Uncoupling Protein 2 Ablation Exacerbates High-Salt Intake-Induced Vascular Dysfunction | Zendy

ShiTang Ma | Zendy; Lingling Ma | Zendy; Dachun Yang | Zendy; Zhigang Luo | Zendy; Xinzhong Hao | Zendy; D. Liu | Zendy; Zhihao Zhu | Zendy

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Uncoupling Protein 2 Ablation Exacerbates High-Salt Intake-Induced Vascular Dysfunction

Author(s) -

ShiTang Ma,

Lingling Ma,

Dachun Yang,

Zhigang Luo,

Xinzhong Hao,

D. Liu,

Zhihao Zhu

Publication year - 2010

Publication title -

american journal of hypertension

Language(s) - Uncategorized

Resource type - Journals

SCImago Journal Rank - 1.009

H-Index - 136

eISSN - 1941-7225

pISSN - 0895-7061

DOI - 10.1038/ajh.2010.73

Subject(s) - medicine , phenylephrine , reactive oxygen species , endocrinology , mesenteric arteries , superoxide , nitric oxide , vasodilation , contraction (grammar) , endothelial dysfunction , oxidative stress , blood pressure , chemistry , biochemistry , artery , enzyme

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.

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