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

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Abstract
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.

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