title: Oxidative stress impairs IKCa- and SKCa-mediated vasodilatation in mesenteric arteries from diabetic rats.
abstract: OBJECTIVE
  To investigate the role of oxidative stress in impaired intermediate-conductance Ca(2+)-activated potassium channels (IKCa)- and small-conductance Ca(2+)-activated potassium channels (SKCa)-mediated relaxation in diabetic resistance arteries.
  
  
  METHODS
  Rat diabetic model was induced by a high fat and high glucose diet and streptozotocin (STZ) injection. Endothelial function of mesenteric arteries was assessed with the use of wire myography. The expression levels of IKCa and SKCa in cultured human umbilical vein endothelial cells (HUVECs) treated with H2O2 and/or antioxidant alpha lipoic acid (ALA) were measured using Western blotting.
  
  
  RESULTS
  IKCa- and SKCa-mediated vasodilatation in response to acetylcholine was impaired in the third-order mesenteric arterioles of diabetic rats. In cultured HUVECs, H2O2 significantly decreased the protein expression of IKCa and SKCa. ALA alleviated the impairment of both vasodilatation function of the mesenteric arterioles ex vivo and enhanced the expression of IKCa and SKCa challenged with H2O2 in cultured HUVECs.
  
  
  CONCLUSIONS
  Our data demonstrated for the first time that impaired IKCa- and SKCa-mediated vasodilatation in diabetes was induced, at least in part, by oxidative stress via down-regulation of IKCa and SKCa channels.
authors.affiliation: Department of Physiology and Pathophysiology, Xi'an Jiaotong University College of Medicine, Xi'an, China. meilizhao@mail.xjtu.edu.cn
authors.forename: Limei
authors.initials: L
authors.lastname: Zhao
authors.forename: Yan
authors.initials: Y
authors.lastname: Wang
authors.forename: Xiaozhen
authors.initials: X
authors.lastname: Ma
authors.forename: Yawen
authors.initials: Y
authors.lastname: Wang
authors.forename: Xiuling
authors.initials: X
authors.lastname: Deng
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism* / Q000503:physiopathology; D061307:Human Umbilical Vein Endothelial Cells / Q000187:drug effects / Q000473:pathology; D006801:Humans; D006861:Hydrogen Peroxide / Q000494:pharmacology; D051660:Intermediate-Conductance Calcium-Activated Potassium Channels / Q000378:metabolism*; D008297:Male; D008638:Mesenteric Arteries / Q000503:physiopathology*; D018384:Oxidative Stress; D051381:Rats; D017207:Rats, Sprague-Dawley; D051640:Small-Conductance Calcium-Activated Potassium Channels / Q000378:metabolism*; D008063:Thioctic Acid / Q000494:pharmacology; D014664:Vasodilation
chemical_list: D051660:Intermediate-Conductance Calcium-Activated Potassium Channels; D051640:Small-Conductance Calcium-Activated Potassium Channels; D008063:Thioctic Acid; D006861:Hydrogen Peroxide