Erdös 1
recognized that biologically active peptides
generated by the renin-angiotensin and kallikrein-kinin systems, e.g., angiotensin II, bradykinin, and kallidin (Lys-bradykinin), are so rapidly metabolized and inactivated that
their transient effects would never be useful medications, but
the role of these peptides in certain physiological or pathological conditions could be determined by agents that directly block their effects or inhibit either their enzymatic
degradation or production. This concept enabled investigators to discover captopril and later other angiotensin I converting enzyme (ACE) inhibitors and turn them into clinically useful drugs for treatment of hypertension and related
cardiovascular diseases. The aim of this presentation is to assess a role of the renin angiotensin system (RAS) and the
kallikrein kinin system (KKS) in a diabetic renal damage.
