ABSTRACT
It is likely that the effects of the ACE inhibitors on endothelial function are central to their antiatherogenic effects.19 Direct clinical evidence of such an effect is lacking but large-scale studies are currently in progress. It is not only through reduced angiotensin II generation that ACE inhibitors can favourably influence endothelial function. As Fig. 11.2 indicates, these drugs also inhibit the kininase responsible for the breakdown of bradykinin (and also of substance P). Bradykinin in particular is known to act directly on endothelial cells to increase nitric oxide release. The relative importance of these two actions of the ACE inhibitors has become increasingly controversial since the introduction of angiotensin receptor (AT1) antagonists (see later).
