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In the kidney, Ca fluxes in the proximal tubule account for reabsorption of 65% of the filtered Ca, coupled to the bulk transport of solutes such as sodium and water [26].

About 20% of filtered Ca is reabsorbed in the cortical thick ascending limb of the loop of Henle (CTAL). In the CTAL, PTH binds to the PTH1R [27, 28], and enhances Ca reabsorption by increasing the activity of the Na/K/2Cl cotransporter that drives NaCl reabsorption and stimulates paracellular Ca and Mg reabsorption. The Ca sensing receptor (CaSR) is also present in the CTAL [29], where increased ECF Ca can bind and activate phospholipase A2, thereby reducing the activity of the Na/K/2Cl cotransporter and of an apical K channel, and diminishing paracellular Ca reabsorption. Consequently, a raised ECF Ca antagonizes the effect of PTH in this nephron segment and ECF Ca can in fact participate in this way as a hormone in the regulation of its own homeostasis.

About 15% of filtered Ca is reabsorbed in the distal convoluted tubule (DCT), where luminal Ca transfer into the renal tubule cell occurs via TRPV5, translocation of Ca across the cell from apical to basolateral surface involving proteins such as calbindin-D28K, and then active extrusion of the Ca from the cell into the blood via a Na⁺/Ca exchanger. PTH markedly stimulates Ca reabsorption in the DCT primarily by augmenting Na⁺/Ca exchanger activity via a cyclic AMP-mediated mechanism.