Mechanism, prevention and therapy of sodium-dependent hypertension

This review considers the mechanism, prevention and therapy of sodium-dependent, low-renin, presumably volume-expanded, hypertension. Certain evidence suggests that in susceptible persons the basic problem is a genetic or acquired deficiency in the ability of the kidney to excrete sodium and hence water. This places them at a disadvantage in a society such as ours in which the salt intake is uniformly high, to a large extent because of the salt content in commercially processed foods. Other evidence suggests that the blood pressure level rises in part because the volume expansion evokes the release of an unknown, slowly-acting, pressor agent which operates by stimulating the contractility of cardiovascular muscle through suppression of the cellular sodium-potassium pump, much in the manner of the cardiac glycosides. Several investigators and the Select Committee on GRAS Substances suggest that the incidence of salt-dependent hypertension could be significantly decreased in a society such as ours if salt intake were reduced from the present level of approximately 10 g/day to 12 g/day. An obvious starting point is a reduction of the salt content in processed foods. The Food and Nutrition Board of the National Research Council suggest that a judicious combination of dietary sodium restriction and the use of an appropriate diuretic is the most rational approach to the treatment and management of diseases characterized by retention of sodium.