Conversion of angiotensin I to angiotensin II and inactivation of bradykinin in canine peripheral vascular beds.

We studied the effects of angiotensin I (AI), angiotensin II (AII), and bradykinin (BK) on systemic blood pressure and blood flow in the renal, mesenteric, coeliac, external iliac, and internal iliac vascular beds in the presence and absence of the converting enzyme inhibitor captopril in pentobarbital-anesthetized dogs. AI and AII caused dose-dependent pressor responses and blood flow reductions, and BK caused dose-related depressor responses and an increase in blood flow. The pressor response to AI was decreased and the depressor response to BK was potentiated by captopril. However, the effectiveness of captopril was greater when the peptides were injected intravenously than when they were injected intraaortically. The average conversion of AI to AII in the mesenteric, coeliac, external iliac, internal iliac, and renal vascular beds was 45.7, 31.6, 30.6, 28.0, and 8.9%, respectively. The dose ratio of equipotent BK-induced responses before and after captopril in the mesenteric, coeliac, external iliac, internal iliac, and renal vascular beds was 4.6, 3.5, 2.8, 2.5 and 1.4, respectively. This order was similar to that of the percentage conversion of AI to AII. These results suggest that the greatest proportion of angiotensin conversion and BK inactivation occurs in the pulmonary circulation and that the least proportion occurs in the kidney.