Vagal stimulation (VS) decreases heart rate and alters the loading conditions of the left ventricle (LV). However, its effects on LV performance are not clearly defined. To evaluate the effects of VS on LV performance, 20 anesthetized open-chest dogs were instrumented to measure LV pressure (LVP) and volume. VS resulted in a decrease in the slope of the end-systolic pressure-volume relationship, without pacing and with pacing, after ansae subclaviae resection and after ansae subclaviae resection plus beta-adrenergic blockade. VS did not alter the time constant of isovolumic relaxation (tau) or the LV end-systolic pressure-tau relationship during vena caval occlusion. No change was noticed in the LV chamber stiffness constant without and with pacing. However, a significant increase in the LV filling fraction at one-third and one-half of diastole was observed. We examined the mechanism of this increase by examining the relationship of left atrial pressure (LAP) and LVP. VS increased mean LAP 44% and increased the LAP-LVP gradient 42%. These data suggest that VS exerts a significant negative inotropic effect that is independent of its bradycardiac effect and the level of sympathetic tone. Despite the absence of lusitropic effects of VS, early filling of the LV is augmented most likely as a result of an increase in LAP.