当期文章

肾脏钠转运体与盐敏感性高血压

唐成斌^1,2, 陈文灏^2,3, 李春凌^2,3, 王蔚东^1,2,*

¹中山大学中山医学院病理生理学教研室，广州 510080；²中山大学中山医学院高血压研究所，广州 510080；³中山大学中山医学院生理学教研室，广州 510080

摘要

高血压是全球重大公共卫生问题，与心脑血管疾病的发生密切相关。盐敏感性高血压是高血压的常见类型，其发病机制与肾脏钠代谢调节缺陷相关。利尿剂可通过抑制肾脏钠的重吸收，减少血容量从而降低血压。肾脏通过位于肾小管和集合管上皮细胞的钠转运体、钠交换体及钠通道重吸收超过99%肾小球滤过的钠离子，肾单位和集合管不同部位上皮细胞的转运体表达和调节各异。近端小管负责重吸收约60%~70%滤过的Na+，主要由位于上皮细胞顶端膜上的Na+-H+交换体3 (sodium-hydrogen exchanger isoform 3, NHE3)和钠-葡萄糖耦联转运体(sodium-glucose linked cotransporter, SGLT)介导，其异常激活与盐敏感性高血压密切相关。髓袢升支粗段的2型Na+-K+-2Cl⁻共转运体(Na+-K+-2Cl- cotransporter type 2, NKCC2)介导了约25%~30%滤过钠的重吸收，同时还参与建立髓质渗透压梯度，对尿液浓缩起到关键作用。远曲小管的Na+-Cl-共转运体(sodium-chloride cotransporter, NCC)介导约5%~10%氯化钠重吸收，其功能受醛固酮等激素调节，NCC表达异常会引发细胞外液容量及血压的变化。集合管的上皮钠通道(epithelial sodium channel, ENaC)负责重吸收少量滤过钠，过度激活会导致高血压发生。本文将系统性综述上述钠转运体、钠交换体及钠通道的生理功能、在高血压中的病理生理变化与调控机制，以及作为新型降压治疗靶点的最新研究进展及靶向干预策略，旨在为盐敏感性高血压患者治疗研究提供新的思路。

关键词： 肾脏; 盐敏感性高血压; 钠转运体; 钠交换体; 上皮钠通道

Renal sodium transporters in salt-sensitive hypertension

TANG Cheng-Bin^1,2, CHEN Wen-Hao^2,3, LI Chun-Ling^2,3, WANG Wei-Dong^1,2,*

¹Department of Pathophysiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China；²Institute of Hypertension, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China；³Department of Physiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China

Abstract

Hypertension is one of the most important risk factors for cardiovascular, cerebrovascular and renal diseases. The molecular mechanism of hypertension is not fully understood largely due to the complexity of pathogenesis involving many factors. The balance of sodium in body fluids plays a key role in blood pressure regulation. High salt intake is an important environmental factor leading to the development of hypertension. In this setting, the kidney plays a major role in the maintenance of blood pressure. The present review aims to summarize the current overview on the involvement of sodium transporters, sodium exchangers and sodium channels in the modulation of blood pressure, including sodium-hydrogen exchanger isoform 3 (NHE3), Na+-K+-2Cl⁻ cotransporter type 2 (NKCC2), sodium-chloride cotransporter (NCC) and epithelial sodium channel (ENaC), which are expressed in different nephron segments and the collecting ducts, respectively. In particular, recent findings on experimental animal models with modified gene of renal ion channels/transporters leading to the identification of several crucial physiological mechanisms involved in hypertension, were also reviewed. These findings could potentially provide novel therapeutic approaches applicable for hypertension.

Key words: kidney; salt-sensitive hypertension; sodium transporters; sodium exchangers; epithelial sodium channel

收稿日期：　　录用日期：

通讯作者：王蔚东　　E-mail:

DOI: 10.13294/j.aps.2026.0035

引用本文：

唐成斌, 陈文灏, 李春凌, 王蔚东. 肾脏钠转运体与盐敏感性高血压[J]. 生理学报 2026; 78 (2): 253-269.

TANG Cheng-Bin, CHEN Wen-Hao, LI Chun-Ling, WANG Wei-Dong. Renal sodium transporters in salt-sensitive hypertension. Acta Physiol Sin 2026; 78 (2): 253-269 (in Chinese with English abstract).