Effects of SQ 20881 and captopril on mesenteric, renal, and iliac vasculatures

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Abstract
The ability of two kininase II inhibitors, SQ 20881 and captopril, to inhibit conversion of angiotensin I to angiotensin II and to potentiate the vascular responsiveness to exogenous bradykinin were compared in the mesenteric, renal, and external iliac vasculatures of the dog. Basal rate of angiotensin I-to-angiotensin II conversion was found to be lower in the renal vasculature, average conversion being 4.7%, than in the mesenteric and iliac vasculatures, in which the average conversion was 30.7 and 26.3%, respectively. Inhibition of angiotensin I conversion by both kininase II inhibitors was independent of the basal angiotensin I conversion rate; however, SQ 20881 was a more potent inhibitor of angiotensin I conversion than captopril in all vascular beds tested. In the presence of equal molar doses of SQ 20881 and captopril, only 20-30% of the control bradykinin doses was needed to produce the same vascular effects in the mesenteric and iliac vasculatures. In the kidney, 70% of the control bradykinin doses was needed to produce the same vascular effects in the presence of SQ 20881; in contrast to SQ 20881, neither an equimolar nor 20 times an equimolar dose of captopril produced any change in the renal vascular responsiveness to bradykinin. In conclusion, 1) SQ 20881 is a more potent inhibitor of angiotensin conversion than captopril, and 2) captopril, unlike SQ 20881, does not alter renal vascular responsiveness to bradykinin.