Thalidomide ameliorates portal hypertension via nitric oxide synthase independent reduced systolic blood pressure

Figure 1 Portal vein ligation and thalidomide increases nitric oxide via endothelial and inducible nitric oxide synthase respectively. Plasma total nitrate (NOx) was measured daily for 7 d in wild type (WT), endothelial nitric oxide synthase (eNOS)^-/- and inducible nitric oxide synthase (iNOS)^-/- mice following portal vein ligation (PVL) or sham surgery. A: Plasma NOx increased following PVL in wild type mice but not following sham surgery. Levels increased to a maximum 2 d after PVL, after which NOx returned to pre-surgical baseline; B: Plasma NOx increased 2 d following PVL in iNOS^-/- but not eNOS mice. In eNOS^-/- mice NO was not increased following PVL; C: Unadulterated 8 wk WT, eNOS^-/- and iNOS^-/- mice were given 50 mg/kg thalidomide or vehicle. Blood was collected by cardiac puncture and plasma was assayed for NOx. Plasma NOx was significantly increased by the administration of thalidomide in WT and eNOS^-/- mice but was reduced in iNOS^-/- mice. ^aP < 0.05 vs other groups.