1. The production of 1,25-dihydroxycholecalciferol (1,25-DHCC) from tritiated 25-hydroxycholecalciferol (25-HCC) 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.