Stimulation by vanadate of tritium labeled noradrenaline release from rabbit pulmonary artery and its inhibition by noradrenaline
Torok, T.L.; Rubanyi, G.; Vizi, E.S.; Magyar, K.
European Journal of Pharmacology 84(1-2): 93-98
ISSN/ISBN: 0014-2999 Accession: 006480813
Vanadate, the +5 oxidation state of V, present in mammalian tissues including nerve tissue, and a competitive inhibitor of NaK-ATPase, significantly enhnaced the release of [3H]noradrenaline [norepinephrine] evoked from rabbit isolated perfused pulmonary artery by electrical stimulation. Its effect was 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 .times. 10-7 M prevented its action. The effect of vanadate was dependent on external K+. 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. The effect is evidently related to the inhibition of NaK-ATPase activity, a condition resulting in transmitter release.