LOW URINE FLOW REDUCES THE CAPACITY TO EXCRETE A SODIUM LOAD IN HUMANS

Recent studies in rats suggest that vasopressin and the resulting urin ary concentrating activity reduce the capacity of the kidney to excret e sodium. The present study investigates the influence of the level of hydration on the excretion of a sodium load in humans. Eight healthy male volunteers (18-35 yr) were studied twice, in random order, under either low (LowH) or high (HighH) hydration. They drank throughout the study either 0.25 (LowH) or 2.0 ml water/kg body wt (HighH) every 30 min. After 1 h equilibration, urine was collected for 2 h before (basa l) and 10 h after the NaCl load (5 g NaCl in 250 mi, infused intraveno usly over 30 min). Differences in excretory patterns between LowH and HighH were mostly confined to the first 4 h after the load. The increa se in Na excretion after the load was more intense under HighH than un der LowH (+10.9 +/- 2.6 vs. +5.8 +/- 2.7 mmol/h in the first 4 postloa d h; P < 0.001). Under HighH, urine flow rate (V) increased markedly ( +41%), with little change in urinary Na concentration (U-Na), whereas under LowH, V declined slightly and U-Na rose significantly (+33%). Th e capacity to raise U-Na seemed to reach a maximum at approximate to 2 80 mM. In both conditions, the changes in U-Na observed after the load were positively correlated with basal U-Na. After the load, urea excr etion increased under HighH and decreased under LowH, whereas K excret ion was unaffected in either condition. These results show that sodium excretion is facilitated by an abundant water supply. The less effici ent sodium excretion occurring at low V is probably due to the influen ce of vasopressin on water, urea, and sodium movements across the coll ecting ducts. These observations suggest that, in everyday Life, a low water intake could limit the capacity to excrete sodium. Whether this could contribute to salt-sensitive hypertension remains to be evaluat ed.