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(Hypertension. 2008;51:39.)
© 2008 American Heart Association, Inc.
Editorial Commentaries |
From the Department of Medicine, Indiana University School of Medicine, and the Richard L. Roudebush Veterans Affairs Medical Center, Indianapolis, Ind.
Correspondence to J. Howard Pratt, 541 Clinical Dr, Indianapolis, IN 46202-5111. E-mail johpratt@iupui.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Whether primary aldosteronism is as widespread as some believe, a topic debated recently in this journal by Calhoun1 and Kaplan,2 may not be as relevant as whether the commonly observed prevailing level of aldosterone is too high for the amount of sodium that we consume. I would like to make the case here (with help from a Nobel Laureate) that the usual level of aldosterone contributes to the development of hypertension in many people, indeed, possibly many more than even the most generous estimate for the prevalence of primary aldosteronism.
Not long after the angiotensinogen gene/hypertension association was described in 1992,3 Oliver Smithies laboratory showed in a transgenic mouse that levels of angiotensinogen and blood pressure were proportional to the number of copies of the angiotensinogen gene.4 It provided proof of principal that blood pressure was under the influence of the endogenous load of angiotensinogen. In the present issue of Hypertension,5 this same laboratory now provides similar complimentary proof to the earlier report by Vasan et al6 that higher but normal levels of aldosterone are predictive of a future elevation in blood pressure. They did this by manipulating the gene for aldosterone synthase (AS; CYP11B2), an essential enzyme for synthesis of aldosterone, by making the 3' untranslated region of its mRNA more stable, thereby increasing its expression; the generated mice are referred to as AShi/hi mice.
The causes of common forms of hypertension or essential hypertension are mostly unknown. Although the Guytonian principle that an increase
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