Aquaporin-2 in the immature rat: expression, regulation, and trafficking

The immature kidney is resistant to arginine vasopressin. To define the role of aquaporin-2 (AQP-2), the developmental expression of this water channel was studied in rats. AQP-2 levels were lower during early postnatal life, reaching maximal expression at 10 wk of age. Concurrently, urine osmolality increased from 242 +/- 60 to 1267 +/- 311 mosmol/kg. To study the regulation of AQP-2, immature and adult rats were kept on ad libitum intake or were water-deprived. Under normal conditions, AQP-2 levels in the immature rat were significantly lower (52.3 +/- 5.8%, P < 0.001) than in the adult. However, after dehydration the expression increased to adult levels. Interestingly, the increase in AQP-2 observed in the immature kidney was not accompanied by a proportional increase in urine osmolality. To rule out a potential alteration in AQP-2 trafficking, the transport of this water channel was investigated in a group of rats subjected to dehydration, treated with desmopressin acetate (dDAVP), or water loaded. Dehydration and dDAVP stimulated translocation of AQP-2 from intracellular vesicles to the plasma membrane, whereas water loading caused a shift of AQP-2 channels back to intracellular vesicles in both adult and immature animals. In summary, AQP-2 expression and trafficking in the immature kidney is appropriately stimulated by water deprivation and dDAVP. However, urine osmolality remained significantly decreased. From this study, it is concluded that although AQP-2 expression may play a role in the development of urine concentrating abilities, there still is a significant defect, yet to be defined, distal to AQP-2.