Peck W A, Dowling I
Endocr Res Commun. 1976;3(2):157-66. doi: 10.3109/07435807609052930.
Treatment with 1, 25-(OH) 2-D3 (1 ng/ml-25 ng/ml) for periods ranging from 2.5 min. to 60 min. did not alter cyclic AMP levels in bone cells isolated from periosteum-free rat calvaria, or in cells isolated from rat periosteal tissues. 1, 25-(OH) 2-D3 failed to modify the acute increases in cyclic AMP elicited by PTH (10 ng/ml-1 ug/ml). Two separate 1, 25-(OH) 2-D3 preparations, biologically active in other systems, were ineffective under a wide variety of experimental conditions. These results suggest that 1, 25-(OH) 2-D3 is not an acute modulator of cyclic AMP metabolism in PTH-treated and untreated bone cells.
用1,25 -(OH)₂-D₃(1纳克/毫升 - 25纳克/毫升)处理2.5分钟至60分钟,并未改变从无骨膜大鼠颅骨分离的骨细胞或从大鼠骨膜组织分离的细胞中的环磷酸腺苷水平。1,25 -(OH)₂-D₃未能改变甲状旁腺激素(10纳克/毫升 - 1微克/毫升)引起的环磷酸腺苷的急性增加。在其他系统中具有生物活性的两种不同的1,25 -(OH)₂-D₃制剂,在各种实验条件下均无效。这些结果表明,1,25 -(OH)₂-D₃不是甲状旁腺激素处理和未处理的骨细胞中环磷酸腺苷代谢的急性调节剂。