Can renin inhibition by Aliskiren prove itself in atherosclerosis prevention?

The renin-angiotensin-aldosterone system (RAAS) regulates inflammation and vascular remodeling thus playing an important role in atherosclerosis, kidney disease and heart failure. As an example of this, the effector hormone Angiotensin II (AngII) was shown to promote oxidative stress, endothelial dysfunction and vascular inflammation [1], all of which would be detrimental. However, inhibiting the RAAS now goes beyond blood pressure reduction and is an important component of the baseline treatment of heart failure, cardiorenal syndrome and diabetic nephropathy. As an example of its protective role in atherosclerosis, the HOPE (Heart Outcomes Prevention Evaluation) trial showed a 37% risk reduction in cardiovascular death by Ramipril in people with diabetes [2]. Angiotensin receptor blockers (ARBs) and angiotensinconverting enzyme inhibitors (ACEIs) reduce effectively the production of AngII, but consequently increase plasma renin concentration because of the loss of negative feedback by AngII on renin. On one hand this might lead to a limited blockade of the RAAS, on the other it could lead to activation of possible alternative pathways by renin [3]. This issue raised the demand for different RAAS inhibitors. In 2007 the US Food and Drug Administration first approved Aliskiren. This orally active drug acts a direct renin antagonist, thereby antagonizing the rate-limiting step of the RAAS without raising the plasma renin activity. Plasma renin activity has