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 PCO2). 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 x 10-6 M). Western blots showed a twofold (3 h) and two- to threefold (24 h) increase in NaP(i)-4 protein after acid exposure. Cycloheximide prevented the late increase in NaP(i)-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 NaP(i)-4 cotransporter that is prevented by dexamethasone.
|Original language||English (US)|
|Journal||American Journal of Physiology - Renal Physiology|
|Issue number||3 42-3|
|State||Published - Sep 1 1997|
- Opossum kidney
- Parathyroid hormone
ASJC Scopus subject areas