The influence of magnesium (Mg) deficiency on the concentration of calcium (Ca) in the aorta, heart, and kidney was evaluated in uremic rats. A total of 32 rats were randomly assigned to two groups: one group made uremic by the 5/6 nephrectomy method, and the other serving as sham-operated controls. Both groups were randomly assigned to two subgroups: one group given a Mg-deficient diet and the other fed a Mg-supplemented diet. After 12 weeks on the regimen, all animals were sacrificed. In Mg-supplemented uremic rats, the concentration of Ca in the aorta was higher than in Mg-supplemented control rats. The concentration of Ca in the aorta was further increased in Mg-deficient uremic rats. The concentrations of Ca in the heart and the kidney were also increased in Mg-deficient uremic rats, as compared with Mg-supplemented uremic rats. The concentration of Mg was decreased in the aorta and increased in the kidney of Mg-deficient rats. There was no significant influence of Mg deficiency on the concentration of phosphate in tissue. Results suggest that Mg deficiency in uremia may increase aortic calcification.
The concentration of calcium was measured in the aorta, heart, and kidney of uremic rats treated with 100 ng/kg/day 1,25-dihydroxyvitamin D3 (1,25 D3) or 60 mg/kg/day diltiazem for 12 weeks. The concentration of calcium was increased in the aorta, heart, and kidney of uremic rats, and was further increased by administration of 1,25 D3. The 1,25 D3-induced increase in calcium in the aorta was inhibited by diltiazem, but this effect was not accompanied by a decrease in serum calcium x phosphate products. Diltiazem had no effect on the 1,25 D3-induced increase of calcium in the heart and kidney. Thus, in uremia 1,25 D3 may promote the calcification of the aorta; calcium antagonists may protect against calcification without a reduction in serum calcium x phosphate products.
The effect of 1,25-dihydroxyvitamin D3 (1,25-D) on the absorption of glucose in the small intestine was studied in five-sixths nephrectomized uremic rats and sham-operated rats. Four weeks after the nephrectomy, the uremic animals were divided into two groups: One group was given 1,25-D (300 pmol/kg body weight/day, three times per week) intraperitoneally, and the other was left untreated. One week after the 1,25-D treatment, an in vivo glucose absorption test was performed at 00.00 h in consideration of the circadian rhythm of glucose absorption. In untreated uremic rats, the glucose absorption rate was lower than in sham-operated rats. In 1,25-D treated uremic rats, the glucose absorption rate was higher than in untreated uremic rats and not lower than in sham-operated rats. These results suggest that the absorption rate of glucose of the small intestine is reduced in uremic rats and that it is recovered on treatment with 1,25-D.
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