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Am J Physiol Renal Physiol 252: F585-F589, 1987;
0363-6127/87 $5.00
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AJP - Renal Physiology, Vol 252, Issue 4 585-F589, Copyright © 1987 by American Physiological Society

ARTICLES

Effects of parathyroid hormone on net proton flux from neonatal mouse calvariae

D. A. Bushinsky

Bone mineral buffers protons during acute metabolic acidosis; whether parathyroid hormone (PTH) augments proton buffering is controversial. To determine whether PTH augments proton buffering by bone, we cultured neonatal mouse calvariae with or without PTH (10(-8) M) for 3 h in medium that was physiologically acid (pH approximately 7.20), neutral (pH approximately 7.40), or alkaline (pH approximately 7.60). Over the entire pH range studied there was less influx of protons into calvariae treated with PTH than into control calvariae, indicating that PTH does not augment but instead inhibits proton buffering by bone. To determine whether chronic exposure to PTH is necessary to augment proton buffering, calvariae were incubated with PTH for 24 h before a 3-h culture. Calcium efflux from calvariae exposed to PTH (10(-8) M) for 24 h exceeded that of controls. When these same calvariae were recultured for 3 h in fresh medium, PTH-treated and control calvariae behaved similarly, with net efflux of protons into acid, neutral, and alkaline media. Regardless of whether PTH is added at the time of exposure to acid medium or 24 h before calvariae cultured with PTH do not buffer protons to a greater extent than controls.


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Chronic acidosis-induced alteration in bone bicarbonate and phosphate
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Effects of in vivo metabolic acidosis on midcortical bone ion composition
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Metabolic, but not respiratory, acidosis increases bone PGE2 levels and calcium release
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