Pure kallikrein and bradykinin, when added to the perfusion medium of the isolated perfused rat lung, produced an equal inhibition in the conversion of angiotensin I to angiotensin II as measured in the venous return superfused over the rabbit aortic strips. Acetylsalicylic acid (ASA) prevented the inhibitory effect of kallikrein and bradykinin. Aprotinin, however, prevented the inhibitory effect of kallikrein without altering that of bradykinin. The recovery brought about by ASA of the bradykinin-produced inhibition of angiotensin I conversion was also prevented by prior addition of prostaglandin E2 (PGE2) into the perfusion medium. Neither kallikrein and bradykinin nor ASA altered the myotropic activity of angiotensin II. 5-Oxo-L-prolyl L-tryptophyl-L-prolyl-L-arginyl-L-prolyl-L-glutaminyl-L-isoleucyl-L-prolyl-L- proline (SQ 20 881), when added to the medium, greatly reduced the responses to angiotensin I but potentiated those of angiotensin II. The possible mechanisms of the inhibitory effects of kallikrein and bradykinin are discussed.