title: Uncoupling protein 2 ablation exacerbates high-salt intake-induced vascular dysfunction.
abstract: BACKGROUND
  Salt-induced vascular dysfunction in which underlying mechanisms involve reactive oxygen species (ROS)-mediated reduction of nitric oxide (NO) bioavailability has been well documented. Uncoupling protein 2 (UCP2) has been implicated in the vascular protection, specifically by decreasing ROS production. However, it is unclear how UCP2 affects vascular function in salt-loaded mice.
  
  
  METHODS
  UCP2-deficient (UCP2(-/-)) and wild-type (WT) mice were placed on either a normal-salt (NS, 0.5%) or a high-salt (HS, 8%) diet for 24 weeks. Blood pressure (BP), mesenteric arterial reactivity, superoxide production, and NO bioavailability in the intact vessels were measured in each group.
  
  
  RESULTS
  UCP2(-/-) mice on a HS diet had a higher BP than those on a NS diet (P < 0.01). However, BP in WT mice was not different between the NS and HS diet group. Phenylephrine (PE)-induced contraction was enhanced while acetylcholine (ACh)-elicited relaxation was impaired in mesenteric resistance arteries from the HS diet-fed WT mice. Importantly, the enhanced contraction and impaired relaxation were both further exacerbated in UCP2(-/-) mice. Similarly, the HS diet led to a moderate increase in superoxide production and a comparable decrease in NO availability in both aortas and mesenteric resistance vessels, and these effects were also remarkably enhanced in UCP2(-/-) mice.
  
  
  CONCLUSIONS
  These findings suggest that UCP2 plays an important role in preventing salt-sensitive hypertension, which may be achieved by suppressing superoxide production and reserving NO bioavailability in blood vessels.
authors.affiliation: Department of Hypertension and Endocrinology, Center for Hypertension and Metabolic Diseases, Daping Hospital, Third Military Medical University, Chongqing Institute of Hypertension, China.
authors.forename: Shuangtao
authors.initials: S
authors.lastname: Ma
authors.forename: Liqun
authors.initials: L
authors.lastname: Ma
authors.forename: Dachun
authors.initials: D
authors.lastname: Yang
authors.forename: Zhidan
authors.initials: Z
authors.lastname: Luo
authors.forename: Xinzhong
authors.initials: X
authors.lastname: Hao
authors.forename: Daoyan
authors.initials: D
authors.lastname: Liu
authors.forename: Zhiming
authors.initials: Z
authors.lastname: Zhu
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects; D007473:Ion Channels / Q000172:deficiency*; D008638:Mesenteric Arteries / Q000187:drug effects; D051379:Mice; D008810:Mice, Inbred C57BL; D024101:Mitochondrial Proteins / Q000172:deficiency*; D009569:Nitric Oxide / Q000378:metabolism; D010656:Phenylephrine / Q000494:pharmacology; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage* / Q000494:pharmacology; D013481:Superoxides / Q000378:metabolism; D000071246:Uncoupling Protein 2; D014661:Vasoconstriction / Q000187:drug effects; D014664:Vasodilation / Q000187:drug effects
chemical_list: D007473:Ion Channels; D024101:Mitochondrial Proteins; D017673:Sodium Chloride, Dietary; C000604390:Ucp2 protein, mouse; D000071246:Uncoupling Protein 2; D013481:Superoxides; D010656:Phenylephrine; D009569:Nitric Oxide; D000109:Acetylcholine