Section 45
Chapter 44,403

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

Török, T.L.; Rubányi, G.; Vizi, E.S.; Magyar, K.

European Journal of Pharmacology 84(1-2): 93-97


ISSN/ISBN: 0014-2999
PMID: 6128238
DOI: 10.1016/0014-2999(82)90161-3
Accession: 044402667

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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 alpha 2-adrenoceptors as evidenced by the finding that yohimbine 3 x 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.

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