The authors studied the effects of changes in aortic input impedance on the force-velocity-length relationship of the left ventricle in six open-chest dogs, using a right heart bypass preparation. The control relationship between wall stress and ventricular diameter or mean velocity of shortening (MVCF) was determined first by using maneuvers (changes in venous return and phenylephrine infusion) that did not alter impedance moduli or phase angle above 0 Hz. Aortic impedance then was increased by occlusion of the descending aorta (+89% increase in the first harmonic P < 0.02; +49% increase in characteristic impedance, P < 0.005; and a constant -20° phase shift between 2 and 10 Hz; P < 0.05). When compared to a phenylephrine infusion at the same mean aortic pressure and cardiac output, aortic occlusion increased the level of peak stress (+43%, P < 0.005) and decreased the extent of shortening (from 28.6 ± 6.9 to 14.6 ± 3.1%, P < 0.01) and the MVCF (from 2.00 ± 0.30 to 1.15 ± 0.14 circ.s.-1; P < 0.02). However, left ventricular end systolic diameter and MVCF fell in the 95% confidence interval of their respective control relations with end-systolic wall stress. Similar data were obtained when aortic occlusion was performed during a nitroprusside infusion or during an inotropic stimulation. Moreover, we found that when venous return was reduced by 25% during aortic occlusion, the characteristic impedance and the aortic input resistance increased further (respectively, +16%, P < 0.01; and +18%, P < 0.035) but the wall stress decreased and the MVCF increased slightly. It is concluded that changes in impedance affect shortening and wall stress but not the force-velocity-length framework and, furthermore, that the wall stress provided a better description of the afterload than the impedance alone.