Aldosterone Regulation in Primary Aldosteronism: Differences between Adenoma and Bilateral Hyperplasia

1976 ◽  
Vol 51 (s3) ◽  
pp. 329s-332s ◽  
Author(s):  
F. Mantero ◽  
M. Gion ◽  
D. Armanini ◽  
G. Opocher

1. The diurnal patterns of plasma aldosterone, plasma renin activity (PRA), Cortisol and adreno-corticotrophic hormone (ACTH) in the supine and in the upright position have been studied in fourteen patients with primary aldosteronism, five with adenoma and nine with bilateral hyperplasia. Blood samples were drawn at intervals from 6 h to 30 min. 2. Supine patients with an adenoma showed marked diurnal variations of aldosterone, with maximal values at 08.00 hours and minimal values at 18.00 hours and secretory spurts beginning after 02.00 hours. Plasma Cortisol paralleled aldosterone, and ACTH seemed to anticipate aldosterone and Cortisol variations; PRA remained unchanged. In patients with hyperplasia, aldosterone was signicantly lower than in the adenoma group at 08.00 hours, and its decline during the day was less marked; fluctuations rather than secretory episodes were seen. 3. After patients assumed the upright posture, aldosterone remained unchanged or decreased in patients with adenoma, whereas it significantly increased in hyperplasia; PRA remained low, although a slight increment was seen in the latter group. The different response of aldosterone in the two groups was not modified by the administration of propranolol, apparently excluding a renin-dependent mechanism. On the other hand, dexamethasone seemed to affect the response of aldosterone to the upright posture in both groups; in adenoma there was a slight but significant increase, and in hyperplasia the usual rise was partially suppressed. 4. It is concluded that ACTH has a predominant role in regulating aldosterone secretion in primary aldosteronism due to adenoma, whereas its action in bilateral hyperplasia is only permissive.

2020 ◽  
Vol 106 (1) ◽  
pp. e45-e60
Author(s):  
Matthieu St-Jean ◽  
Isabelle Bourdeau ◽  
Marc Martin ◽  
André Lacroix

Abstract Context In primary aldosteronism (PA), aldosterone secretion is relatively independent of the renin–angiotensin system, but can be regulated by several other stimuli. Objective To evaluate aldosterone response to several stimuli in a series of patients with PA secondary either to bilateral adrenal hyperplasia (BAH) or unilateral aldosterone-producing adenoma (APA). Design and setting Prospective cohort study conducted in a university teaching hospital research center. Patients Forty-three patients with confirmed PA and subtyped by adrenal vein sampling (n = 39) were studied, including 11 with BAH, 28 with APA, and 4 with undefined etiology. We also studied 4 other patients with aldosterone and cortisol cosecretion. Interventions We systematically explored aberrant regulation of aldosterone using an in vivo protocol that included the following stimulation tests performed over 3 days under dexamethasone suppression: upright posture, mixed meal, adrenocorticotropin (ACTH) 1-24, gonadotropin-releasing hormone (GnRH), vasopressin, and serotonin R4 agonist. Main outcome measures Positive response was defined as >50% renin or ACTH-independent increase in plasma aldosterone/cortisol concentration following the various stimulation tests. Results Renin-independent aldosterone secretion increased in response to several aberrant stimuli (upright posture, GnRH) in up to 83% of patients with APA or BAH in whom ACTH 1-24 and HT4R agonists also produced aldosterone oversecretion in all patients. The mean significant aberrant responses per patient was similar in BAH (4.6) and in APA (4.0). Conclusions Aldosterone secretion in PA is relatively autonomous from the renin–angiotensin system, but is highly regulated by several other stimuli, which contributes to the large variability of aldosterone levels in PA patients.


1972 ◽  
Vol 71 (1) ◽  
pp. 153-159 ◽  
Author(s):  
Fred H. Katz ◽  
Peggy Romfh ◽  
Judith A. Smith

ABSTRACT The increase in plasma aldosterone and reduction in plasma renin activity induced by 30 to 60 minutes of mildly pressor angiotensin II infusion in man can be largely abolished when recent prior stimulation of the adrenal cortex by upright posture has been applied. A similar prevention of the ACTH-induced increase in plasma aldosterone can be achieved by previous upright ambulation. These results indicate the intermittent refractoriness of aldosterone secretion and that care must be exerted in the timing of any tests of aldosterone stimulation.


1971 ◽  
Vol 41 (4) ◽  
pp. 321-331 ◽  
Author(s):  
T. A. Kotchen ◽  
P. J. Mulrow ◽  
L. B. Morrow ◽  
P. M. Shutkin ◽  
N. Marieb

1. The renin-aldosterone system was studied in seventy-one selected hypertensive patients. Nine (13%) were diagnosed as having primary aldosteronism. Of the twenty-three patients who presented with a history of unprovoked hypokalaemia, the incidence of primary aldosteronism was 40%. 2. Renin and aldosterone responses to the combined stimuli of a low sodium diet and the upright posture were suppressed in patients with essential hypertension. There was no evidence that the suppression was due to abnormal adrenal function, sympathetic neuropathy, or the level of the blood pressure. The mechanism of the suppressed plasma renin activity response and its significance in the pathogenesis of hypertension are unknown.


2020 ◽  
Vol 52 (06) ◽  
pp. 345-346 ◽  
Author(s):  
Martin Reincke ◽  
Felix Beuschlein ◽  
Tracy Ann Williams

Primary aldosteronism (PA) is characterized by hypertension caused by inappropriately high adrenal aldosterone secretion, consecutively low plasma renin, and an elevated aldosterone to renin ratio. It is nowadays the universally accepted main cause of endocrine hypertension. According to the most recent epidemiological data, PA is present in 5.8% of unselected hypertensives in primary care, 6–12% of hypertensives treated in hypertension centers, and up to 30% in subjects with resistant hypertension 1. Despite this high prevalence, a recent survey demonstrated that screening for PA is not universally followed. Renin and aldosterone measurements, the basis for PA screening, are currently performed by only 7% of general practitioners in Italy and 8% in Germany 2. Accordingly, the prevalence of PA was low with 1% among hypertensives in Italy and 2% in Germany. In a retrospective cohort study of 4660 patients with resistant hypertension in California the screening rate for PA was 2.1% 3. Based on these data, it is clear that we still miss the majority of PA cases, despite advances in diagnosis and therapy.


1994 ◽  
Vol 131 (3) ◽  
pp. 215-220 ◽  
Author(s):  
Atsuko Yagi ◽  
Shuichi Ichikawa ◽  
Tetsuo Sakamaki ◽  
Zempei Ono ◽  
Kunio Sato ◽  
...  

Yagi A, Ichikawa S, Sakamaki T, Ono, Z, Sato K, Nakamura T, Sakamoto H, Murata K. Aldosterone response to adrenocorticotrophin and furosemide in primary aldosteronism after prolonged spironolactone treatment. Eur J Endocrinol 1994;131:215–20. ISSN 0804–4643 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 μg·1−1 · 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), 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. Atsuko Yagi, Second Department of Internal Medicine, Gunma University School of Medicine, 3-39-15, Showa-machi, Maebashi, Gunma 371, Japan


2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Jing Xu ◽  
Yumei Yang ◽  
Yan Ling ◽  
Zhiqiang Lu ◽  
Xin Gao ◽  
...  

Objectives. Long-term exposure to excessive aldosterone secretion from the adrenal gland may cause renal damage in patients with primary aldosteronism (PA). The aldosterone-to-renin ratio (ARR) may be significantly affected by renal function, especially in patients with renal damage related to long-term PA. The objective of this study was to investigate the association between the estimated glomerular filtration rate (eGFR) and ARR as well as its effect on screening for PA. Methods. This study was performed in Zhongshan Hospital, Fudan University, China. 803 patients with hypertension were consecutively recruited from 2012 to 2015. All participants underwent routine biochemical measurements, including plasma renin activity (PRA) and plasma aldosterone concentration (PAC). In all patients with a PAC higher than 10 ng/dl, a saline perfusion test was conducted, and a CT scan or adrenal venous sampling was also performed if needed. Receiver operating characteristic (ROC) analysis was conducted in all eGFR < 90 and eGFR ≥ 90 groups separately to determine the optimal cut-off values of ARR. Results. The optimal cut-off point for PA was an ARR of 40 ng/dl per ng/ml.h in the whole population, 52 ng/dl per ng/ml.h in subjects with an eGFR higher than 90 ml/min/1.73 m2, and 18 ng/dl per ng/ml.h in subjects with an eGFR lower than 90 ml/min/1.73 m2. Patients with an eGFR higher than 90 ml/min/1.73 m2 had significantly lower PRA and higher ARR levels than patients with an eGFR lower than 90 ml/min/1.73 m2 (P<0.05). Conclusions. Unsuppressed renin and lower ARR levels were associated with decreased eGFR in patients with primary aldosteronism. Diagnostic criteria of ARR by stratified eGFR may be an optimal strategy for the screening of primary aldosteronism.


1973 ◽  
Vol 45 (3) ◽  
pp. 347-373 ◽  
Author(s):  
D. H. P. Streeten ◽  
T. G. Dalakos ◽  
M. Souma ◽  
H. Fellerman ◽  
G. V. Clift ◽  
...  

1. On constant high (200 mmol)- and low (10 mmol)-sodium diets, thirty-one patients with idiopathic oedema have been compared with six non-oedematous control subjects while upright from 08.00 to 20.00 hours for 3 days and while recumbent all day for 2 days. 2. The cumulative weight rise in the upright posture and fall in recumbency were ‘normal’ in five patients (‘non-orthostatic oedema’) and excessive in twenty-six (‘orthostatic oedema’). 3. Leg volume showed a cumulative rise during the upright period, which was excessive in the orthostatic oedema patients only. 4. When the orthostatic oedema patients were in the upright posture, fifteen retained sodium excessively (‘orthostatic sodium retainers’), while eleven retained ‘normal’ amounts of sodium (‘orthostatic water retainers’). 5. The ‘orthostatic sodium retainers’ experienced excessive acute orthostatic falls in inulin and para-aminohippurate (PAH) clearances. Half of them showed excessive aldosterone excretion and secretion rates and excessive potassium excretion in the upright posture on the 200 mmol of sodium diet. Plamsa volume fell excessively after 1 h in the upright posture in these patients. None of these changes was significant or consistent in the other patients with oedema. 6. Plasma renin activity and plasma protein and albumin concentrations were ‘normal’ in all patients in all circumstances. 7. Idiopathic oedema is a group of disorders each associated with: (I) orthostatic fall in filtered sodium often with orthostatic hyperaldosteronism and consequent orthostatic sodium retention; (II) orthostatic water retention possibly related to orthostatic hypervasopressinism and occasionally associated with occult heart failure; or (III) non-orthostatic factors.


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