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1 Nephrology Unit, Department of Medicine, University of Rochester School of Medicine, Rochester, New York 14642; and 2 Enrico Fermi Institute, Department of Physics, University of Chicago, Chicago, Illinois 60637
Chronic metabolic
acidosis increases urine calcium excretion without altering intestinal
calcium absorption, suggesting that bone mineral is the source of the
additional urinary calcium. During metabolic acidosis there appears to
be an influx of protons into bone mineral, lessening the magnitude of
the decrement in pH. Although in vitro studies strongly support a
marked effect of metabolic acidosis on the ion composition of bone,
there are few in vivo observations. We utilized a high-resolution
scanning ion microprobe with secondary ion mass spectroscopy to
determine whether in vivo metabolic acidosis would alter bone mineral
in a manner consistent with its purported role in buffering the
increased proton concentration. Postweanling mice were provided
distilled drinking water with or without 1.5%
NH4Cl for 7 days; arterial blood
gas was then determined. The addition of
NH4Cl led to a fall in blood pH
and HCO
3 concentration. The animals
were killed on day
7, and the femurs were dissected and split longitudinally. The bulk cortical ratios Na/Ca,
K/Ca, total phosphate/carbon-nitrogen bonds
[(PO2 + PO3)/CN], and
HCO3/CN each fell after 1 wk of
metabolic acidosis. Because metabolic acidosis induces bone Ca loss,
the fall in Na/Ca and K/Ca indicates a greater efflux of bone Na and K
than Ca, suggesting H substitution for Na and K on the mineral. The
fall in (PO2 + PO3)/CN indicates release of
mineral phosphates, and the fall in
HCO3/CN indicates release of mineral
HCO3. Each of these mechanisms would
result in buffering of the excess protons and returning the systemic pH
toward normal.
ion microprobe; calcium; mouse femurs; proton
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