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Hypertension. 2007;49:761-762
Published online before print March 5, 2007, doi: 10.1161/01.HYP.0000260141.30703.0c
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(Hypertension. 2007;49:761.)
© 2007 American Heart Association, Inc.


Editorial Commentaries

Aldosterone Excess, Hypertension, and Chromosome 7p22

Evidence Continues to Mount

Michael Stowasser; Richard D. Gordon

From the Endocrine Hypertension Research Centre, University of Queensland School of Medicine, Greenslopes and Princess Alexandra Hospitals, Brisbane, Australia.

Correspondence to Michael Stowasser, Endocrine Hypertension Research Centre, University of Queensland School of Medicine, Princess Alexandra Hospital, Ipswich Road, Woolloongabba, Brisbane 4102, Australia. E-mail m.stowasser@uq.edu.au


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

In recent years, numerous groups of investigators have reported primary aldosteronism (PAL) to be much more common than previously thought.1–4 This has followed recognition of the aldosterone/renin ratio (ARR) as an improved, more sensitive method of screening for PAL and the application of ARR testing to a wider population, to include normokalemic, as well as hypokalemic, hypertensive subjects. The degree of selectedness of the populations involved in those studies has varied widely, from relatively "unselected" (including subjects randomly selected from general practitioner databases3) to highly selected. Despite this, the great majority of these studies have reported prevalence rates of PAL that have fallen within the range of 5% to 15%, making it the most common specifically treatable and potentially curable form of hypertension.

Importantly, clinical responses to specific medical or surgical treatment in patients found in this way to have PAL have been highly gratifying. However, careful steps need to be taken to avoid misdiagnosis. These include controlling posture and avoiding interfering medications during diagnostic testing, performing careful suppression testing to definitively confirm or exclude the diagnosis of PAL, and using adrenal venous sampling to differentiate unilateral from bilateral forms.5

In the wake of these reports, the article by Newton-Cheh et al6 appearing in this edition of Hypertension is highly relevant and should be of great interest to readers of this journal. Following on their recent report describing significant relationships of aldosterone levels with blood pressure progression and hypertension development among Framingham study participants,7 the authors have found similar . . . [Full Text of this Article]


Related Article:

Clinical and Genetic Correlates of Aldosterone-to-Renin Ratio and Relations to Blood Pressure in a Community Sample
Christopher Newton-Cheh, Chao-Yu Guo, Philimon Gona, Martin G. Larson, Emelia J. Benjamin, Thomas J. Wang, Sekar Kathiresan, Christopher J. O’Donnell, Stacy L. Musone, Amy L. Camargo, Jared A. Drake, Daniel Levy, Joel N. Hirschhorn, and Ramachandran S. Vasan
Hypertension 2007 49: 846-856. [Abstract] [Full Text] [PDF]



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J. R. Sowers, A. Whaley-Connell, and M. Epstein
Narrative Review: The Emerging Clinical Implications of the Role of Aldosterone in the Metabolic Syndrome and Resistant Hypertension
Ann Intern Med, June 2, 2009; 150(11): 776 - 783.
[Abstract] [Full Text] [PDF]