title: Oxidative stress and endothelial function in chronic renal failure.
abstract: This study aimed to investigate the relationship between oxidative stress and endothelium-dependent vasodilation in patients with chronic renal failure (CRF). Thirty-seven patients with CRF underwent evaluation of endothelium-dependent vasodilation and endothelium-independent vasodilation by means of forearm blood flow measurements with venous occlusion plethysmography during local intra-arterial infusions of methacholine (evaluating endothelium-dependent vasodilation) and sodium nitroprusside (evaluating endothelium-independent vasodilation). Lag phase of lipoprotein fraction to oxidation, total antioxidative activity, diene conjugates, thiobarbituric acid reactive substances, lipid hydroperoxide, reduced glutathione (GSH), oxidized GSH (GSSG), and the GSH redox ratio (GSSG/GSH) were all measured as markers of oxidative stress. Two groups of healthy subjects (61 and 37 subjects, respectively) were used as controls. In one group, oxidative stress markers were measured, whereas endothelium-dependent vasodilation and endothelium-independent vasodilation were assessed in the other group. Compared with controls, the patients with renal insufficiency had an impaired endothelium-dependent vasodilation, a shorter lag phase of lipoprotein fraction, and higher levels of diene conjugates, lipid hydroperoxide, and GSSG levels. The GSSG/GSH ratio was lower in patients with CRF. Endothelium-dependent vasodilation was positively correlated with total antioxidative activity (r = 0.41, P = 0.016), GSH (r = 0.44, P < 0.0098), and lag phase of LDL (r = 0.35, P = 0.036) and negatively correlated with GSSG (r = -0.40, P < 0.018), GSSG/GSH (r = -0.47, P = 0.0057), and diene conjugates (r = -0.53 P < 0.0015) in patients with CRF. These results show that an impaired endothelium vasodilation function and oxidative stress are related to each other in patients with CRF.
authors.affiliation: *Department of Medical Sciences, University Hospital, Uppsala, Sweden; and Department of Biochemistry, University of Tartu, Estonia.
authors.forename: Margus
authors.initials: M
authors.lastname: Annuk
authors.affiliation: *Department of Medical Sciences, University Hospital, Uppsala, Sweden; and Department of Biochemistry, University of Tartu, Estonia.
authors.forename: Mihkel
authors.initials: M
authors.lastname: Zilmer
authors.affiliation: *Department of Medical Sciences, University Hospital, Uppsala, Sweden; and Department of Biochemistry, University of Tartu, Estonia.
authors.forename: Lars
authors.initials: L
authors.lastname: Lind
authors.affiliation: *Department of Medical Sciences, University Hospital, Uppsala, Sweden; and Department of Biochemistry, University of Tartu, Estonia.
authors.forename: Torbjörn
authors.initials: T
authors.lastname: Linde
authors.affiliation: *Department of Medical Sciences, University Hospital, Uppsala, Sweden; and Department of Biochemistry, University of Tartu, Estonia.
authors.forename: Bengt
authors.initials: B
authors.lastname: Fellström
mesh_terms: D000368:Aged; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D005978:Glutathione / Q000378:metabolism; D019803:Glutathione Disulfide / Q000378:metabolism; D006801:Humans; D007676:Kidney Failure, Chronic / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress; D012016:Reference Values; D014664:Vasodilation
chemical_list: D005978:Glutathione; D019803:Glutathione Disulfide