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See related article, pp 62–69The International Society on Hypertension in Blacks consensus statement in 2010 noted that, in the setting of high dietary sodium intake, hypertensive blacks have particularly impressive responses to renin-angiotensin-aldosterone system (RAAS) blockade.1 The statement went on to point out that the excessive target-organ damage (TOD) in hypertensive blacks can be attributed to RAAS activation. Although a normal-to-“high-renin” hypertensive state is most prevalent, the classic hypertension literature has categorized blacks as typically having a “low-renin” state.2 There is somewhat of a paradox in the observation that blacks, despite having a low-renin state, have high serum aldosterone concentrations.3 Blacks experience disproportionately higher rates of hypertension-related TOD compared with whites.4 The mediators of the higher rates of TOD noted in blacks are most likely directly attributed to high levels of downstream mediators of the RAAS, such as aldosterone and angiotensin II. The mechanism by which a low-renin state can be associated with such an apparently active RAAS is not clearly defined.The article by Michel et al,5 in this issue of Hypertension , addresses the mechanism by which RAAS activation affects blood pressure (BP) …

Unraveling the Mechanism of Renin-Angiotensin- Aldosterone System Activation and Target Organ Damage in Hypertensive Blacks