Therapeutic value of calcium antagonists in autonomous hyperaldosteronism

The chronic effect of the calcium antagonist nitrendipine was investigated on blood pressure (BP), plasma aldosterone concentration (PAC), plasma renin activity (PRA), and serum potassium in six patients with primary aldosteronism, either due to an (unilateral) aldosterone-producing adenoma (APA;n=3; age, 44±4 years; PAC, 312±96 pg/ml; PRA, <0.1 ng/l·h; serum potassium, 2.8±0.3 mmol/l) or to bilateral idiopathic hyperaldosteronism (IHA;n=3; age, 49±1 years; PAC, 212±32 pg/ml; PRA, 0.1±0.1 ng/l·h; serum potassium, 3.3±0.2 mmol/l). After with-drawal of antihypertensive medications at least 3 weeks prior to the study, nitrendipine was given orally in a daily dosage of 40 to 60 mg. BP, PAC, PRA, and serum potassium were determined before (see data above) and after 4 weeks of nitrendipine therapy. After 4 weeks, BP was significantly reduced (178±10 to 165±6 mmHg systolic, 109±7 to 101±6 mmHg diastolic) in three patients with APA and in two with IHA. No significant changes of PAC, PRA, and serum potassium were observed in these patients. However, one patient with clinical characteristics of IHA and a long-term history of diuretic therapy showed a complete normalization of BP, PAC, PRA, and serum potassium, suggesting that the etiology of autonomous hyperaldosteronism in this patient might differ from typical primary aldosteronism. From these findings we conclude that calcium antagonists may be helpful in lowering BP in those patients with primary aldosteronism who develop intolerable side effects under treatment with spironolactone or trilostane. However, calcium antagonists do not normalize hormonal and electrolyte abnormalities in primary aldosteronism. Normalization of PAC, PRA, BP, and serum potassium after calcium channel blockade in some patients with clinical characteristics of IHA might point to a calcium-dependent subset of autonomous hyperaldosteronism, provisionally termed “diuretic-induced tertiary hyperaldosteronism.”