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(Hypertension. 2006;48:820.)
© 2006 American Heart Association, Inc.

Editorial Commentaries

The Adrenergic Nervous System Conversing With the Adrenal Cortex

New Implications for Salt-Sensitive Hypertension

From the Department of Medicine, Indiana University School of Medicine, and the Richard L. Roudebush VA Medical Center, Indianapolis, Ind.

Correspondence to J. Howard Pratt, Richard L. Roudebush VA Medical Center, 1481 West 10th St, Indianapolis, IN 46202. E-mail johpratt@iupui.edu

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

Aldosterone signals the distal nephron to reabsorb sodium and secrete potassium. The regulation of aldosterone secretion is driven by the need to defend against sodium deficiency or an elevated potassium. With a high-salt diet, the one typically consumed today, the rigorous relationship of aldosterone to sodium balance begins to break down with the result that more aldosterone is produced than is needed, driving the distal nephron, the guardian of overall sodium homeostasis, to a state of overactivity. Why is aldosterone secretion not more contained under conditions of high salt intake? One explanation is that there were no teleologic pressures applied to the renin–angiotensin system to appropriately dampen stimulation of aldosterone secretion: early ancestral survival depended on there being only sufficiently high levels of aldosterone.¹

In the current issue of Hypertension, Pojoga et al² provide evidence for a new mechanism whereby secretion of aldosterone is sustained under conditions of generous salt intake and when, in the interest of avoiding hypertension, a lower secretion rate would be preferred. They report on an intriguing observation that certain haplotypes (more specifically, diplotypes) of the ß-2 adrenergic receptor (ß2AR) gene associate with low-renin hypertension that seems to be because of higher plasma aldosterone levels. Theoretically, when something other than the usual stimuli (angiotensin II and potassium) are increasing aldosterone secretion, the usual stimuli downregulate their contribution, and there is no net increase in secretion; but, as already noted, this type of counterregulation may be less than complete under conditions of high salt consumption.

In . . . [Full Text of this Article]

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