Bradykinin and coronary artery disease

Although the benefits of angiotensin-converting enzyme (ACE) inhibitors in limiting the progression of a variety of cardiovascular diseases are well k nown, their mechanisms of action have not been completely discovered. A red uction in the synthesis of the potent vasoconstricting agent angiotensin II has for a long time been considered to be the leading mechanism to account for the effects of ACE inhibitors. However, another action of these relati vely old drugs is emerging: the increased availability of bradykinin. This kinin, which is broken down by ACE, has potent cardioprotective, antithromb otic antitrophic and vasodilator effects occurring through the stimulation of specific receptors on several cells. The recent development of a specifi c bradykinin-receptor blocking agent, icatibant, has allowed better underst anding of the therapeutic propel:ties of ACE inhibitors mediated by bradyki nin both in experimental and clinical studies.