New insights into sodium transport regulation in the distal nephron: Role of G-protein coupled receptors

Figure 1 Schematic representation of the different sodium transport systems along the nephron. A: In TAL, the apical entry of Na⁺ is mediated by the NKCC2. At the basolateral side, the Na⁺ exits the cell through the NKA and the Cl^- through a channel of the CLC-K family; B: DCT consists of two different sub-structures, the DCT1 and the DCT2. In DCT1, the entry of Na+ and Cl- is mediated by the NCC and in DCT2, a ENaC is also involved. In both structures, the exit of Na⁺ and Cl^- is mediated by the NKA and a CLC-K conductance; C: In the CD, the Na⁺ enters the principal cells through ENaC and exits through the NKA. The system is more complex in the B-intercalated cells. The apical entry of of Na⁺ and Cl^- is mediated by the functional association between the pendrin, bicarbonate/Cl^- exchanger (Pds), and NDBCE. The system is energized by the vacuolar proton pump (H⁺-ATPase) and the generation of bicarbonate mediated by a CA. The exit of Na⁺ and Cl^- is mediated by an AE4 and a Cl^--conductance, respectively. TAL: Thick ascending limb; NKCC2: Na⁺/K⁺/2Cl^--cotransporter; NKA: Na,K-ATPase; DCT: Distal convoluted tubule; NCC: Na⁺/Cl^--cotransporter; ENaC: Na⁺ channel; CD: collecting duct; Pds: Bicarbonate/Cl^- exchanger; CA: Carbonic anhydrase; NDBCE: Na⁺-driven bicarbonate/Cl^- exchanger; AE4: Anion exchanger.