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JRAAS 2001;2:89–92 Introduction Certain drugs that block the renin-angiotensinaldosterone system (RAAS), namely angiotensin converting enzyme inhibitors (ACE-I) and spironolactone, have been shown to improve symptoms, reduce hospital admission rates and increase survival in patients with chronic heart failure (CHF). Consequently, angiotensin II (Ang II) type 1 receptor antagonists or Ang II type 1 receptor (AT1receptor) blockers (ARBs) may also have a role in the treatment of CHF. Two therapeutic strategies have been considered for ARBs, the first as an alternative to ACE-I and the second in combination with ACE-I. Interestingly, the rationale behind these strategies is quite different. In the first, the kinase II property of ACE is considered disadvantageous, in that bradykinin is directly or indirectly blamed for the undesirable effects of ACE-I such as cough and angio-oedema. The second strategy sees bradykinin as a desirable substance, with vasodilator, anti-thrombotic and growth inhibiting properties. Both strategies,however, regard ACEI as sub-optimal antagonists of the action of Ang II, reflecting the belief that non-ACE pathways also contribute to the generation of Ang II (and this can only be blocked by an ARB). An even more theoretical difference between ACE-I and ARBs concerns the postulated role of the Ang II type 2 receptor (AT2-receptor). This receptor is considered by some to exert the opposite effects to the AT1-receptor. ACE inhibition leads to reduced stimulation of both types of Ang II receptor, whereas selective AT1receptor blockade, in theory, leads to hyperstimulation of the unblocked AT2-receptor. The alternative strategy of combination ACE-I and ARB therapy in CHF will not have this effect (Figure 1).

Angiotensin II receptor antagonists for the treatment of heart failure: what is their place after ELITE-II and Val-HeFT?