 or 6 wk.The combined oral contraceptive ethinylestradiol plus drospirenone is capable of significantly increasing ARR with risk of false-positive results during screening for primary aldosteronism, but only if DRC is used to calculate the ratio. Subdermal etonogestrel had no effect on ARR after 6 wk.

Plasma aldosterone to renin ratio (ARR) is the most popular screening test for primary aldosteronism (PAL). Certain medications are known to cause false-negative or -positive ARRs by affecting renin and aldosterone levels. There are no previously published data on the effects of antidepressants on ARR.Normotensive, depressed male patients (n = 26) underwent measurement (seated, midmorning) of plasma aldosterone, direct renin concentration (DRC), renin activity (PRA), electrolytes and creatinine and urinary aldosterone, cortisol, electrolytes, and creatinine at baseline and after 2 and 6 wk treatment with sertraline (n = 14) or escitalopram (n = 12).For both antidepressants, treatment was associated with rises in aldosterone [sertraline: baseline, mean ± sd, 243 ± 34; 2 wk, 256 ± 33; 6 wk, 267 ± 34 pmol/liter (P0.01 by ANOVA); escitalopram, 261 ± 36, 269 ± 38, 282 ± 40 pmol/liter (P0.05)], DRC [19.5 ± 2.2, 33.5 ± 2.0, 39.0 ± 2.4 mU/liter (P0.001); 24.5 ± 2.4, 34.0 ± 2.7, 42.8 ± 2.4 mU/liter (P0.001)], and PRA [2.24 ± 0.21, 2.58 ± 0.26, 4.68 ± 0.42 ng/ml · h (P0.001); 4.31 ± 0.22, 5.57 ± 0.36, 6.42 ± 0.53 ng/ml · h (P0.001)]. ARR fell significantly whether calculated using DRC [sertraline, 13.7 ± 2.2, 7.5 ± 0.7, 6.8 ± 0.7 (P0.001); escitalopram, 11.5 ± 1.9, 8.0 ± 1.1, 6.6 ± 1.0 (P0.001)], or PRA [116.6 ± 15.8, 108.4 ± 15.6, 60.4 ± 6.2 (P0.001); 61.2 ± 8.1, 50.0 ± 7.7, 45.6 ± 6.0 (P0.01)].Selective serotonin reuptake inhibitor antidepressants can significantly reduce ARR and therefore potentially increase the risk of false-negative results when screening for PAL. Further studies in hypertensive patients, including patients with confirmed PAL, are required.

Because primary aldosteronism is not uncommon, specifically treatable and in some cases curable, and carries higher risks for cardiovascular morbidity and mortality than essential hypertension, screening hypertensive patients for its presence by measuring aldosterone to renin ratio (ARR) is increasingly common. A significantly higher false-positive ARR rate for women than men, resulting in unnecessary suppression tests has previously been reported.Using a new, highly accurate aldosterone assay and both of the currently widely used renin assays, ARR was measured in 19 normal, ovulating women at three time points in the menstrual cycle and compared with single measurements in 21 normal males of similar age.ARRs in males were possibly too well down in the current normal range. Although normotensive and normokalemic, two women had raised ARRs in the luteal phase but only when direct renin concentration (DRC) was used. Their DRC levels were low at all sampling times [despite midrange plasma renin activity levels], whereas their progesterone and aldosterone levels were highest for the group. Saline suppression testing, performed in one of them, showed normal aldosterone suppressibility.False-positive ARRs in normal women during the luteal phase only when DRC is used may explain the higher incidence of false-positive ARRs in hypertensive women than men and suggest the following: 1) plasma renin activity is preferable to DRC in determination of ARR and 2) new reference ranges for ARR that take into account gender and sex hormone levels are required.

In 22 patients with unilateral primary aldosteronism (UPA), unilateral laparoscopic adrenalectomy (ADX) not only corrected hypokalemia and led to cure or improvement of hypertension, but also significantly improved quality of life (QOL).In this pilot study, QOL was evaluated prospectively using SF-36 questionnaire before and 3 and 6 months after ADX in 22 patients [14 males] with UPA who underwent ADX within the Endocrine Hypertension Research Center, Greenslopes and Princess Alexandra Hospitals, between June 2007 and June 2008.Eighty-six percent of patients were cured of hypertension, and the remainder improved. Plasma potassium normalized and, whereas renin concentration increased, plasma aldosterone, aldosterone/renin ratio, and number of antihypertensive agents decreased. Preoperatively, SF-36 scores for each QOL domain were lower for UPA patients than reported for the Australian general population, especially for physical functioning, role physical, vitality, and general health. Significant improvements were seen at 3 months in physical functioning, role physical, social functioning, role emotional, general health, mental health, and vitality and at 6 months in physical functioning, role physical, general health, role emotional, mental health, and vitality.Unilateral adrenalectomy had positive impacts not only on blood pressure and biochemical parameters, but also on QOL, which was impaired preoperatively but significantly improved by 3 months postoperatively.

The aim of the study was to examine blood pressure and biochemical responses to unilateral adrenalectomy in patients with bilateral primary aldosteronism (PA) and identify predictive parameters.PA considered due to bilateral autonomous production of aldosterone is usually treated medically. Unilateral adrenalectomy has been considered ineffective. Because quality outcome data are lacking and medical treatment may cause adverse effects or fail to control hypertension, defining the role for unilateral adrenalectomy in bilateral PA is an important clinical issue.Between 1984 and 2004, 51 of 684 patients diagnosed with bilateral PA underwent unilateral adrenalectomy. This report is based on the records of the 40 considered suitable for inclusion, who were followed for at least 12 (median, 56.4) months.Hypertension was cured in 15% of patients and improved in 20%, usually within 1 yr of unilateral adrenalectomy. The proportion with controlled hypertension was significantly (P0.001) higher after adrenalectomy (65%) than before (25%). Mean systolic (P0.001) and diastolic (P0.001) blood pressure, left ventricular mass index (P0.05), plasma upright aldosterone (P0.05), and aldosterone/renin ratio (P0.001) fell. Serum creatinine independently predicted hypertension cure.Although this retrospective analysis of patients from a single center does not permit prediction of response rates among patients diagnosed elsewhere, it suggests that unilateral adrenalectomy can be beneficial in some patients with apparent bilateral PA and should not be dismissed as a treatment option.

In familial hyperaldosteronism type I, inheritance of a hybrid 11β-hydroxylase/aldosterone synthase gene leads to ACTH-regulated overproduction of aldosterone (causing hypertension) and of“ hybrid” steroids, 18-hydroxy- and 18-oxo-cortisol. To determine whether complete suppression of the hybrid gene is necessary to normalize blood pressure, we sought evidence of persisting expression in eight patients who were rendered normotensive for 1.3–4.5 yr by glucocorticoid treatment. At the time of the study, six patients were receiving dexamethasone (0.125–0.25 mg/day) and two patients were taking prednisolone (2.5 or 5 mg/day). Urinary 18-oxo-cortisol levels during treatment demonstrated close correlation with mean “day curve” (blood collected every 2 h for 24 h) cortisol (r = 0.74), consistent with regulation by ACTH. Although urinary 18-oxo-cortisol levels were lower during than before treatment (mean 12.6 ± 2.4 semvs. 35.0 ± 5.6 nmol/mmol creatinine; P < 0.01), they remained above normal (0.8–5.2 nmol/mmol creatinine) in all eight patients. Although mean upright plasma potassium levels during treatment were higher, aldosterone levels lower, PRA levels higher, and aldosterone to PRA ratios lower than before treatment, PRA levels were uncorrected (65) during treatment in four patients. For each of the eight patients, day curve aldosterone levels during treatment correlated more tightly with cortisol (mean r for the eight patients, 0.87 ± 0.05 sem) than with PRA (mean r = 0.36 ± 0.10 sem). Hence, control of hypertension by glucocorticoid treatment was associated, in all patients, with only partial suppression of ACTH-regulated hybrid steroid and aldosterone production. Normalization of urinary hybrid steroid levels and abolition of ACTH-regulated aldosterone production is not a requisite for hypertension control and, if used as a treatment goal, may unnecessarily increase the risk of Cushingoid side effects.

In familial hyperaldosteronism type I (FH-I), inheritance of a hybrid 11 beta-hydroxylase/aldosterone synthase gene causes ACTH-regulated aldosterone overproduction. In an attempt to understand the marked variability in hypertension severity in FH-I, we compared clinical and biochemical characteristics of 9 affected individuals with mild hypertension (normotensive or onset of hypertension after 15 yr, blood pressure never >160/100 mm Hg, less than or equal to 1 medication required to control hypertension, no history of stroke, age >18 yr when studied) with those of 17 subjects with severe hypertension (onset before 15 yr, or systolic blood pressure >180 mm Hg or diastolic blood pressure >120 mm Hg at least once, or greater than or equal to 2 medications, or history of stroke). Severe hypertension was more frequent in males (11 of 13 males vs. 6 of 13 females; P

We examined in detail biochemical characteristics of 10 normotensive individuals (6 females; age range, 11–43 yr) with glucocorticoid-suppressible hyperaldosteronism (familial hyperaldosteronism type I) in an attempt to understand the development of hypertension in this disorder. All were normokalemic (median plasma potassium, 3.7 ± 0.4 mmol/L sd), and upright plasma aldosterone levels (478 ± 333 pmol/L) were within the normal range (140–1110 pmol/L) in nine subjects. However, upright PRA levels (3.3 ± 30.5 pmol/L·min) were suppressed ( 65) in all but one subject. All subjects had elevated 24-h urinary levels of 18-oxo-cortisol (34.3 ± 11.2 nmol/mmol creatinine; normal range, 0.8–6.5 nmol/mmol creatinine). Plasma aldosterone failed to rise by at least 50% during 2 h of upright posture in five of seven subjects, or during a 1-h infusion of angiotensin II (2 ng/kg·min) in each of six subjects so studied. Serial, second-hourly (d...

Familial hyperaldosteronism type II (FH-II) is characterized by autosomal dominant inheritance and hypersecretion of aldosterone due to adrenocortical hyperplasia or an aldosterone-producing adenoma; unlike FH type I (FH-I), hyperaldosteronism in FH-II is not suppressible by dexamethasone. Of a total of 17 FH-II families with 44 affected members, we studied a large kindred with 7 affected members that was informative for linkage analysis. Family members were screened with the aldosterone/PRA ratio test; patients with aldosterone/PRA ratio greater than 25 underwent fludrocortisone/salt suppression testing for confirmation of autonomous aldosterone secretion. Postural testing, adrenal gland imaging, and adrenal venous sampling were also performed. Individuals affected by FH-II demonstrated lack of suppression of plasma A levels after 4 days of dexamethasone treatment (0.5 mg every 6 h). All patients had negative genetic testing for the defect associated with FH-I, the CYP11B1/CYP11B2 hybrid gene. Genetic li...

We compared the aldosterone-producing potency of the angiotensin II-sensitive wild-type aldosterone synthase genes and the ACTH-sensitive hybrid 11 beta-hydroxylase/aldosterone synthase gene by examining aldosterone, PRA, and cortisol day-curves (2-hourly levels over 24 h) in patients with familial hyperaldosteronism type I, before and during long-term (0.8-13.5 yr) glucocorticoid treatment. In 8 untreated patients, PRA levels were usually suppressed, and aldosterone correlated strongly with cortisol (r = 0.69-0.99). Fourteen studies were performed on 10 patients receiving glucocorticoid treatment that corrected hypertension, hypokalemia, and PRA suppression in all. ACTH was markedly and continuously suppressed in 6 studies, 3 of which demonstrated strong correlations between aldosterone and PRA (r = 0.77-0.92). ACTH was only partially suppressed in the remaining 8 studies; aldosterone correlated strongly: 1) with cortisol alone in 5 (r = 0.71-0.98); 2) with cortisol (r = 0.90) and PRA (r = 0.74) in one; 3) with PRA only in one (r = 0.80); and 4) with neither PRA nor cortisol in one. Unless ACTH is markedly and continuously suppressed, aldosterone is more responsive to ACTH than to renin/angiotensin II, despite the latter being unsuppressed. This is consistent with the hybrid gene being more powerfully expressed than the wild-type aldosterone synthase genes in familial hyperaldosteronism type I.

There is an apparent circadian rhythm in the secretion of aldosterone by normal active subjects which is reflected in the excretion of larger quantities of aldosterone in the forenoon than at other times of the day. The aldosterone rhythm is not abolished by the administration of dexamethasone in doses sufficient to suppress 17-hydroxycorticosteroids to negligible values. The aldosterone rhythm can be suppressed, however, by having the subjects remain recumbent at all times. When normal subjects assume the upright posture at 8 pm rather than at 8 am, their aldosterone values are higher at night than during the day. The increase in aldosterone excretion which occurs after assumption of upright posture at 8 am is followed by a decrease in aldosterone values in the afternoon, despite continued maintenance of upright posture. Under all these circumstances changes in plasma renin activity tend to parallel those in aldosterone excretion. It is concluded that posture is the dominant factor conferring apparent ci...