Effects of Diet, Salt Intake and Salt-Loading on Tissue Sodium Concentration and Turnover

Abstract

The effects of alterations in salt exchange and of salt loads on tissue Na turnover and distribution were studied in normal adult rats. In most of these studies Na22 was administered in tracer doses. In acute and subacute studies, Na22Cl was injected intraperitoneally. In chronic studies, Na22Cl was fed in the drinking solution. The soft tissue turnover of Na22, as exemplified in muscle, was greatly retarded by a low sodium diet and accelerated by saline feeding. Neither condition appeared to alter the rapid attainment of maximum muscle concentration relative to plasma. In animals in which a high Na turnover was induced by saline feeding, single intraperitoneal doses of Na22Cl appeared to be distributed in soft tissues parallel to Na23 during the 96 hours following injection. During the early part of this interval the organs most directly in the routes of absorption and excretion in liver and kidney were prone to exhibit unduly high Na22 concentrations. After 96 hours the specific activity in nearly all tissues, notably in heart, lung and skin, fell significantly below that of plasma. On chronic feeding of Na22Cl in saline, the distribution of Na22 in soft tissues required more than 2 weeks to achieve constancy. The principal discrepancy during this early interval was again due to disproportionately high concentrations along the absorption route, notably in stomach and liver. After the 3d week, soft tissue equilibration appeared quite complete, and showed little change over periods as long as 14 weeks. Equilibration in bone appeared a more complex process, with indications that bone Na is composed of 2 fractions. One, apparently comprising about 50% of the total, equilibrated as rapidly as did soft tissue Na. The remaining fraction equilibrated very slowly, the process being nearly complete only after 14 weeks. The data suggest that all bone Na is completely exchangeable, when sufficient time is allowed. Both saline feeding and salt loading were followed by differential increases in the total Na concentrations of certain tissues. The tissues principally involved were bone, lung, spleen and muscle. The most consistent increases were observed in striated muscle, where the Na concentration rose disproportionately with increasing plasma concentrations. The data presently at hand do not indicate whether these differential increases in tissue Na concentrations were due to a rise in the relative amount of extracellular fluid, to an increase in intracellular Na, or to both. The sum of the results indicates that the total Na concentration of a tissue is a complex and somewhat labile function, which can be modified in direction and degree by such common influences as fasting, the composition of the diet, and the nature and extent of the oral and parenteral fluid intake.