Kraut J A, Mishler D R, Kurokawa K
Kidney Int. 1984 Apr;25(4):608-12. doi: 10.1038/ki.1984.64.
To examine the mechanism responsible for enhanced calcium mobilization from bone in metabolic acidosis, we evaluated the effect of colchicine and calcitonin, two blockers of cell-mediated bone resorption, on the calcemic response to acute metabolic acidosis in thyroparathyroidectomized rats. Metabolic acidosis lasting 16 hr and induced by the feeding of NH4Cl led to a significant rise in serum calcium of 1.2 to 1.9 mg/dl. The administration of colchicine or calcitonin led to a decrement in serum calcium of 1.1 +/- 0.2 (P less than 0.01) and 0.7 +/- 0.2 mg/dl (P less than 0.05), respectively. Cyclic AMP levels in calvaria from rats with metabolic acidosis and from control rats were not different. These data suggest that mobilization of calcium from bone which occurs in metabolic acidosis is due, in part, to increased bone resorption, which is mediated by a cAMP-independent mechanism.
为研究代谢性酸中毒时骨钙动员增强的机制,我们评估了秋水仙碱和降钙素(两种细胞介导性骨吸收阻滞剂)对甲状旁腺切除大鼠急性代谢性酸中毒血钙反应的影响。通过喂食氯化铵诱导的持续16小时的代谢性酸中毒,导致血清钙显著升高1.2至1.9mg/dl。给予秋水仙碱或降钙素分别导致血清钙下降1.1±0.2(P<0.01)和0.7±0.2mg/dl(P<0.05)。代谢性酸中毒大鼠和对照大鼠颅骨中的环磷酸腺苷水平无差异。这些数据表明,代谢性酸中毒时发生的骨钙动员部分归因于骨吸收增加,这是由一种不依赖环磷酸腺苷的机制介导的。