Sevoflurane anaesthesia causes a transient decrease in aquaporin-2 and impairment of urine concentration

Sevoflurane anaesthesia is occasionally associated with polyuria, but theexact mechanism of this phenomenon has not been clarified. Aquaporin-2(AQP2) is an arginine vasopressin (AVP)-regulated water channel proteinlocalized to the apical region of renal collecting duct cells and isinvolved in the regulation of water permeability. To elucidate the effectof sevoflurane anaesthesia on urine concentration and AQP2, we havecompared serum and urinary concentrations of AVP, AQP2 and osmolar changesduring sevoflurane and propofol anaesthesia. General anaesthesia wasinduced with sevoflurane or propofol in 30 patients for a variety of majorsurgical procedures. Blood and urine samples were obtained from patients atbaseline, and 90 and 180 min after induction of anaesthesia. AVP and AQP2concentrations were measured by radioimmunoassay. In both groups, plasmaand urinary concentrations of AVP increased similarly during anaesthesiaalthough plasma osmolality remained unchanged. Although urinary AQP2excretion in the propofol group increased together with changes in plasmaand urinary AVP, urinary AQP2 was significantly lower at 90 min in thesevoflurane group. Urine osmolality in the sevoflurane group also showed atransient but significant decrease in parallel with suppression of AQP2.Our data suggest that sevoflurane anaesthesia transiently produced animpaired AQP2 response to an increase in intrinsic AVP.