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Calcium and magnesium transport in the thick ascending limb

Calcium and magnesium transport in the thick ascending limb
Na is reabsorbed via the apical Na-K-2Cl cotransporter (NKCC2) and pumped out basolaterally by the Na-K-ATPase, Cl exits via the Cl channel composed of chloride channel Kb (ClC-Kb) and barttin, and K is recycled apically via the inwardly rectifying K channel, ROMK, thereby generating a lumen-positive transtubular voltage. In addition, transcellular reabsorption of NaCl generates a concentration gradient in the late thick ascending limb (TAL) favoring NaCl backflux. In the presence of Na-selective paracellular permeability mediated by a complex of claudin-16 and -19 (CLDN16/19), this generates a NaCl diffusion potential that augments the transepithelial voltage. Ca and Mg are reabsorbed passively across the paracellular pathway, driven by the lumen-positive electrical potential. The identity of the paracellular divalent cation pore may be made up of claudin-16 and possibly -19. Blood Ca levels regulate this process by stimulating the Ca-sensing receptor (CaSR), which negatively regulates calcineurin and nuclear factor of activated T-cells cytoplasmic-1 (NFATc1). NFATc1 increases transcription of the microRNAs, miR-9 and miR-374, which inhibit expression of claudin-14 (CLDN14), a protein that normally binds to and inhibits claudin-16 and -19.
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