Phosphatemic action of 1,25-dihydroxyvitamin D3

Th, Steele; Engle, J A; Tanaka, Yoshihisa; Rs, Lorenc; Dudgeon, KL; DeLuca, H. F.

doi:10.1152/ajplegacy.1975.229.2.489

Cited by 78 publications

(21 citation statements)

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“…These differing conclusions appear to arise from several reasons: differences in the vitamin D status of animals (4,9), differences in doses and kinds of vitamin D metabolites administered (4,9), changes in the serum calcium concentration and filtered load ofcalcium (13), and differences in the status ofthe function of PTH (10), a hormone that has a direct action on the renal tubular calcium reabsorption. Since one or more ofthese factors was not controlled or taken into account in most studies, it is often difficult to determine whether or not vitamin D has any direct action on the renal tubular transport of calcium.…”

Section: Introductionmentioning

confidence: 99%

Vitamin D deficiency and renal calcium transport in the rat.

Yamamoto¹,

Kawanobe²,

Takahashi³

et al. 1984

J. Clin. Invest.

129

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A bstract. To examine the role of vitamin D in the renal tubular handling of calcium, clearance studies were performed in three groups of rats: group A rats fed a standard vitamin D-deficient diet (Ca 0.45%, P 0.3%) for 6 wk, were hypocalcemic with secondary hyperparathyroidism; group B rats fed the same diet as in group A but with high calcium (Ca 1.4%) and 20% lactose, were normocalcemic and without secondary hyperparathyroidism; group C rats fed the same diet as in group A but supplemented with 25 U of vitamin D3 orally twice a week, were normocalcemic, vitamin D-replete, and euparathyroid. After thyroparathyroidectomy (TPTX), each rat was infused intravenously with an electrolyte solution that contained a fixed concentration of calcium (0-30 mM) with or without parathyroid hormone (PTH; 0.75 or 2.5 U/h) at a rate of 3 ml/h. Urinary calcium excretion and serum calcium concentrations were measured between 16 and 19 h of the infusion, and the apparent threshold of calcium excretion was determined.The threshold of calcium excretion was lower in vitamin D-deficient TPTX rats (groups A and B) than in vitamin D-replete TPTX rats (group C), and not different between group A and group B. Administration of PTH at a dose of 0.75 U/h increased the threshold of calcium excretion by -0.6 mM in group C, but did not alter the threshold either in group A or group B. Administration

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Section: Introductionmentioning

confidence: 99%

Vitamin D deficiency and renal calcium transport in the rat.

Yamamoto¹,

Kawanobe²,

Takahashi³

et al. 1984

J. Clin. Invest.

129

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“…Phosphate depletion in rats is associated with hypophosphatemia, hypophosphaturia, hyperealcemia, and hypercalciuria (1)(2)(3)(4)(5)(6). Because renal tubular transport of calcium may share a common reabsorptive mechanism or pathway with magnesium (7)(8)(9), one might expect magnesuria with phosphate depletion.…”

Section: Introductionmentioning

confidence: 99%

Effect of Phosphate Depletion on Magnesium Homeostasis in Rats

Kreußer¹,

Kurokawa²,

Aznar³

et al. 1978

J. Clin. Invest.

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A B S T R A C T The effects of phosphate depletion on magniesiumni (NMg) homeostasis were evaluated in rats fed a diet containing 0.03% phosphorus for periods up to 8 wk. Plasma phosphorus fell signiificantly (P < 0.01) from 10.1+0.27 (SE) to 5.0±0.54 mgIl00 ml within 1 day and conitiniued to fall gradually to a level of 1.2±0.21 mg/100 ml by the end of the 8th wk. A signiificant (P < 0.01) increment in urinary Mg excretion (UMgV) from 46±2.7 to 126±24 ,ueq/24 h occurred during the 1st day of phosphate depletion; UMgV reached a peak of 300±+24 pieq/24 h by the 3rd day and remained high ranging between 150-300 ,ueq/24 h, thereafter. The magnittude of the magnesuria was related to the degree of hypophosphatemia and was not affected by lowering the calcium intake and reducing the hypercalciuria. The concentration of plasma Mg fell significantly (P < 0.01) from 1.2±0.02 to 0.79±0.10 meq/liter by the 1st day of the study and remained low throughout.Mg balance became negative during the 1st day of phosphate depletion and remained so during the entire study. This occurred despite a significant increment in the fraction of ingested Mg absorbed which becarmie evident by the 3rd wk of phosphate depletion. Mg contenit of muscle, kidney, and liver were not affected but bone Mg was reduced significantly. The change in bone Mg was not due to an overall reduction in bone mineral contenit because bone calcium content was not affected. Supplementation of large amounts of Mg (800-1,000 ,ueq/day) in the drinking water produced a normalization of serum Mg but did not bring about restoration of bone Mg despite a positive Mg balance. The disturbances in Mg metabolism were independent of the age or veight of the animals.Our results indicate that phosphate depletion is Dr. Kreusser is a Fellow of the Deutsche Forschungsgemeinschaft.Dr. Aznar is a Fellow of the Del Amo Foundation.

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“…Recently, we have carried out phosphate loading studies in chronic TPTX phosphorus-depleted rats which were also vitamin D-deficient (4 (32). Other studies from the same laboratory have demonstrated that a progressive reduction in the dietary phosphorus intake, proportionate to the degree of reduction in GFR, resulted in the maintenance of a normal fractional Pi reabsorption in dogs with reduced nephron populations (33).…”

Section: Resultsmentioning

confidence: 99%