The renin-angiotensin-aldosterone system (RAAS) is one of the main targets in the pharmacotherapy of cardiovascular diseases. Inhibitors of the angiotensin- converting enzyme (ACE) have been in clinical use for years and a great deal of experience exists with this particular group of drugs. However, the therapeutic effect is based on the inhibition of an enzyme (ACE) that is not very specific. Another substrate is bradykinin, a well-known mediator of inflammation and a potent inductor of vasodilatation and bronchoconstriction. Dur ing therapy with an ACE inhibitor, the inactivation of bradykinin by cleavage of the carboxyterminal end of this nonpeptide is blocked as well, with the result of bradykinin accumulation. The pattern of adverse effects seen with ACE inhibitors is mainly determined by bradykinin-mediated actions such as edema and cough. Therefore, the inhibition of the RAAS at the level of the transmitter-receptor interaction seems to be a logical development. Because nonpeptide (ie, orally active) angiotensin II (AT) receptor antagonists are available, this concept can be proven.