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In cardiovascular disease, especially hypertension, chronic heart failure, and atherosclerosis, angiotensin II (Ang II) is generally a culprit while nitric oxide exerts beneficial effects. Accordingly, inhibiting angiotensin-converting enzyme (ACE) has become established as one of the most successful therapeutic options in the treatment of chronic cardiovascular disorders. However, an estimated 20–40% of patients do not respond to and/or tolerate ACE inhibition.1 The introduction of drugs selectively blocking Ang II receptors of type 1 (ARBs) has definitely brought some relief from unwanted side effects. In the paper by Company et al. , appearing in the current issue of Cardiovascular Research ,2 reasons are now given for why one should expect ARBs to be even more beneficial than ACE inhibitors in all cardiovascular conditions with an inflammatory component.The reasoning and evidence are compelling and centre on the fact that the mast cell enzyme chymase is able to generate Ang II independently of the activity of ACE. In experiments conducted on the mouse cremaster muscle microcirculation, the authors show that degranulating mast cells release chymase in amounts great enough to circumvent the functional protection otherwise provided by an ACE inhibitor under non-inflammatory conditions. In contrast, stimulated mast cells lose much of their microcirculatory destabilizing potential if an ARB is applied instead …

All because of the mast cell: blocking the angiotensin receptor-1 should be better than inhibiting ACE (theoretically)