Abstract

Parathyroid hormone (PTH) has been shown to stimulate the formation of 1,25-dihydroxycholecalciferol (1,25(OH)2D3), the most biologically active form of vitamin D3, by the kidney (1, 2). It has been postulated that 1,25(OH)2D3 or other vitamin D3 metabolites might directly influence the secretion of PTH. Receptors for 1,25(OH)2D3 have been identified in chick (3) and pig (4) parathyroid glands and in human parathyroid adenoma (5). Accumulation of 1,25(OH)2D3 by the parathyroid gland has been reported in the chick (6), and 1,25(OH)2D3 when administered to-gether with 24,25-dihydroxycholecalciferol (24,25(OH)2D3), caused the size of the parathyroid glands in vitamin D-deficient chicks to regress (7). The effect of vitamin D metabolites on PTH secretion has been examined in several species. Studies several years ago by Oldham, et al, showed that the administration of pharmacological amounts of 25-hydroxycholecalciferol (250H D3) to vitamin D-deficient dogs appeared to decrease the circulating concentrations of immunoreactive parathyroid hormone (IPTH) before significant increases in serum calcium concentration occurred (8). Chertow, et al, reported a decrease in IPTH in rats administered 1,25(OH)2D3 and an inhibition of IPTH released from slices of bovine parathyroid tissue in vitro when 1,25(OH)2D3 was added to the culture medium (9).KeywordsSerum CalciumParathyroid GlandMalachite GreenSerum Calcium ConcentrationSerum IPTHThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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