The administration of 100,000 to 200,000 U of calciferol to adult dogs daily for 5 weeks caused marked hypercalcemia and significant decreases in plasma concentrations of sodium, potassium, magnesium and chloride. Cellular concentrations of calcium were increased by 30 to 300 % in muscle, myocardium, pancreas and aorta and were unchanged in liver, brain and nerve. Bone uptake of 47Ca was increased by 45 %. The exchangeable body and tissue pools of calcium were increased by 100% but the fractional rate of exchange of tissue calcium was unaltered. The magnesium concentrations of liver, pancreas and bone were increased by 16 to 20 % by calciferol and the fractional rate of exchange of tissue magnesium with 28Mg was increased by 23 %. Calciferol administration had a minor effect on tissue concentrations of acidsoluble phosphorus. The sodium concentrations of 5 tissues and the chloride concentrations of 3 tissues were significantly decreased, whereas the potassium concentrations of 2 tissues were increased significantly. These data support the hypothesis that vitamin D, like parathyroid hormone, stimulates the cellular transport of calcium and magnesium. However, the different quantitative effects of these agents on the distribution and transport of divalent cations and the inability of vitamin D, in contradistinction to parathyroid hormone, to influence the tissue concentrations of phosphorus and of univalent electrolytes which are usually present in hypercalcemia suggest that different loci and/or modes of action are involved in the effects of vitamin D and parathyroid hormone on cellular transport processes.(Endocrinology79: 773, 1966)
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Wallach et al. (1966) studied this question.