[Metabolism of vitamin D in exogenous hypercorticism in rats].

Short-term administration of hydrocortisone into rats (within 7 days) stimulated 1.25(OH)2D3 synthesis in kidney and led to accumulation of the metabolite in blood serum, small intestinal mucose and bones. After long-term administration of hydrocortisone within 28 days synthesis of 1.

[Effect of 1,25-dihydroxycholecalciferol and 24,25-dihydroxycholecalciferol on calcium homeostasis in rats treated with hydrocortisone].

Physiological dose of 1,25(OH)2D3 (0.03 microgram) normalized the phosphorus-calcium metabolism and improved the state of bone tissue in rats treated with hydrocortisone. An increased dose of 1,25(OH)2D3 (0.

[Effect of 1,25-dioxycholecalciferol and 24,25-dioxycholecalciferol on calcium homeostasis in rats given hydrocortisone in the diet with various phosphorus contents].

High content of phosphorus in the diet (1.8% of phosphorus in the diet, Ca:P ratio 1:3) accelerated the development of hypocalcemia and osteoporosis and increased their degree in rats which received hydrocortisone (3.5 mg/10 g bw a day for 4 weeks).

[Effect of phosphorus intake on calcium homeostasis and bone tissue status in rats receiving hydrocortisone].

The increase of phosphorus content up to 1.2-1.8% in the diet (the calcium/phosphorus ratio 1:2 or 1:3) accelerates the development and raises the rate of hypocalcemia and osteoporosis in rats administered pharmacological doses of hydrocortisone (3.