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Aquaporin-1 (AQP1) and endothelial NO synthase (eNOS) expression on the endothelium of peritoneal vessels modulates ultrafiltration during peritoneal dialysis (PD) by different mechanisms. Protracted eNOS activation may, in the long term, be deleterious for peritoneal functioning. We aimed at examining the effect of peritoneal dialysis solutions (PDSs) and glucose degradation products (GDPs) on the expression of AQP1 and eNOS in cultured endothelial cells.An endothelial cell line (t End.1) was incubated for 24 hours with 2 GDPs (2-furaldehyde [Fur] or methylglyoxal [MGly] at concentrations found in traditional PDSs) or with a different PDS (1.36% glucose, 3.86% glucose and 7.5% icodextrin) in Transwell culture devices. AQP1 and eNOS gene expression were detected by reverse transcriptase polymerase chain reaction.Fur and MGly at concentrations reported in traditional PDSs (Fur 0.8 microM; MGly 35 microM) significantly up-regulated eNOS mRNA and tended to down-regulate AQP1 mRNA in cultured endothelial cells. Glucose-based PDS as well as icodextrin PDS significantly up-regulated basal AQP1 and eNOS mRNA. The effect of 3.86% glucose PDS on AQP1 was significantly higher than that of icodextrin.In cultured endothelial cells, all PDSs triggered both AQP1 and eNOS in a likely feedback mechanism. GDPs stimulated e-NOS expression only, and this effect might favor PD ultrafiltration failure in the long term.