The RAAS is a major regulator of BP [3, 4] . In addition, the RAAS has a role in the vascular response to injury and inflammation [4] . Chronic RAAS activation, through both angiotensin (Ang) II and aldosterone, leads to hypertension and perpetuates a cascade of proinflammatory, prothrombotic, and atherogenic effects associated with endorgan damage [3, 4] . Based on these facts, several drugs have been developed that work by (a) reduction of Ang II levels, (b) inhibition of the Ang II type 1 receptor (AT1R), (c) blockade of the aldosterone receptor, and (d) renin receptor blockade [5, 6] . During the last 25 years several clinical trials have shown the benefits with these drugs that inhibit the RAAS with regard to BP reduction, regression of cardiac hypertrophy, prevention of kidney damage and reduction of cardiovascular morbidity reduction in hypertensive patients. Besides, with most of these RAAS blockers, quality of life as well as survival has been significantly improved in patients with heart failure. Consequently, the RAAS is currently a main therapeutic target in hypertension treatment [3, 4] . Aggressive BP control improves outcomes in patients with CV disease, stroke, and nephropathy and might have beneficial effects beyond BP lowering [7] .