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Previous Volume 351:8-10 July 1, 2004 Number 1 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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The two primary regulators of aldosterone secretion are potassium and the renin–angiotensin system. The latter is involved in volume homeostasis, with high salt intake suppressing the renin–angiotensin system and aldosterone levels and low salt intake having the opposite effect. Secondary hyperaldosteronism, a physiologic response to dietary salt restriction, promotes renal sodium conservation. In this setting, hyperaldosteronism is a bystander that has no cardiovascular consequences. Hyperaldosteronism emerges as villain in persons whose dietary salt intake is normal if the production of aldosterone is inappropriate for the level of sodium intake, resulting in excessive renal sodium retention, potassium wasting, hypertension, and cardiovascular . . . [Full Text of this Article]

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From the Division of Endocrine, Diabetes, and Hypertension, Brigham and Women's Hospital; and Harvard Medical School — both in Boston.

Related Letters:

Aldosterone Revisited
Haddy F. J., Kleta R., O'Brien K., Syed A. A., Redfern C. P.F., Weaver J. U., Vasan R. S., Benjamin E. J., Levy D., Dluhy R. G., Williams G. H.
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N Engl J Med 2004; 351:2131-2133, Nov 11, 2004. Correspondence

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