Relative Aldosterone Excess

Abstract

There is clear evidence that the vessel wall is an aldosterone target tissue, and that aldosterone at physiological levels produces vasoconstriction by genomic and rapid nongenomic actions.1 Similarly, in clinical studies cited by Duffy et al,2 patients with primary aldosteronism show impaired flow-mediated dilatation among other indices of endothelial dysfunction;3,4 in addition, mineralocorticoid receptor blockade reverses endothelial dysfunction in patients with hypertension or heart failure.4,5 In this issue of the journal Duffy et al2 explore vasodilator responses to methacholine, nitroprusside, and verapamil over a wide dose range in good-sized cohorts of hypertensive and normotensive subjects, to establish possible correlations with renin-angiotensin-aldosterone status. This is clearly a worthwhile undertaking, although the authors candidly admit they had expected to find elevated renin in hypertensives to be correlated with most marked impairment in vasodilatation and, in fact, found the opposite. That said, there are several issues of interpretation and analysis that need to be raised. First is the usage “relative aldosterone excess” in the title and throughout the article. No differences between hypertensives and normotensives were seen in plasma aldosterone levels nor in either group divided into quartiles, with the exception of the highest renin quartile among normotensives: the significantly …