[Pharmacologic modification of the converting enzyme--local and systemic effects on the heart and blood vessels]

The renin-angiotensin system (RAS) has long been perceived as basically humoral. Since recent findings in molecular biology extended this view to local, possibly independent, tissue-RAS, both the RAS and the kallikrein-kinin cascade are understood as mixed local-systemic interacting systems, which explains local and systemic effects of converting enzyme (CE) inhibitors well. The key enzyme of both systems, CE, catalyzes the activation of the vasopressor and possibly trophic peptide, angiotensin II, and also inactivates the vasodilatory and, according to our observations, cardioprotective bradykinin. Thus, it is consistent that CE-inhibitors lower blood pressure, reduce cardiac hypertrophy, improve metabolic state and attenuate arrhythmias, particularly in ischemic hearts. It is evident from animal experiments that the tight binding favours new oral CE inhibitors, such as ramipril, not only for prevention but also for treatment of tissue injuries due to hypertension or ischemia.