Net calcium efflux from live bone during chronic metabolic, but not respiratory, acidosis.

In vivo chronic metabolic acidosis induces bone mineral dissolution. Whether the dissolution is due to alterations in physicochemical factors alone, as in acute metabolic acidosis, or requires participation of bone cells is not clear. The effect of chronic respiratory acidosis on bone has also not been established. To determine the effects of chronic metabolic and respiratory acidosis on net calcium flux from bone, we cultured live and dead neonatal mouse calvariae for 99 h in control medium or in medium acidified (pH approximately equal to 7.1) either by lowering the bicarbonate concentration (Met) or by increasing the PCO2 (Resp). We measured net calcium flux (JCa) over 0-48, 48-96, and 96-99 h. Over the first 48 h, there was greater net calcium efflux from live and dead Met than from both Resp groups. All four acidic groups had greater net calcium efflux than controls. Over the last 51 h of the chronic 99 h culture, there was net calcium efflux only from live Met (JCa = 285 +/- 129 nmol.bone-1.3 h-1) and not from any of the other groups (live control, JCa = -183 +/- 24; live Resp, JCa = -110 +/- 22; dead control, JCa = -256 +/- 12; dead Met, JCa = 11 +/- 78; dead Resp, JCa = -27 +/- 47; each P less than 0.02 vs. live Met). There is net calcium efflux from live cultured neonatal mouse calvariae during chronic metabolic, but not respiratory, acidosis. During chronic acidosis, decreased medium bicarbonate, and not just a fall in pH, is necessary to enhance net calcium efflux from live bone.