The calcium channel blocker nifedipine was administered to patients with chronic obstructive pulmonary disease (COPD) to determine its efficiency as a pulmonary vasodilator. Since nifedipine has been shown to decrease elevated pulmonary artery pressures in patients with hypoxic pulmonary hypertension, we hypothesized that nifedipine would attenuate acute hypoxic pulmonary vasoconstriction in patients without pulmonary hypertension. We studied 11 clinically stable patients with mild to moderate COPD and normal pulmonary artery pressures using a randomized single-blind cross-over design. The patients were studied before and after nifedipine (20 mg) or placebo, given sublingually, at room air and subsequently during inhalation of a hypoxic gas mixture containing 13% O2, 5% CO2 and 72% N2. During normoxia, nifedipine significantly increased cardiac index from 4.2 +/- 0.3 to 4.9 +/- 0.5 liters/min/m2 (p less than 0.05) and the coefficient of oxygen delivery from 4.15 +/- 0.3 to 4.91 +/- 0.5 (p less than 0.05), whereas placebo treatment did not. During isocapnic hypoxia, a significant increase in mean pulmonary artery pressure (from 15.7 +/- 0.7 to 24.4 +/- 1.2 mm Hg; p less than 0.005) and mean pulmonary vascular resistance index (from 2.6 +/- 0.3 to 4.2 +/- 0.5 mm Hg; p less than 0.005) could be observed. Pretreatment with nifedipine significantly attenuated the hypoxia-induced increase in mean pulmonary artery pressure by 53% and of the mean pulmonary vascular resistance index by 50%. This was accomplished without significant changes in systemic arterial pressure and in the systemic vascular resistance index. Thus, nifedipine acutely dilates the constricted vascular bed associated with hypoxia in these patients with COPD.