GREATER UNIDIRECTIONAL CALCIUM EFFLUX FROM BONE DURING METABOLIC, COMPARED WITH RESPIRATORY, ACIDOSIS

There is a smaller net calcium efflux from bone in vitro during respiratory (increased PCO2) than metabolic (decreased [HCO3-]) acidosis. This could be due to the elevated PCO2, which would lessen the driving force for mineral dissolution and increase the driving force for mineralization with respect to carbonated apatite in the bone mineral. To test this hypothesis, we injected neonatal mice with Ca-45 and dissected the radiolabeled calvariae 24 h later. The live calvariae were then cultured for 24 h under conditions simulating respiratory acidosis (Resp, pH = 7.225 +/- 0.003, PCO2 = 87.5 +/- 0.1 mmHg), severe respiratory acidosis (SResp, pH = 7.072 +/- 0.004, PCO2 = 103.0 +/- 0.5 mmHg), metabolic acidosis (Met, pH = 7.212 +/- 0.003, HCO3- = 15.5 +/- 0.1 meq/l), or normal acid-base status (Ctl, pH = 7.452 +/- 0.003, PCO2 = 40.0 +/- 0.2 mmHg, HCO3- = 27.8 +/- 0.2 meq/l) and bidirectional net calcium flux (J(Ca)) and unidirectional Ca-45 release were determined. There was greater J(Ca) from bone during Met than Resp, and J(Ca) was not different from Met during SResp despite the latter having a significantly lower pH. There was greater unidirectional Ca-45 release from bone during Met than Resp, SResp, or Ctl. There was a similar direct correlation between J(Ca) and Ca-45 efflux in the respiratory and metabolic groups. However, when calvarial osteoclast activity was inhibited with calcitonin, although there was again greater J(Ca) and Ca-45 release with metabolic compared with respiratory acidosis, there was a greater proportion of Ca-45 release than J(Ca) from bone. Thus the decreased net calcium efflux during respiratory compared with metabolic acidosis appears to be due to a combination of decreased unidirectional calcium efflux from the mineral coupled to deposition of medium calcium on the bone surface during hypercapnia.