To evaluate the potential value of nifedipine treatment for primary pulmonary hypertension, hemodynamic and scintigraphic measurements were made before and 15 to 30 minutes after nifedipine, 10 to 20 mg, was given sublingually to nine patients. Nifedipine treatment increased cardiac output (mean +/- SD, 3.6 +/- 1.7 to 5.3 +/- 2.8 L/min, p less than 0.001) and decreased mean aortic pressure (99 +/- 19 to 85 +/- 12 mm Hg, p less than 0.001) and total pulmonary and total systemic resistances (1605 +/- 787 to 1025 +/- 540 dyn X s X cm-5 and 2761 +/- 1557 to 1591 +/- 823 dyn X s X cm-5, respectively; p less than 0.005). Heart rate and mean pulmonary arterial pressure did not change significantly. Right ventricular end-diastolic volume decreased 10% (p = 0.01), end-systolic volume decreased 15% (p less than 0.01), and right ventricular ejection fraction increased 18% (p less than 0.05) in eight patients. After 4 to 14 months (mean, 7.3 +/- 3.8) of treatment with nifedipine, 40 to 120 mg/d, in six patients, cardiac output increased (3.6 +/- 2.0 to 5.0 +/- 1.8 L/min, p less than 0.01) and total pulmonary resistance decreased (1572 +/- 730 to 987 +/- 586 dyn X s X cm-5, p = 0.025), whereas pulmonary arterial pressure remained unchanged (59 +/- 23.2 to 55 +/- 28.6 mm Hg, p greater than 0.05) compared with baseline values. We conclude that nifedipine therapy may be useful in the chronic management of patients with primary pulmonary hypertension.