SODIUM APPETITE, THIRST, AND BODY-FLUID REGULATION IN HUMANS DURING REHYDRATION WITHOUT SODIUM REPLACEMENT

After a 7-h H2O and Na+ depletion period (DP), produced by intermittent light exercise (8 bouts) at 35 degrees C, we examined thirst and taste palatability responses to 10 different NaCl solutions during 23 h of rehydration (RH) at 25 degrees C. During DP, net H2O and Na+ loss were 27.2 +/- 2.9 ml/kg and 3.29 +/- 0.45 meq/kg, respectively. Plasma osmolality (P-Osm) and plasma Na+ concentration ([Na+](p)) increased significantly during DP by 3.4 +/- 1.2 mosmol/kgH(2)O and 3.0 +/- 1.0 meq/kgH(2)O, respectively. Plasma volume (PV) decreased by 6.5 +/- 1.9%. Thirst rating, renal fractional reabsorption of H2O, and plasma arginine vasopressin concentration (P-AVP) increased as P-Osm increased. This increased thirst was accompanied by increased palatability ratings to H2O. During RH, subjects drank deionized H2O ad libitum and ate a Na+-free diet for 23 h. P-Osm and [Na+](p) returned to control levels within 1 h RH and remained at or below the control thereafter. PV remained reduced by similar to 5% throughout RH. The increased thirst and P-AVP returned to their respective control levels within 1 h of RH as P-Osm decreased, but thirst rating increased again between 17 and 23 h of RH without an increase in P-Osm or P-AVP. Palatability ratings to a 1 M NaCl solution at and after 3 h RH and palatability ratings to 0.3 M at 17 and 23 h RH were significantly higher than control. Plasma aldosterone concentration (P-Aldo) increased after DP, decreased with drinking, and increased again between 6 and 23 h of RH, accompanied by a marked decrease in fractional Na+ excretion to <0.07%. Thus both Na+ preference and thirst in humans are influenced by body fluid and electrolyte status. The increased Na+ palatability (Na+ appetite) was preceded by osmotically induced thirst, and accompanied by nonosmotically driven thirst [extracellular fluid (ECF) thirst] and increased P-Aldo. The ''Na+ appetite'' and ''ECF thirst'' along with increased renal Na+ retention could contribute to ECF volume regulation after thermally induced H2O and Na+ depletion.