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- Title
Uncoupling Protein 2 Ablation Exacerbates High-Salt Intake-Induced Vascular Dysfunction.
- Authors
Shuangtao Ma; Liqun Ma; Dachun Yang; Zhidan Luo; Xinzhong Hao; Daoyan Liu; Zhiming Zhu
- Abstract
BackgroundSalt-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.MethodsUCP2-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.ResultsUCP2−/− 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.ConclusionsThese 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.American Journal of Hypertension 2010; doi:10.1038/ajh.2010.73
- Subjects
VASCULAR diseases; NITRIC oxide; HYPERTENSION; BIOAVAILABILITY; BLOOD pressure; SUPEROXIDES; PHENYLEPHRINE; LABORATORY mice
- Publication
American Journal of Hypertension, 2010, Vol 23, Issue 8, p822
- ISSN
0895-7061
- Publication type
Article
- DOI
10.1038/ajh.2010.73