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To investigate the mechanism of antianginal action of the calcium channel blocker nisoldipine and to determine the reproducibility of the clinical and hemodynamic events induced by supine leg exercise, 30 patients with stable effort angina pectoris were studied. They were divided into two groups; one group of 19 patients received a single 10-mg dose of nisoldipine orally, and the other group of 11 patients received a single dose of placebo orally. Chest pain was induced in all of 30 patients during the control exercise test. After nisoldipine administration, chest pain was not induced in 13 of 19 patients and was of lessened severity in five patients with the same work load as those performing control exercise. ST segment at peak exercise showed less severe depression after nisoldipine. Systemic vascular resistance was reduced by 38% (p<0.001) at rest and 22% (p <0.001) at peak exercise, and coronary vascular resistance was reduced by 31% (p<0.01) at rest and 18% (p <0.01) at peak exercise. Pulmonary artery wedge pressure fell from 6±1 to 3±1 mm Hg (p<0.001) at rest and from 28±3 to 11+2 mm Hg (p<0.001) at peak exercise. Coronary sinus flow at rest and myocardial oxygen uptake both at rest and during exercise was not modified by nisoldipine. However, coronary sinus flow at peak exercise increased significantly from 219±24 to 249±31 ml/min (p<0.01) after nisoldipine, and myocardial oxygen uptake was not significantly changed despite decreased coronary vascular resistance. The clinical and hemodynamic events induced by the exercise during invasive studies (except pulmonary artery wedge pressure at rest) were reproducible after placebo administration. Our data demonstrate that increased coronary blood flow could be the major mechanism of the antianginal action of nisoldipine in supine leg exercise-induced angina. (Circulation 1990;81:1887-1898 C alcium channel blockers have obtained wide acceptance in the treatment of exerciseinduced angina pectoris. Recently, much interest has been focused on the mechanisms of their antianginal actions and their effects on exercise performance in patients with angina. The exact mechanisms are multifactorial and complex and are related to a combination of effects on heart rate, myocardial contractility,'-3 possibly myocardial oxygen supply through coronary vasodilation,4 and peripheral vascuFrom the