Vanadyl ions stimulate K+ uptake into isolated perfused rat liver via the Na+/K+-pump by a tyrosine kinase-dependent mechanism

Rafael Bruck, Zamir Halpern, Hussein Aeed, Yoram Shechter, Steven J.D. Karlish

Research output: Contribution to journalArticlepeer-review

Abstract

Vanadium salts mimic most metabolic effects of insulin in vitro. We report here that vanadyl sulfate (VOSO4) and sodium vanadate (NaVO3) stimulate net K+ uptake in isolated perfused rat liver. Stimulation was evident at low concentrations of vanadyl ions (range 1-20 μM) and occurred within minutes following the addition of VOSO4. By comparison with VOSO4, insulin had less of a stimulatory effect on K+ uptake. Ouabain prevented the activating effect of VOSO4 on K+ uptake. Following a VOSO4 challenge, measured intracellular Na+ concentration ([Na+](i)) fell (control, 17.1 ± 1.2; VOSO4-treated, 13.0 ± 1.1 mmol·g-1 wet weight, P = 0.027). The results indicate that active K+ uptake via the Na+/K+-ATPase was stimulated by vanadyl ions. An indirect mechanism-due to changes in [Na+](i) can be excluded. The tyrosine kinase inhibitor genistein was found to inhibit stimulation of K+ by vanadyl and vanadate ions which are known inhibitors of phosphotyrosine phosphatases. We conclude that stimulation of active K+ influx involves a tyrosine kinase. Possible mechanisms include phosphorylation at tyrosine residues and direct activation of the Na+/K+-ATPase, or phosphorylation of other proteins that regulate the activity or number of pumps in the cells.

Original languageEnglish
Pages (from-to)610-616
Number of pages7
JournalPflugers Archiv European Journal of Physiology
Volume435
Issue number5
DOIs
StatePublished - 1998

Keywords

  • Insulin-like effects
  • Na/K-ATPase
  • Perfused rat liver
  • Vanadium

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