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Recent insight into therapy of congestive heart failure: focus on ACE inhibition and angiotensin-II antagonism

^a Baker Medical Research Institute, Melbourne, 8008, Australia

View larger version (29K): [in a new window]   Figure 1 Cascades of RAS and kinins and mechanisms of action of ACE inhibitors and AT1 receptor antagonists. Conversion from Ang I to Ang II promoted by ACE and non-ACE pathways. Accordingly, ACE inhibitors cannot completely inhibit Ang II formation. Angiotensin II effects are mediated by AT1- and AT2-receptors. While AT1-receptor mediated effects are well defined, AT2-receptor mediated effects are less clear. Angiotensin II type 1 receptor effects can be inhibited by AT1 receptor antagonists while AT2 receptor mediated effects and the formation of Ang III and IV are unconstrained by them. Angiotensin II type 2 receptor stimulation might increase bradykinin levels. Thus, it is possible that increased bradykinin levels may be caused not only by ACE inhibition, but also by AT1 receptor antagonism to a lesser extent. AT = Ang II receptors; t-PA = tissue plasminogen activator; SNS = sympathetic nervous system; GFR = growth factors; PAI = plasminogen activator inhibitor. White arrows indicate enzymatic activation, black arrows formation of substances, double arrows receptor or substance mediated effects.