The Acute Effect of 25-Hydroxycholecalciferol on Renal Handling of Phosphorus

Popovtzer, Mordecai M.; Robinette, John B.; DeLuca, Hector F.; Holick, Michael F.

doi:10.1172/jci107632

Cited by 93 publications

(19 citation statements)

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“…In the experiments described in Table 1 Vitamin D3 analog, M dent uptake of phosphate (12) and with reports of others that the acute effect of infusion of 1,25-(OH)2D3 in the intact animal was to decrease phosphate excretion (5,6). The present findings also agree with the previously reported effect of the vitamin in increasing phosphate uptake by organ culture preparations of chick ileum explants and isolated intestinal cells (13,14).…”

Section: Methodsmentioning

confidence: 86%

“…The effect of 1,25-(OH)2D3 on the reabsorption of phosphate in the kidney is in dispute. In some studies, infusion of the vitamin has been found to decrease phosphate excretion (5,6), whereas in other investigations 1,25-(OH)2D3 has been reported to be phosphaturic (7) or without effect on urinary phosphate (8). Some of the difficulties in resolving the apparent discrepancies stem, in part, from whether 1,25-(OH)2D3 is administered chronically or acutely and from the complex interactions in the animal in vivo of the vitamin D metabolic and phosphate transport systems with various regulatory factors, including parathyroid hormone and other endocrines, dietary status, and calcium (9)(10)(11).…”

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confidence: 99%

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In vitro stimulation of phosphate uptake in isolated chick renal cells by 1,25-dihydroxycholecalciferol.

Liang¹,

Barnes²,

Balakir³

et al. 1982

Proc. Natl. Acad. Sci. U.S.A.

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Renal cells isolated from vitamin D-deficient chicks had an increased Na+-dependent phosphate uptake when preincubated with 1,25-dihydroxycholecalciferol [1,25-(OH)2D3]. Phosphate uptake in the absence of Na+ and methyl a-glucoside uptake dependent on Na+ were not affected. Phosphate uptake was stimulated 15% by 0.010 pM 1,25-(OH)2D3. Maximal enhancement of 30% was obtained with 100 pM. The uptake when fully stimulated by preincubation in vitro approximated the uptake of cells isolated from chicks that were previously repleted with 1,25-(OH)2D3 in vivo. Cells from repleted chicks were not stimulated additionally when preincubated with 1,25-(OH)2D3 in vitro. The increase in phosphate uptake could be measured after a 1-hr preincubation period; full response required at least 2 hr. Phosphate uptake induced by 1,25-(OH)2D3 was blocked by cycloheximide and actinomycin D. Enhancement of phosphate uptake was relatively specific for the 1,25-(OH)2D3 analog of vitamin D3. * To whom reprint requests should be addressed. 3532The publication costs ofthis article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U. S. C. §1734 solely to indicate this fact.

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Section: Methodsmentioning

confidence: 86%

mentioning

confidence: 99%

In vitro stimulation of phosphate uptake in isolated chick renal cells by 1,25-dihydroxycholecalciferol.

Liang¹,

Barnes²,

Balakir³

et al. 1982

Proc. Natl. Acad. Sci. U.S.A.

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“…Also, urinary Pi excretion was lower in the 1,25LD or 1,25HD groups for any given level of serum Pi. Popovtzer et al (31) and Puschett et al (32) both reported an antiphosphaturic action of 25(OH)D3 in rats that was dependent upon the presence of parathyroid hormone (PTH). The quantities of 25(OH)D3 utilized in their studies were considerably greater than the amount of vitamin D3 given here and much greater than the amount of 1,25(OH)2D3 employed.…”

Section: Resultsmentioning

confidence: 99%

Interactions between Vitamin D Deficiency and Phosphorus Depletion in the Rat

Brautbar¹,

Walling²,

Coburn³

et al. 1979

J. Clin. Invest.

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A B S T R A C T To evaluate the role of vitamin D in the physiologic response to phosphorus depletion (P depleton) and the response to vitamin D administration in P depletion, we studied vitamin D-deficient (-D) INTRODUCTIONWith dietary phosphorus restriction and the appearance of phosphorus depletion, several physiologic events consistently occur: These include a marked reduction in urinary phosphorus excretion, the appearance of hypophosphatemia, hypercalciuria, and, in certain species, the development of hypercalcemia (1)(2)(3)(4)(5). There is indirect evidence in animals (3, 6) and direct measurements in humans (7) suggesting that physiologic hypoparathyroidism develops during phosphate depletion. However, it has been shown that administration of parathyroid hormone does not modify renal phosphate conservation during phosphorus depletion (8,9) and only partially reduces the hypercalciuria (3).It

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“…Vitamin D (25,26) and its metabolites (26,27), when administered in pharmacologic doses, accelerate Pi reabsorption, although the presence of PTH may be required for such an action in the rat (28). Recently, we have carried out phosphate loading studies in chronic TPTX phosphorus-depleted rats which were also vitamin D-deficient (4 (32).…”

Section: Resultsmentioning

confidence: 99%