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

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 [ 3 H]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 [ 3 H]noradrenaline. The effect of noradrenaline is mediated via α 2 -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 [ 3 H]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.