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(Hypertension. 2005;45:849.)
© 2005 American Heart Association, Inc.

Editorial Commentaries

Contributions of Sodium and Chloride to NaCl-Induced Hypertension

Theodore A. Kotchen

From the Department of Medicine, Medical College of Wisconsin, Milwaukee, Wis.

Correspondence to Theodore A. Kotchen, MD, Department of Medicine, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226. E-mail tkotchen@mcw.edu

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

The recommendation to avoid high dietary "salt" intake for the prevention and treatment of hypertension is often expressed in terms of dietary sodium. However, a consistent body of evidence suggests that the chloride component of salt is an important contributor to NaCl-induced elevations of blood pressure.¹ In several rat models of salt-sensitive hypertension (Dahl salt-sensitive [S] rat, DOCA-salt hypertension, stroke-prone SHR [SHRSP], angiotensin II-induced salt-sensitive hypertension), selective dietary sodium loading, in the absence of chloride, fails to produce hypertension. In various feeding protocols, anions provided with sodium included various combinations of bicarbonate, phosphate, aspartate, glutamate, and glycinate. Overall, the failure of selective dietary sodium loading to produce hypertension in these studies was not related to group differences of body weight, net sodium balance, blood pH, or serum concentrations of sodium, potassium, or chloride.

Similarly, a limited number of clinical observations also indicate that blood pressure is not increased in humans by high dietary sodium intakes in the absence of chloride. In 1929, Berghoff et al reported that blood pressure increased in 7 hypertensive individuals on a high NaCl intake, but not on a high sodium bicarbonate intake.² This observation was subsequently confirmed.³ Similarly, other investigators have also observed that in contrast to the increase of blood pressure induced by a high NaCl intake in hypertensive patients, blood pressure is not increased by a high sodium intake provided as sodium phosphate or sodium citrate.¹ Further suggesting a modulating effect of dietary chloride on blood pressure, in hypertensive and normotensive subjects, substitution . . . [Full Text of this Article]

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