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Articles in PresS, published online ahead of print July 12, 2001
Am J Physiol Renal Physiol, 10.1152/ajprenal.0355.2000
Submitted on December 28, 2000
Accepted on July 9, 2001
1 Nephrology Unit, University of Rochester School of Medicine, Rochester, NY, USA
* To whom correspondence should be addressed. E-mail: david_bushinsky{at}urmc.rochester.edu.
Clinically, a decrease in blood pH may be due to either a reduction in bicarbonate concentration ([HCO3-], metabolic acidosis) or to an increase in the partial pressure of carbon dioxide (Pco2, respiratory acidosis). In mammals, metabolic acidosis induces a far greater increase in urine calcium excretion than respiratory acidosis and this increase occurs without an alteration in intestinal calcium absorption, indicating that the additional urinary calcium is derived from the bone mineral. In cultured bone, metabolic acidosis induces a marked increase in calcium efflux, a decrease in osteoblastic collagen synthesis and an increase in osteoclastic bone resorption, while isohydric respiratory acidosis has little effect on any of these parameters. MRecently we have shown that metabolic acidosis increases bone prostaglandin E2 production and that this increase is correlated with net calcium efflux from bone. Inhibition of PGE2 production with indomethacin significantly inhibits this acid-induced calcium efflux. Given the marked differences in the osseous response to metabolic and respiratory acidosis, we hypothesized that incubation of neonatal mouse calvariae in medium simulating respiratory acidosis would not lead to the increase in medium PGE2 levels which is observed during metabolic acidosis. To test this hypothesis, we determined medium PGE2 levels and net calcium efflux from neonatal mouse calvariae incubated at pH~7.1 to model either metabolic (Met, [HCO3-]~11 mM), or respiratory (Resp, Pco2~83 mmHg), acidosis or at pH~7.5 as a control (Ntl). We found that after 24-48 hrs in culture, a period when cell mediated calcium efflux predominates, medium PGE2 levels and net calcium flux were increased with Met, but not Resp when compared to Ntl. Medium PGE2=0.35±0.14 ng/mL/24h (Ntl); 2.26±0.34 (Met, p<0.001 vs Ntl); 0.44±0.16 (Resp, p=NS vs Ntl and p<0.001 vs Met). Net calcium flux=293±74 nmol/bone/24h (Ntl); 850±115 (Met, p<0.001 vs Ntl); 383±70 (Resp, p=NS vs Ntl and p<0.001 vs Met). There was a strong, direct, correlation between medium PGE2 levels and net calcium flux (r=0.777, n=34, p<0.001). These differences and interrelationships were maintained during a subsequent 48-51 hr time period. We found that after 48 and 51 hrs in culture medium PGE2 levels and net calcium efflux from bone were increased with metabolic, but not respiratory, acidosis. During both time periods there was a strong, direct, correlation between medium PGE2 levels and net calcium release. Thus metabolic, but not respiratory, acidosis induces the release of bone PGE2 which is tightly correlated with net calcium efflux from bone.
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