In ten patients with coronary heart disease molsidomine achieved a clear-cut decrease in pre- and after-load of the heart at rest. Due to decreased venous return at rest there was a fall in stroke volume resulting in a fall of systolic and diastolic aortic pressure. But at the same level of standardised exercise, systolic and diastolic arterial pressure and cardiac output were similar with or without molsidomine. Without changing after-load, there was a fall in pulmonary artery mean pressure (P less than 0.005), probably due to an increase in left-ventricular compliance and (or) a fall in pulmonary vascular resistance. A rise in venous capacity or a decrease in venous return during exercise was excluded as a possible mechanism of molsidomine action.