Stimulation by vanadate of [3H]noradrenaline release from rabbit pulmonary artery and its inhibition by noradrenaline

Tamás L. Török, Gábor Rubányi, E. Sylvester Vizi, Kalman Magyar

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Vanadate, the +5 oxidation state of vanadium, present in mammalian tissues, even in nerve tissue, and a competitive inhibitor of NaK-ATPase, significantly enhanced the release of [3H]noradrenaline evoked from rabbit isolated perfused pulmonary artery by electrical stimulation. Its effect proved to be concentration-dependent. Noradrenaline (10-6 M) reduced the vanadate-potentiated release of [3H]noradrenaline. The effect of noradrenaline is mediated via α2-adrenoceptors as evidenced by the finding that yohimbine 3×10-7 M prevented its action. The effect of vanadate was dependent on external K ions. When the effect of vanadate on [3H]noradrenaline release was studied under conditions when the NaK-ATPase enzyme activity was inhibited by removal of external K for 45 min, vanadate was ineffective. This finding indicates that the effect is related to the inhibition of NaK-ATPase activity, a condition known to result in transmitter release.

Original languageEnglish
Pages (from-to)93-97
Number of pages5
JournalEuropean Journal of Pharmacology
Volume84
Issue number1-2
DOIs
Publication statusPublished - Oct 15 1982

Keywords

  • NaK-ATPase
  • Noradrenaline
  • Rabbit pulmonary strip
  • Vanadate
  • [H]Noradrenaline release

ASJC Scopus subject areas

  • Pharmacology

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