Effect of spironolactone on fluid volumes and adrenal steroids in primary aldosteronism.

Ichikawa, Shûichi; Tajima, Yoshihiro; Sakamaki, Tatsuya; Matsuo, H; Kogure, Masami; Hirano, Yoko; Yagi, Shunichi; Murata, Katsuyuki

doi:10.1253/jcj.48.1184

Cited by 16 publications

(13 citation statements)

References 27 publications

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“…Our previous study revealed that aldosterone secretion is affected significantly by sodium ion intake in patients with primary aldosteronism receiving SPL. In patients with a sodium intake of 80mEq/day, the plasma aldosterone level during SPL treatment was the same as in untreated patients, but plasma aldosterone levels were higher in patients with a low sodium intake of 15mEq/day (8). In addition, other studies of ours have shown that the plasma renin activity (PRA) increases to normal during SPL therapy (9,10).…”

supporting

confidence: 51%

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

Yagi

Ichikawa²,

Sakamaki³

et al. 1994

European Journal of Endocrinology

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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.

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supporting

confidence: 51%

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

Yagi

Ichikawa²,

Sakamaki³

et al. 1994

European Journal of Endocrinology

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“…In addition to age, BMI, sex, plasma lipids and glucose, the medicated groups were matched for the use of beta adrenoceptor blockers, as this class drugs interferes with both cardiac function and regulation of systemic vascular resistance [35]. Figure 1, except that in extracellular water analyses, BMI was replaced with lean body mass, and in PWV analyses, the results were also adjusted for mean aortic blood pressure; *P < 0.05, **P < 0.01, ***P < 0.001 In separate previous reports, PA has been associated with increased ECW volume [5,6], increased cardiac output [36] and increased large arterial stiffness [9,10,37] (see Supplementary Table S1 for a summary of haemodynamic findings in PA). Our results showed that SVRI and AIx@75 were corresponding in all hypertensive groups, whilst medicated PA patients had higher ECW balance, cardiac index and PWV than medicated EH patients.…”

Section: Discussionmentioning

confidence: 92%

Primary aldosteronism: Higher volume load, cardiac output and arterial stiffness than in essential hypertension

et al. 2020

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Background. The diagnostics of primary aldosteronism (PA) are usually carried out in patients taking antihypertensive medications. We compared haemodynamics between medicated PA, medicated essential hypertension (EH), never-medicated EH and normotensive controls (n = 130 in all groups). Methods. The hypertensive groups were matched for age (53 years), sex (84 male/46 female) and body mass index (BMI) (30 kg m À2); normotensive controls had similar sex distribution (age 48 years, BMI 27 kg m À2). Haemodynamics were recorded using whole-body impedance cardiography and radial pulse wave analysis, and the results were adjusted as appropriate. Radial blood pressure recordings were calibrated by brachial blood pressure measurements from the contralateral arm. Results. Radial and aortic systolic and diastolic blood pressure was similar in PA and never-medicated EH, and higher than in medicated EH and normotensive controls (P ≤ 0.001 for all comparisons). Extracellular water balance was~4% higher in PA than in all other groups (P < 0.05 for all), whilst cardiac output was~8% higher in PA than in medicated EH (P = 0.012). Systemic vascular resistance and augmentation index were similarly increased in PA and both EH groups when compared with controls. Pulse wave velocity was higher in PA and never-medicated EH than in medicated EH and normotensive controls (P ≤ 0.033 for all comparisons). Conclusions. Medicated PA patients presented with corresponding systemic vascular resistance and wave reflection, but higher extracellular water volume, cardiac output and arterial stiffness than medicated EH patients. Whether the systematic evaluation of these features would benefit the clinical diagnostics of PA remains to be studied in future.

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“…In PA, there is an increase in plasma volume due to increased sodium reabsorption 5 . A previous study demonstrated that patients with PA had greater values for plasma volume and extracellular fluid volume than did patients with essential hypertension 6 . There is limited information about the effect of prolonged aldosterone excess and treatment on body fluid.…”

mentioning

confidence: 91%

Effect of Treatment on Body Fluid in Patients with Unilateral Aldosterone Producing Adenoma: Adrenalectomy versus Spironolactone

Yang

Hung

et al. 2015

Sci Rep

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Aldosterone affects fluid retention in the body by affecting how much salt and water that the kidney retains or excretes. There is limited information about the effect of prolonged aldosterone excess and treatment on body fluid in primary aldosteronism (PA) patients. In this study, body composition changes of 41 PA patients with unilateral aldosterone producing adenoma (APA) were assessed by a bio-impedance spectroscopy device. Patients with APA receiving adrenalectomy, as compared with those treated with spironolactone, had significantly lower relative overhydration (OH) and urine albumin excretion, and significantly higher urine sodium excretion four weeks after treatment. These differences dissipated 12 weeks after the initial treatment. Independent factors to predict decreased relative OH four weeks after treatment were male patients and patients who experienced adrenalectomy. Patients who underwent adrenaelctomy had significantly decreased TNF-α and increased serum potassium level when compared to patients treated with spironolactone 4 and 12 weeks after treatment. In this pilot study, we found that adrenalectomy leads to an earlier increase in renal sodium excretion and decreases in body fluid content, TNF-α, and urine albumin excretion. Adrenalectomy yields a therapeutic effect more rapidly, which has been shown to ameliorate overhydration in PA patients.

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Effect of spironolactone on fluid volumes and adrenal steroids in primary aldosteronism.

Cited by 16 publications

References 27 publications

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

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

Primary aldosteronism: Higher volume load, cardiac output and arterial stiffness than in essential hypertension

Effect of Treatment on Body Fluid in Patients with Unilateral Aldosterone Producing Adenoma: Adrenalectomy versus Spironolactone

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