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  • Title: Effects of 1,25-dihydroxycholecalciferol on phosphate transport in vitamin D-deprived rats.
    Author: Kurnik BR, Hruska KA.
    Journal: Am J Physiol; 1984 Jul; 247(1 Pt 2):F177-84. PubMed ID: 6331201.
    Abstract:
    To clarify the role of vitamin D in renal phosphate transport, weanling rats were fed a vitamin D-deficient diet containing 1.8% calcium and 1.2% phosphorus. After 5-6 wk, the rats were normocalcemic, normophosphatemic, and had normal levels of PTH. Assays of vitamin D metabolites revealed undetectable plasma levels of 25(OH)D, and 1,25(OH)2D levels of 92 +/- 16 pg/ml in partially vitamin D-depleted (PVDD) rats and 169 +/- 58 pg/ml in normal rats. PVDD rats had increased phosphate excretion, both absolute and fractional, and a decrease in Na+ gradient-dependent Pi transport in proximal tubular brush border membrane vesicles (BBMV) prepared from their kidneys. Vitamin D repletion of PVDD rats with 1,25(OH)2D3, 15 pmol/100 g body wt, decreased fractional excretion of Pi from 22.6 +/- 1.9 to 13.5 +/- 1.3%; the latter values were similar to normal rats. Repletion with 1,25(OH)2D3 also increased Na+-dependent phosphate transport in BBMV from 322 +/- 24 pmol X mg protein-1 X 15 s-1 in BBMV from PVDD rats to 698 +/- 70 pmol X mg protein-1 X 15 s-1. Repletion with larger doses of 1,25(OH)2D3 produced hypercalcemia and hyperphosphatemia from intestinal absorption, an increase in phosphate excretion, and a blunted response of Pi transport to 1,25(OH)2D3. Prevention of hyperphosphatemia by dietary adjustments allowed full expression of the stimulatory effects of 1,25(OH)2D3 on Pi transport. These later data may partially explain the inhibitory effects reported in prior studies in which plasma Pi was not controlled and the larger doses of 1,25(OH)2D3 administered.(ABSTRACT TRUNCATED AT 250 WORDS)
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