We examined the effect of converting enzyme inhibition with captopril (SQ 14,225) on pulmonary hemodynamics and on accumulation of extravascular lung water after microembolization in dogs. Pulmonary microembolization, induced with glass beads (200 microns diam), increased the mean pulmonary arterial pressure to approximately 40 Torr in both control and captopril-treated animals. The increase in pulmonary vascular resistance (PVR) in control animals was sustained during the 75 min of study and was associated with an increase in the extravascular lung water content-to-bloodless dry lung weight ratio (W/D) from a normal value of 2.84 +/- 0.22 to 4.53 +/- 0.24 ml/g (P less than 0.01) after embolization. In the captopril-treated group, the PVR increased gradually, such that the value at 75 min postembolization was greater than in controls (P less than 0.05). The W/D in the captopril-treated group of 4.62 +/- 0.19 ml/g was greater than the value of 2.83 +/- 0.10 ml/g in nonembolized captopril-treated animals, but the degrees of edema in the control and captopril-treated animals were not different. A similar degree of embolization induced during infusion of 5 micrograms X kg-1 X h-1 of bradykinin also did not enhance the pulmonary edema, and there was also a greater increase in PVR than in control animals after embolization. These findings suggest that bradykinin does not contribute to the degree of pulmonary edema after microembolization.