Acid-induced stimulation of Na-Pi cotransport in OK cells: molecular characterization and effect of dexamethasone
Jehle, A.W.; Forgo, J.; Biber, J.; Lederer, E.; Krapf, R.; Murer, H.
American Journal of Physiology 273(3 Pt 2): F396-F403
1997
ISSN/ISBN: 0002-9513 PMID: 9321912 Document Number: 473587
Alterations in systemic acid/base balance affect renal P-i excretion. In the present study, the effects of an acidic pH on apical Na-dependent P-i (Na-P-i) cotransport were analyzed using OK cells (opossum kidney cell line). Cells were maintained at either pH 7.4 or 7.1 (altered HCO-3- concentration at constant PCO-2). Incubation in acidic medium led to an increase in Na-P-i cotransport activity, which was characterized by a transient, initial response (2-4 h, 25% increase) followed by a sustained response (24 h, 75% increase). Increased Na-P-i cotransport activity (24 h) was sensitive to inhibition by parathyroid hormone. Actinomycin D did not abolish the acid-induced increases (initial and sustained responses). Cycloheximide abolished the increase in Na-P-i cotransport observed after 24 h. The increase in Na-P-i cotransport (24 h) was prevented by dexamethasone (2 times 10-6 M). Western blots showed a twofold (3 h) and two- to threefold (24 h) increase in NaPi-4 protein after acid exposure. Cycloheximide prevented the late increase in NaPi-4 protein abundance. Also dexamethasone reduced the increase in specific protein content. In conclusion, the exposure of OK cells to an acidic medium causes a stimulation of the NaPi-4 cotransporter that is prevented by dexamethasone.