Cyclooxygenase inhibitors suppress inhibitory effect of PGE2 on Na-K-ATPase in MDCK cells

Rivka Cohen-Luria, Arie Moran, Gilad Rimon

Research output: Contribution to journalArticlepeer-review

12 Scopus citations

Abstract

In a previous work, we showed that picomolar concentrations of prostaglandin E2 (PGE2) inhibit Na-K-ATPase activity and ouabain binding in a clone of Madin-Darby canine kidney (MDCK) cells. In the present study, we demonstrate that the inhibitory effects of PGE2 on Na-K-ATPase activity, ouabain-sensitive Rb+ uptake, and ouabain binding in MDCK cells were diminished by treatment of the cells with nonsteroidal antiinflammatory drugs. These results suggested that products of arachidonic acid synthesized through the cyclooxygenase pathway are involved in the inhibitory mechanism of PGE2. Treatment of the cells with arachidonic acid resulted in inhibition of ouabain binding, and the inhibition was eliminated by cyclooxygenase inhibitors. These observations further support the involvement of cyclooxygenase products in the PGE2-induced inhibitory process. Finally, we demonstrated that dopamine inhibits Rb+ influx and ouabain binding in MDCK cells similarly to PGE2. Cyclooxygenase inhibitors suppressed the inhibition of ouabain binding by dopamine, thus also suggesting the involvement of cyclooxygenase products in the inhibitory effect of dopamine.

Original languageEnglish
Pages (from-to)F94-F98
JournalAmerican Journal of Physiology - Renal Fluid and Electrolyte Physiology
Volume267
Issue number1 36-1
StatePublished - 1 Jan 1994

Keywords

  • Arachidonic acid
  • Cultured renal cells
  • Dopamine
  • Nonsteroidal anti-inflammatory drugs
  • Sodium pump

ASJC Scopus subject areas

  • Physiology

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