Amelioration of AngiotensinII-induced salt-sensitive hypertension by L-FABP in proximal tubules

L-FABP 改善近曲小管中血管紧张素 II 诱导的盐敏感性高血压

• 批准号: 22790803
• 负责人: TANIFUJI Chiaki
• 金额: $ 2.5万
• 依托单位: Juntendo University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 财政年份: 2010
• 资助国家: 日本
• 起止时间: 2010 至 2011
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-22790803/
• 关键词: L-FABP; 食塩感受性高血圧; レニン・アンジオテンシン系; 酸化ストレス; レニン・アンギオテンシン系; レニン-アンジオテンシン系

Recent findings indicated that inappropriate activation of the intrarenal renin-angiotensin system(RAS) induces reactive oxygen species production, which may contribute to salt-sensitive hypertension. On the other hand, L-FABP is expressed in renal proximal tubules in humans and may play an endogenous antioxidant role. The present study is to examine the antioxidative effect of L-FABP on salt-sensitive hypertension. The present findings indicated that L-FABP in proximal tubules may protect against AngII-induced SSHT in combination with attenuation of intrarenal RAS activation, oxidative stress. Therefore, L-FABP of proximal tubules may play a pathological role in SSHT.

最近的研究表明，肾内肾素-血管紧张素系统（RAS）的不适当激活诱导活性氧的产生，这可能有助于盐敏感性高血压。另一方面，L-FABP在人类肾脏近端小管中表达，并可能发挥内源性抗氧化作用。本研究旨在探讨L-脂肪酸结合蛋白对盐敏感性高血压的抗氧化作用。目前的研究结果表明，L-FABP在近端小管可以保护对血管紧张素II诱导的SSHT与肾内RAS激活，氧化应激的衰减相结合。因此，近曲小管L-FABP可能在SSHT中起一定的病理作用。