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A decade before aldosterone was isolated and characterized, Hans Selye showed that administration of deoxycorticosterone acetate to rats sensitized by salt loading produced a vascular inflammatory response (polyarteritis) and tissue fibrosis. Fifty years later, Karl Weber and his colleagues showed that aldosterone and inappropriate salt intake produced cardiac hypertrophy and fibrosis1; this response is bilateral, independent of blood pressure,2 and preceded by progressive perivascular and interstitial inflammation.3 Clinically, patients with primary aldosteronism are more at risk than essential hypertensive patients with comparable blood pressure elevation, similarly suggesting a pathophysiological role for aldosterone in the cardiovascular system. On the basis of this evidence, experimental and clinical, there is thus no doubt that blocking aldosterone action in such circumstances is beneficial in terms of progression and outcomes.It is, however, not as simple as that. In the present issue of Hypertension , Nagata et al4 show that mineralocorticoid receptor blockade attenuates cardiac hypertrophy and failure in low-renin, low-aldosterone hypertensive rats. The model is straightforward: salt sensitive Dahl rats are started at 7 weeks on an uncompromisingly high (8%) salt intake to which they not surprisingly respond by marked cardiac hypertrophy and clear signs of cardiac failure at age 19 weeks. Animals given eplerenone (30 or 100 mg/kg bw in the chow) to block mineralocorticoid receptors are progressively protected in terms of a number of cardiac/pulmonary indices. The authors conclude that in this model, mineralocorticoid receptor activation is not by the low levels of aldosterone, but by corticosterone, which circulates at total concentrations ≈2000× those of …

Mineralocorticoid Receptors and Cardiovascular Damage