Sodium intake and essential hypertension.

Abstract

This review briefly considers the hypothesis that a generous dietary sodium intake contributes to the development or maintenance of essential hypertension. Three lines of evidence are presented that are not mutually exclusive. Epidemiological studies examining sodium intake, prevalence of hypertension, and increases of blood pressure with age provide circumstantial support for the concept that hypertension is related to sodium intake. Analyses of cellular electrolyte transport suggest that hypertensives and their relatives are at a disadvantage with respect to extruding sodium from cells. A conceptual framework indicates that blood pressure is determined by a balance between the natriuretic effect of increased blood pressure and the pressor effect of sodium retention. Clinical studies in humans support the sodium hypothesis. The kidney's ability to excrete sodium and its sodium regulatory system are genetically determined. In hypertensive humans, blood pressure is directly correlated with total body and exchangeable sodium, a relationship that increases with age. Groups at risk for hypertension excrete sodium less well then those at less risk. Yet both hypertensives and normotensives exhibit heterogeneous blood pressure responses when sodium-loaded or -depleted. It has not been shown that sodium restriction will prevent the development of hypertension in normal individuals; however, it is clear that sodium restriction is an important aspect of management. In three prospective randomized controlled trials, practical sodium restriction lowered blood pressure by 8 mm Hg. Such a decrease would lower cardiovascular morbidity by 10% to 15%. Were means available to detect "salt-sensitive" hypertensives, sodium restriction could be conducted in a more appropriate fashion.