High salt diet elevates the mean arterial pressure of SLC14α1 gene depletion mice

高盐饮食可升高 SLC14α1 基因缺失小鼠的平均动脉压

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作者:Song Wang, Jinshu Liu, Hongwei Cai, Keyuan Liu, Yayu He, Shuxiang Liu, Yingze Guo, Lirong Guo

Aims

Urea transporter B (UTB) is encoded by the SLC14α1 gene, and exerts its activity in the choroid plexus (CP) by regulating [Na+] in the cerebrospinal fluid (CSF) and maintaining normal blood pressure in mice fed on high salt diet. The aim of this study is to investigate the effect of high salt diet on the mean arterial pressure (MAP) in SLC14α1 depletion mice and its possible molecular mechanism. Main

Methods

Adult male mice were divided into four groups: 1) UTB+/+(wild type) mice + normal salt diet (0.3% NaCl, NS); 2) UTB+/+ mice + high salt diet (8% NaCl, HS); 3) UTB-/- (SLC14α1 knockout) mice + NS; 4) UTB-/- mice + HS, each group consisted of 6 mice. The MAP of mice was measured by non-invasive detection method after HS diet for 4 weeks, followed by euthanization for brain and blood collection. Key findings: HS significantly elevated the MAP and CSF [Na+] in UTB-/- mice in comparison with wild type mice; however, NS didn't alter the MAP and CSF [Na+] in either wild type mice or UTB-/- mice. HS also induced the expression of ENaC-α and α1-Na+-K+-ATPase in UTB-/- mice as confirmed by RT-PCR and Western blot. Significance: These

Significance

These results suggest that the depletion of SLC14α1 gene in mice may contribute to the HS-induced abnormality of sodium transportation in the CSF, and lead to the elevation of MAP, which eventually promote the development of salt-sensitive hypertension.

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