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(Hypertension. 2005;46:1259.)
© 2005 American Heart Association, Inc.

Editorial Commentaries

Neurogenic Mechanisms and Salt Sensitivity

Heimo Ehmke

From the Institut für Vegetative Physiologie und Pathophysiologie, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany.

Correspondence to Heimo Ehmke, MD, Institut für Vegetative Physiologie und Pathophysiologie, Universitätsklinikum Hamburg-Eppendorf, Martinistraße 52, D-20246 Hamburg, Germany. E-mail ehmke@uke.uni-hamburg.de

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

The concept of salt sensitivity is based on the observation that some individuals respond to a high salt intake with a marked increase in blood pressure, whereas others experience little or no blood pressure changes. Salt sensitivity is found much more frequently in hypertensive than in normotensive subjects,¹ and its presence predicts a significantly greater increase of blood pressure with age,² suggesting that salt sensitivity plays some role in the pathogenesis of hypertension. In addition, the risk for the occurrence of cardiovascular events is >3-fold higher in salt-sensitive than in salt-resistant hypertensive subjects.³ In this issue of Hypertension, Coruzzi et al⁴ show that in individuals with essential hypertension, even modest levels of salt sensitivity are associated with alterations in autonomic cardiovascular control. Their study strongly supports the idea that neurogenic mechanisms are involved in the pathophysiology of salt sensitivity in essential hypertension.

Because the kidney is the primary site for the regulation of salt and water homeostasis, most of the previous search for mechanisms leading to salt sensitivity has focused on functional and genetic differences in renal sodium handling. In their classical analysis of long-term blood pressure control, Guyton et al predicted that any reduction of the steepness of the chronic pressure–natriuresis curve, such as a loss of kidney mass or an aldosterone-producing adenoma, will induce salt sensitivity of blood pressure.⁵ This proposal was confirmed by experimental and clinical observations, most elegantly in monogenic disorders, which functionally mimic an excess of aldosterone (glucocorticoid remediable aldosteronism, apparent mineralocorticoid excess, and . . . [Full Text of this Article]

Related Article:

Effects of Salt Sensitivity on Neural Cardiovascular Regulation in Essential Hypertension

Paolo Coruzzi, Gianfranco Parati, Lorenzo Brambilla, Valerio Brambilla, Massimo Gualerzi, Almerico Novarini, Paolo Castiglioni, and Marco Di Rienzo
Hypertension 2005 46: 1321-1326. [Abstract] [Full Text] [PDF]