Reduction in the synthesis of the potent vasoconstricting agent angiotensin II has long been considered as the principal mechanism accounting for angiotensin-converting enzyme inhibition and the ensuing limitation in the progression of a variety of cardiovascular diseases. Recently, a new mechanism of action of these relatively old drugs has been proposed, ie, the increased availability of bradykinin. This kinin, which is broken down by angiotensin-converting enzyme, has a potent vasodilator effect resulting from the stimulation of specific receptors on endothelial cells and the release of nitric oxide, prostacyclin, and the endothelium-derived hyperpolarizing factor. The recent development of a specific bradykininreceptor blocking agent, icatibant, has allowed better understanding of the beneficial properties of angiotensin-converting enzyme inhibitors on endothelial dysfunction, both in experimental and clinical studies...