Calcium regulates parathyroid hormone messenger ribonucleic acid (mRNA), but not calcitonin mRNA in vivo in the rat. Dominant role of 1,25-dihydroxyvitamin D.

Abstract

In vivo 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) decreased PTH and calcitonin gene transcription. A low calcium is the major signal for PTH secretion, and a high calcium for calcitonin secretion. We report here that calcium has no effect on calcitonin messenger RNA (mRNA) levels in vivo in the rat, but that a low calcium markedly stimulates PTH mRNA levels. Serum calcium was decreased by ip phosphorus and increased by calcium gluconate (ip or iv infusion) and demonstrated that a low serum calcium markedly increased PTH mRNA levels whereas a high serum calcium had no effect. There was no change in mRNAs for calcitonin or actin in the same thyroparathyroid extracts. After phosphorus ip serum calcium decreased from 10.4 to 8.5 mg/dl and PTH mRNA increased up to 3-fold at 1, 3, and 6 h. Gel blots showed that a low calcium increased PTH mRNA levels with no change in its size (833 base pairs). Calcitonin ip decreased both serum calcium and phosphorus with an up to 5-fold increase in PTH mRNA at 1 h, thus demonstrating that the effect of phosphorus on PTH mRNA was due to the low serum calcium and not the high serum phosphorus. When phosphorus and 1,25(OH)2D3 (100 pmol/100 g) were injected together, despite the low serum calcium, there was a decrease in PTH mRNA levels. These results show a linear relationship between calcium and PTH gene expression, but not calcitonin or actin, with a dominant role for 1,25(OH)2D3.