Dahl盐敏感大鼠高血压形成的肾脏代谢机制
陈萌, 杨鹏飞, 田中民*
西安交通大学生命科学与技术学院,生物医学信息工程教育部重点实验室,西安 710049
摘要
肾脏调控着机体的水盐代谢、血容量和血管阻力,是参与血压调节的主要靶器官。高盐饮食会诱发盐敏感个体水钠潴留以及持续性的内皮功能障碍,并促成血压升高。Dahl盐敏感(Dahl salt sensitive, Dahl-SS)大鼠作为研究盐敏感高血压的经典动物模型,具备血压的盐敏感性、高脂血症、胰岛素抵抗、肾功能衰竭、尿蛋白分泌增加以及低血浆肾素活性等和人类盐敏感高血压患者相类似的病理生理学特征,并能够稳定遗传。本文结合近年对Dahl-SS大鼠肾脏生理学和生物化学方面的研究以及多组学研究成果,对盐敏感高血压的发生、发展与肾脏氧化还原代谢、一氧化氮代谢、氨基酸代谢、糖脂代谢之间的关系进行了归纳和总结。
关键词: 盐敏感高血压; Dahl盐敏感大鼠; 氧自由基; 一氧化氮; 氨基酸代谢; 糖代谢; 脂代谢
The renal metabolic mechanism of salt sensitive hypertension in Dahl-SS rats
CHEN Meng, YANG Peng-Fei, TIAN Zhong-Min*
The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi’an Jiaotong University, Xi’an 710049, China
Abstract
The kidney is one of the main target organs involved in hypertension, and it regulates water and salt metabolism, blood volume and vascular resistance. High salt intake induces salt and water retention, persistent endothelial dysfunction and elevation of blood pressure in salt sensitive individuals. Dahl salt sensitive (Dahl-SS) rats, as a classic animal model for salt sensitive hypertension, have many similar stably inherited physiological characteristics to human with salt sensitive hypertension, such as salt sensitivity, hyperlipidemia, insulin resistance, renal failure, increased urinary protein secretion and low plasma renin activity. Based on renal physiology and biochemistry researches and multi-omics analyses in Dahl-SS rats, this review will summarize the relationship between salt sensitive hypertension and renal redox, NO, amino acids, glucose and lipid metabolism.
Key words: salt sensitive hypertension; Dahl-SS rats; oxygen free radicals; nitric oxide; amino acid metabolism; glucose metabolism; lipid metabolism
收稿日期: 录用日期:
通讯作者:田中民 E-mail: zmtian@mail.xjtu.edu.cn
DOI: 10.13294/j.aps.2022.0005
引用本文:
陈萌, 杨鹏飞, 田中民. Dahl盐敏感大鼠高血压形成的肾脏代谢机制[J]. 生理学报 2022; 74 (1): 47-58.
CHEN Meng, YANG Peng-Fei, TIAN Zhong-Min. The renal metabolic mechanism of salt sensitive hypertension in Dahl-SS rats. Acta Physiol Sin 2022; 74 (1): 47-58 (in Chinese with English abstract).