高血压中近端肾小管盐转运的调节：最新进展
The regulation of proximal tubular salt transport in hypertension: an update.
作者信息
Wang Xiaoyan, Armando Ines, Upadhyay Kiran, Pascua Annabelle, Jose Pedro A
机构信息
Center for Molecular Physiology Research, Children's Research Institute, Children's National Medical Center, Washington, District of Columbia, USA.
出版信息
Curr Opin Nephrol Hypertens. 2009 Sep;18(5):412-20. doi: 10.1097/MNH.0b013e32832f5775.
PURPOSE OF REVIEW
Renal proximal tubular sodium reabsorption is regulated by sodium transporters, including the sodium glucose transporter, sodium amino acid transporter, sodium hydrogen exchanger isoform 3 and sodium phosphate cotransporter type 2 located at the luminal/apical membrane, and sodium bicarbonate cotransporter and Na+/K+ATPase located at the basolateral membrane. This review summarizes recent studies on sodium transporters that play a major role in the increase in blood pressure in essential/polygenic hypertension.
RECENT FINDINGS
Sodium transporters and Na+/K+ATPase are segregated in membrane lipid and nonlipid raft microdomains that regulate their activities and trafficking via cytoskeletal proteins. The increase in renal proximal tubule ion transport in polygenic hypertension is primarily due to increased activity of NHE3 and Cl/HCO3 exchanger at the luminal/apical membrane and a primary or secondary increase in Na+/K+ATPase activity.
SUMMARY
The increase in renal proximal tubule ion transport in hypertension is due to increased actions by prohypertensive factors that are unopposed by antihypertensive factors.
综述目的
肾近端小管钠重吸收受钠转运体调节，包括位于管腔/顶端膜的钠葡萄糖转运体、钠氨基酸转运体、钠氢交换体3型和钠磷共转运体2型，以及位于基底外侧膜的钠碳酸氢根共转运体和钠钾ATP酶。本综述总结了近期关于在原发性/多基因高血压中导致血压升高起主要作用的钠转运体的研究。
最新发现
钠转运体和钠钾ATP酶在膜脂质和非脂质筏微区中分隔，这些微区通过细胞骨架蛋白调节它们的活性和转运。多基因高血压中肾近端小管离子转运增加主要是由于管腔/顶端膜处NHE3和氯/碳酸氢根交换体活性增加以及钠钾ATP酶活性原发性或继发性增加。
总结
高血压中肾近端小管离子转运增加是由于升压因子作用增强，而降压因子未起拮抗作用。
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