Bicarbonate reabsorption in proximal renal tubule: molecular mechanisms and metabolic acidosis.
- Author:
Yi-Min GUO
1
;
Ying LIU
;
Li-Ming CHEN
Author Information
1. Department of Biophysics and Molecular Physiology, Key Laboratory of Molecular Biophysics of Ministry of Education, Huazhong University of Science & Technology School of Life Science & Technology, Wuhan 430074, China. liming.chen@mail.hust.edu.cn.
- Publication Type:Journal Article
- MeSH:
Acidosis;
physiopathology;
Animals;
Bicarbonates;
metabolism;
Humans;
Kidney Tubules, Proximal;
physiopathology;
Sodium-Hydrogen Exchangers;
physiology;
Vacuolar Proton-Translocating ATPases;
physiology
- From:
Acta Physiologica Sinica
2014;66(4):398-414
- CountryChina
- Language:Chinese
-
Abstract:
HCO3(-) reabsorption in the renal tubules plays a critically important role in maintaining the global acid-base balance. Loss of HCO3(-) causes metabolic acidosis. Proximal renal tubule is the major site for HCO3(-) reabsorption, accounting for more than 80% of total HCO3(-) reabsorption along the nephron. Over the past more than half centuries, tremendous progresses have been made on understanding the molecular mechanisms underlying the HCO3(-) reabsorption in proximal tubules. The transepithelial movement of HCO3(-) involves the coordinated operation of machineries on both the apical and the basolateral membranes of the epithelial cells. On the apical domain, Na(+)-H(+) exchanger NHE3 and the vacuolar H(+)-ATPase are two major pathways mediating the apical uptake of HCO3(-)-related species. Taken together, NHE3 and H(+)-ATPase are responsible for about 80% of HCO3(-) reabsorption in the proximal tubule. The remaining 20% is likely mediated by pathways yet to be characterized. On the basolateral membrane, NBCe1 represents the only major known pathway mediating the extrusion of HCO3(-) coupled with Na(+) into the interstitial space. In the present article, we provide a historical view about the studies on the mechanisms of HCO3(-) reabsorption since 1940s. Moreover, we summarize the latest progresses emerging over the past decade in the physiological as well as pathological roles of acid-base transporters underlying the HCO3(-) reabsorption in proximal tubules.
