Journal of the American College of Nutrition, Vol 6, Issue 3 261-270, Copyright © 1987 by American College of Nutrition

JOURNAL ARTICLE

Dietary sodium and potassium in the genesis, therapy, and prevention of hypertension

F. J. Haddy

In this review, we first summarized the evidence from animals and man for and against a role for dietary sodium in the genesis and treatment of hypertension. The evidence for a role for dietary sodium in the genesis of hypertension is strongest in those subjects with impaired ability to excrete sodium due to organic renal disease or mineralocorticoid excess. Here restriction of dietary sodium promptly lowers arterial pressure. Its role in the genesis of essential hypertension is still controversial. Nevertheless, it appears that some patients with mild to moderate essential hypertension respond to moderate sodium restriction with a modest fall in blood pressure. This restriction also seems to reduce the amount of antihypertensive medication needed to keep blood pressure under control. We next considered the mechanism of the pressure response to dietary sodium chloride, concentrating upon the increase in extracellular fluid volume, potassium depletion, and increased plasma levels of prohypertensive sodium pump inhibitor and antihypertensive atrial natriuretic factor. We next summarized the evidence for a primary role for dietary potassium in the genesis of hypertension and pointed out that certain subsets of subjects with a high incidence of hypertension also have a lower dietary potassium intake. Some investigators find that dietary potassium supplementation lowers blood pressure in established hypertension. This may result from natriuresis and from vasodilation subsequent to stimulation of Na+, K+-ATPase in vascular smooth muscle and adrenergic nerve terminals. We then considered practical aspects of dietary sodium restriction and dietary potassium supplementation in the therapy for established hypertension. The review concludes with comments on their possible roles in the prevention of hypertension.

This article has been cited by other articles:

				V. Vallon, D. Y. Huang, F. Grahammer, A. W. Wyatt, H. Osswald, P. Wulff, D. Kuhl, and F. Lang SGK1 as a determinant of kidney function and salt intake in response to mineralocorticoid excess Am J Physiol Regulatory Integrative Comp Physiol, August 1, 2005; 289(2): R395 - R401. [Abstract] [Full Text] [PDF]