S U M M A R Y1, The production of 1,25-dihydroxycholecalciferol (1,25-DHCC) from tritiated 25-hydroxycholecalciferol was assessed in renal tubules prepared from vitamin D-deficient chicks.2. Cyclic AMP and dibutyryl cyclic AMP enhanced the production of 1,25-DHCC. 3. Bovine parathyroid hormone (BPTH) and its synthetic analogue either had no effect or inhibited the production of 1,25-DHCC when calcium was present in the extracellular medium, but enhanced the conversion when calcium was absent. BPTH increased adenylate cyclase activity and cyclic AMP content of the renal tubule cells.4. Synthetic salmon calcitonin enhanced the production of 1,25-DHCC, whereas human calcitonin had no effect at the concentrations tested. Salmon calcitonin did not increase chick renal adenylate cyclase activity or cyclic AMP levels. 5. A short period of incubation in media containing strontium gluconate (5 mmol/l) significantly increased production of 1,25-DHCC, whereas no effect was seen after more prolonged exposure to strontium. Calcium depletion decreased production of 1,25-DHCC, but when some calcium was present, variation in extracellular concentration of calcium did not affect conversion. Variation in extracellular phosphate concentration did not affect conversion. 6. A small quantity of 1,25-DHCC added to the medium inhibited the conversion of 25-HCC into 1,25-DHCC.7. The production of 1,25-DHCC is subject to complex control, and intracellular concentrations of calcium, cyclic AMP and 1,25-DHCC may all be important regulatory influences.

No abstract

No abstract

SUMMARY The effect of nephrectomy on the response to thyrocalcitonin was studied in three groups of rats: intact animals on stock diet; parathyroidectomized rats on stock diet; and parathyroidectomized rats on high calcium, low phosphorus diet. In intact rats and in parathyroidectomized rats on a high calcium, low phosphorus diet, nephrectomy did not alter the fall in plasma calcium and phosphate produced by thyrocalcitonin. In parathyroidectomized rats on stock diet, however, plasma calcium was not changed by the hormone, but there was an isolated fall in phosphate which was prevented by previous nephrectomy. Experiments with 45Ca showed that when plasma calcium was lowered by thyrocalcitonin this was caused by inhibition of bone resorption. Since the hormone also causes phosphaturia, it was concluded that there are two sites of action: bone and kidney. The skeletal effect is usually dominant and the renal effect is the major one only when the rate of bone resorption is low.

No abstract