Effect of water deprivation and hypertonic saline infusion on urinary AQP2 excretion in healthy humans.

Arginine vasopressin (AVP) mediates water transport in the renal collecting ducts by forming water channels of aquaporin-2 (AQP2) in the apical plasma membrane. AQP2 is excreted in human urine. We wanted to test the hypothesis that urinary excretion of AQP2 (u-AQP2) reflects the effect of AVP on the renal collecting ducts during water deprivation and hypertonic saline infusion in healthy subjects. Fifteen healthy subjects underwent a 24-h period of fluid restriction. Urine and blood samples were collected at timed intervals. Fifteen healthy subjects were given 7 ml/kg 3% hypertonic saline infusion for 30 min. Urine and blood samples were collected at timed intervals. During fluid restriction, the u-AQP2 rate increased from 3.9 (25th percentile: 3.1; 75th percentile: 5.2) to 7.6 (5.9-9.1; P < 0.001) ng/min, and the plasma AVP (p-AVP) level increased from 0.5 (0.4-0.6) to 3 (1.7-3.3) pmol/l. There was a positive correlation between the maximum change in u-AQP2 rate and the maximum change in p-AVP (r = 0.57, P < 0.03). During the infusion study, u-AQP2 rate was at maximum 90 min after the infusion [baseline: 4.5 ng/min (3.5-4.8); 90 min: 5 ng/min (4.5-6.0) P < 0.02]. p-AVP increased from 1.0 (0.9-1.1) to 1.5 (1.2-1.8; P < 0.002) pmol/l. There was a positive correlation between the maximum change in u-AQP2 rate and the maximum change in p-AVP (r = 0.83; P < 0.0001). It can be concluded that p-AVP and u-AQP2 are increased during thirst and hypertonic saline infusion and that u-AQP2 reflects the action of AVP on the collecting ducts.