Low urine flow reduces the capacity to excrete a sodium load in humans

Recent studies in rats suggest that vasopressin and the resulting urinary concentrating activity reduce the capacity of the kidney to excrete 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 (basal) and 10 h after the NaCl load (5 g NaCl in 250 ml, infused intravenously over 30 min). Differences in excretory patterns between LowH and HighH were mostly confined to the first 4 h after the load. The increase in Na excretion after the load was more intense under HighH than under LowH (+10.9 ± 2.6 vs. +5.8 ± 2.7 mmol/h in the first 4 postload h; P < 0.001). Under HighH, urine flow rate (V) increased markedly (+41%), with little change in urinary Na concentration (UNa), whereas under LowH, V declined slightly and UNa rose significantly (+33%). The capacity to raise UNa seemed to reach a maximum at ≈280 mM. In both conditions, the changes in UNa observed after the load were positively correlated with basal UNa. After the load, urea excretion increased under HighH and decreased under LowH, whereas K excretion was unaffected in either condition. These results show that sodium excretion is facilitated by an abundant water supply. The less efficient sodium excretion occurring at low V is probably due to the influence of vasopressin on water, urea, and sodium movements across the collecting 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 evaluated.