In nine patients with severe congestive heart failure, the acute response to the infusion of a nonspecific vasodilator, sodium nitroprusside, was compared with the infusion of the converting enzyme inhibitor, teprotide (SQ 20, 881). The hemodynamic effects were similar. Nitroprusside and teprotide increased cardiac index 24 and 20 percent, respectively, reduced mean arterial pressure 11 and 14 percent and pulmonary wedge pressure 21 and 24 percent, and produced no significant change in heart rate (-0.5 and -0.7 percent). Arterial partial pressure of oxygen decreased in response to nitroprusside infusion from 75.8 ± 4.1 to 65.4 ± 3.2 mm Hg (p < 0.05) but did not change in response to teprotide infusion (77.0 ± 4.5 before and 76.3 ± 3.0 mm Hg after). Circulating norepinephrine levels were lowered in response to both agents in spite of the decrease in mean arterial pressure (nitroprusside 754 ± 126 to 580 ± 82 pg/ml, p < 0.05; teprotide 807 ± 136 to 518 ± 92 pg/ml, p < 0.05). Although the control plasma renin activity did not correlate closely with the hemodynamic response to either agent in this small series, this level did correlate directly with the dose of nitroprusside required to produce the desired hemodynamic response. Therefore, converting enzyme inhibition produces an acute hemodynamic response in severe congestive heart failure comparable with that of sodium nitroprusside with less detrimental acute effect on pulmonary oxygen transport. Long-term oral therapy with converting enzyme inhibitor deserves evaluation in congestive heart failure.