ALDOSTERONE RESPONSE TO ADRENOCORTICOTROPIN AND FUROSEMIDE IN PRIMARYALDOSTERONISM AFTER PROLONGED SPIRONOLACTONE TREATMENT

We evaluated the effects of prolonged spironolactone treatment on aldo sterone secretion in patients with primary aldosteronism. The patients were hospitalized and underwent a furosemide test with or without dex amethasone, as well as an adrenocorticotrophin (ACTH) test. In untreat ed patients, neither plasma renin activity (PRA) nor plasma aldosteron e showed a response in the furosemide test. In patients receiving spir onolactone, furosemide increased significantly both the PRA and the pl asma aldosterone concentration (from 2.6 +/- 0.8 to 7.0 +/- 2.0 mu g.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 h ad no effect on the results of the furosemide test (p > 0.1). However, dexamethasone tended to decrease the basal plasma aldosterone concent ration in the untreated patients, but not in the patients receiving sp ironolactone. In the ACTH test, the plasma aldosterone concentration i ncreased 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 aldo sterone response in the spironolactone-treated patients (from 885.5 +/ - 204.9 to 1260.3 +/- 289.2 ng/l, p > 0.1). We conclude that aldostero ne secretion is mainly dependent on ACTH in the untreated patients wit h primary aldosteronism and is more strongly regulated by the renin-an giotensin system during spironolactone treatment.