Decreased bone carbonate content in response to metabolic, but not respiratory, acidosis

Abstract

In vitro cultured neonatal mouse calvariae release calcium and buffer the medium proton concentration in response to a decrease in the medium pH caused by a reduction in bicarbonate concentration ([HCO3-]), a model of metabolic acidosis, but not to an equivalent decrease in pH caused by an increase in the partial pressure of carbon dioxide (PCO2), a model of respiratory acidosis. We have postulated that the medium is in equilibrium with the carbonated apatite in bone. To determine whether bone carbonate is depleted during models of acidosis, we cultured calvariae in control medium (pH approximately 7.4, PCO2 approximately 43, [HCO3-] approximately 26) or in medium in which the pH was equivalently reduced by either a decrease in [HCO3-] (metabolic acidosis, pH approximately 7.1, [HCO3-] approximately 13) or an increase in PCO2 (respiratory acidosis, pH approximately 7.1, PCO2 approximately 86) and determined net calcium flux (JCa) and bone carbonate content. We found that compared with control, after 3, 24, and 48 h there was a decrease in bone carbonate content during metabolic but not during respiratory acidosis. Compared with control, at 3 h JCa increased with both respiratory and metabolic acidosis; however, at 24 and 48 h JCa increased only with metabolic acidosis. JCa was correlated inversely with percent bone carbonate content in control and metabolic acidosis at all time periods studied (r = -0.809, n = 23, P < 0.001). Thus a model of metabolic acidosis appears to increase JCa from bone, perhaps due to the low [HCO3-] inducing bone carbonate dissolution.(ABSTRACT TRUNCATED AT 250 WORDS)

Dynamics of Parathyroid Hormone Secretion in Health and Secondary Hyperparathyroidism

“…Previous in vitro and in vivo studies (62)(63)(64) showed that even in the absence of PTH, metabolic acidosis increases calcium efflux from bone. Moreover, Fraley and Adler (65) showed that the administration of PTH to parathyroidectomized animals that received an acid load increased survival; therefore, the results of these studies suggest not only that in acute metabolic acidosis calcium release from bone is increased independent of PTH but also that PTH acts to enhance calcium release further from bone and to increase buffering capacity.…”

Metabolic, but not respiratory, acidosis increases bone PGE2levels and calcium release

“…During models of metabolic acidosis, there is marked calcium efflux from cultured bone, depletion of bone carbonate, stimulation of osteoclastic resorption, inhibition of osteoblastic formation, and a decrease in the formation of mineralized bone nodules (5-7, 13, 14, 17, 20-25, 27-29, 31, 36, 38, 46, 47). However, isohydric respiratory acidosis causes far less calcium efflux, does not appear to affect bone carbonate or osteoblastic or osteoclastic function, and has far less effect on the formation and mineralization of bone nodules (6,7,11,22,27,28,31,70).…”

“…The additional protons present in the medium during metabolic acidosis are buffered by the bone mineral whereas there is little buffering of protons during respiratory acidosis (5,6,18,21). The proton buffering during metabolic acidosis is apparently due, at least in part, to the depletion of bone carbonate that occurs during metabolic, but not respiratory, acidosis (22,23).During longer term incubations, there is a significant cell-mediated component of calcium efflux from bone during models of metabolic, but not respiratory, acidosis (7,11,47). Although we have shown that metabolic acidosis increases the resorptive activity of…”

“…During short-term (3-h) incubations, both types of acidosis cause a net calcium efflux from bone; however, isohydric metabolic acidosis causes a far greater net efflux than does respiratory acidosis (22,27,28,31). Respiratory acidosis not only causes less unidirectional calcium efflux but has been shown to cause deposition of medium calcium onto bone (28).…”

“…The additional protons present in the medium during metabolic acidosis are buffered by the bone mineral whereas there is little buffering of protons during respiratory acidosis (5,6,18,21). The proton buffering during metabolic acidosis is apparently due, at least in part, to the depletion of bone carbonate that occurs during metabolic, but not respiratory, acidosis (22,23).…”