Acid-induced stimulation of Na-P(i) cotransport in OK cells: Molecular characterization and effect of dexamethasone

Andreas W. Jehle, Judith Forgo, Jürg Biber, Eleanor Lederer, Reto Krapf, Heini Murer

Research output: Contribution to journalArticlepeer-review

13 Scopus citations

Abstract

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 languageEnglish (US)
Pages (from-to)F396-F403
JournalAmerican Journal of Physiology - Renal Physiology
Volume273
Issue number3 42-3
StatePublished - Sep 1 1997
Externally publishedYes

Keywords

  • Acidemia
  • Acidosis
  • Opossum kidney
  • Parathyroid hormone
  • Phosphate

ASJC Scopus subject areas

  • Physiology
  • Urology

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