Almost all of the 240 mmol of calcium filtered daily in the kidney is reabsorbed by three mechanisms (Friedman, 2000):
1. In the proximal tubules, calcium absorption is mainly by a paracellular route that is not regulated by hormones.
2. In the thick ascending limbs, there are bothparacellular and transcellular routes: the active transcellular route is regulatedbyparathyroidhormone (increasing reabsorption) and calcitonin (reducing reabsorption), the paracellular route by cotransport with sodium.
3. In the distal tubule, reabsorption is entirely transcellular, and is regulated by parathyroid hormone and calcitriol (increasing reabsorption) and calcitonin (reducing reabsorption).
Although calcitriol is synthesized only in the proximal renal tubule, after the administration of [3 H]calcidiol, radioactivity in the kidney accumulates only in the distal and collecting tubules. This is the region in which selective resorption of calcium from the urine occurs and, in response to calcitriol, there is induction of calbindin-D28k. As in the intestinal mucosa, calbindin in the kidney is a cytosolic protein and is presumably involved in the intracellular accumulation and transport of calcium.
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