Therapeutic Effect of Calcium Channel Blockade in Primary Aldosteronism*

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Abstract
To determine the potential therapeutic effect of calcium entry blockade in primary aldosteronism, 10 patients (5 adenoma and 5 hyperplasia) documented by endocrine testing and/or surgery were given nifedipine (20 mg, sublingually) in the afternoon. In all patients, nifedipine acutely lowered systolic and diastolic blood pressure to normal for up to 6 h. Plasma cortisol and potassium did not change in the acute study. The basal plasma renin concentration was suppressed and was not altered by nifedipine. However, nifedipine reduced aldosterone within 120 min [22 ± 5 (±SE) to 10 ± 2 ng/dl; P < 0.02], including the 5 patients with adenomas (22 ± 3 to 10 ± 3; P < 0.02). In a 4-week study, nifedipine controlled blood pressure (134 ± 5 mm Hg systolic and 85 ± 3 mm Hg diastolic) and normalized serum K+ (3.0 ± 0.1 to 3.7 ± 0.1 meq/liter; P < 0.01) while reducing plasma aldosterone levels (46 ± 8 to 20 ± 3; P < 0.02). These results suggest that Ca+2 channel blockers may provide a new medical therapy, both controlling blood pressure and reducing aldosterone levels, for patients with primary aldosteronism.