Sepsis-induced urinary concentration defect is related to nitric oxide–dependent inactivation of TonEBP/NFAT5, which downregulates renal medullary solute transport proteins and aquaporin-2
Critical Care Medicine, 06/01/2012
Küper C et al. – The present data demonstrate that lipopolysaccharide increases medullary nitric oxide production by iNOS induction, resulting in impairment of the transcriptional activity of TonEBP/NFAT5 by S–nitrosylation. The consequence thereof is reduced expression of TonEBP/NFAT5 target genes ClC–K1, Barttin, urea transporter–A1, and aquaporin 2 that are required for urinary concentration.