Effects of osmolality on the expression of brain aquaporins in AQP11-null mice.

Water transport in the brain is tightly controlled by blood-brain-barrier (BBB) composed of capillary endothelial cells expressing AQP1/AQP11 and glial foot processes expressing AQP4. Here we examined each AQP mRNA expression in acute hyponatremic and hypernatremic mouse models of wild type (WT) and AQP11 KO mice (KO). The expressions of AQP1, AQP4 and AQP11 mRNAs were quantified by real-time qRT-PCR analysis of whole brain RNA. Acute hyponatremia enhanced AQP4 expression without changing AQP1 expression in KO, whereas it did not change the expression of all AQPs in WT. On the other hand, acute hypernatremia increased AQP4 but decreased AQP1 expression by half in KO, whereas it decreased AQP1 and AQP11 by half without changing AQP4 expression in WT. Enhanced AQP4 expression by osmotic challenges with sodium in KO seems to be a compensation for the loss of AQP11. A stronger hypertonic stimulation with mannitol decreased all AQPs by 30-80% in WT. Since AQP4 plays an important role in the regulation of brain edema at BBB, the results suggest that AQP11 may also be involved in the osmotic regulation of the brain.