Metabolic acidosis induces resorption of cultured bone, resulting in a
net efflux of calcium (Ca) from the bone and an apparent loss of mine
ral potassium (K), However, in these organ cultures, there is diffusio
n of K between the medium and the crystal lattice, causing difficulty
in interpretation of the acid-induced changes in mineral ion compositi
on, To determine the effects of acidosis on bone mineral K, we injecte
d 4-day-old neonatal mice with pure stable isotope K-41, equal to simi
lar to 5% of their total body K. Calvariae were dissected 24 h later a
nd then cultured for 24 h in medium without added K-41, either at pH s
imilar to 7.4 (Ctl) or at pH similar to 7.1 (Ac), with or without the
osteoclastic inhibitor calcitonin (3 x 10(-9) M, CT), The bone isotopi
c ion content was determined with a high-resolution scanning ion micro
probe utilizing secondary ion mass spectrometry, K-41 is present in na
ture at 6.7% of total K, The injected K-41 raised the ratio of bone K-
41/(K-39 + K-41) to 9.8 +/- 0.5% On the surface (ratios of counts per
second of detected secondary ions, mean +/- 95% confidence interval) b
ut did not alter the ratio in the interior (6.9 +/- 0.4%), indicating
biological incorporation of the K-41 into the mineral surface, The rat
ios of K-41/Ca-40 on the surface of Ctl calvariae was 14.4 +/- 1.2, in
dicating that bone mineral surface is rich in K compared with Ca, Comp
ared with Ctl, Ac caused a marked increase in the net Ca efflux from b
one that was blocked by CT, Ac also induced a marked fall in the ratio
of K-41/Ca-40 on the surface of the calvariae (4.3 +/- 0.5, p < 0.01
VS, Ctl), which was partially blocked by CT (8.2 +/- 0.9, p < 0.01 vs,
Ctl and vs, Ac), indicating that Ac causes a greater release of bone
mineral K than Ca which is partially blocked by CT, Thus, bone mineral
surface is rich in K relative to Ca, acidosis induces a greater relea
se of surface mineral K than Ca, and osteoclastic function is necessar
y to support the enriched levels of surface mineral K in the presence
of acidosis.