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(Hypertension. 2005;46:643.)
© 2005 American Heart Association, Inc.

Editorial Commentaries

Relative Aldosterone Excess

Relative to What?

John W. Funder

From Prince Henry’s Institute of Medical Research, Clayton, Victoria, Australia.

Correspondence to Professor John W. Funder, Prince Henry’s Institute of Medical Research, Monash Medical Centre, 247 Clayton Rd, PO Box 5152, Clayton, Victoria, Australia 3168. E-mail john.funder@phimr.monash.edu.au

An extract of the first 250 words of the full text is provided, because this article has no 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 higher aldosterone levels in this subgroup may reflect nothing more sinister than lower sodium intake, which was unfortunately neither measured nor controlled. "Relative aldosterone excess" is thus relative to measured plasma renin levels, which makes the common but dangerous assumption that the major determinant of aldosterone secretion is the renin-angiotensin system. The most . . . [Full Text of this Article]

Related Article:

Low-Renin Hypertension With Relative Aldosterone Excess Is Associated With Impaired NO-Mediated Vasodilation

Stephen J. Duffy, Elizabeth S. Biegelsen, Robert T. Eberhardt, David F. Kahn, Bronwyn A. Kingwell, and Joseph A. Vita
Hypertension 2005 46: 707-713. [Abstract] [Full Text] [PDF]

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