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Journal of Clinical Endocrinology & Metabolism, Vol 60, 896-899, Copyright © 1985 by Endocrine Society

ARTICLES

Therapeutic effect of calcium channel blockade in primary aldosteronism

JL Nadler, W Hsueh and R Horton

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 less than 0.02], including the 5 patients with adenomas (22 +/- 3 to 10 +/- 3; P less than 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 less than 0.01) while reducing plasma aldosterone levels (46 +/- 8 to 20 +/- 3; P less than 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.


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