A radioimmunoassay has been established to measure urinary aquaporin-2 excretion (u-AQP2). To elucidate how u-AQP2 changes when endogenous vasopressin is increased independently of plasma osmolality, we estimated u- AQP2 during general anesthesia for surgery. We collected urine and blood samples from 50 patients before and 90 and 180 min after anesthetic induction. Plasma (29.1 ± 12.6 pg/mL) and urinary (565.1 ± 207.0 ng/gCr) vasopressin levels were markedly increased after anesthetic induction. Although no significant alteration of plasma osmolality or serum sodium concentration was observed during 180 min, u-AQP2 was significantly increased (preinduction 224.5 ± 24.2 fmol/mgCr; 90 min 243.3 ± 31.8; 180 min 331.4 ± 45.9), paralleling an increase of plasma and urinary vasopressin. The plasma vasopressin concentration after anesthetic induction was far in excess of that expected based on plasma osmolality. Individual plasma and urinary vasopressin concentrations correlated significantly with u-AQP2. At 180 min after anesthesia, plasma osmolality did not change, but urine osmolality decreased despite increased u-AQP2, and a preanesthetic positive correlation between urine osmolality and u-AQP2 disappeared. Thus, although u-AQP2 correlates with increased intrinsic vasopressin levels, the increase in u- AQP2 did not directly contribute to urine concentration. Apparently, an escape from the physiologic effects of high vasopressin level occurs during anesthesia via a mechanism independent of aquaporin-2. We conclude that the anesthetic would interfere with the urinary concentrating capacity at the level of AQP2-action. Implications: The excessive increase of intrinsic vasopressin exactly augmented urinary aquaporin-2 excretion, resulting in urine concentration; however, anesthesia seemed to modify this process possibly by interfering with the aquaporin-2 action.
ASJC Scopus subject areas
- Anesthesiology and Pain Medicine