Pauló T, Tóth P T, Nguyen T T, Forgács L, Török T L, Magyar K
J Pharm Pharmacol. 1986 Sep;38(9):668-73. doi: 10.1111/j.2042-7158.1986.tb03107.x.
Vinpocetine (10(-6)-3 X 10(-5) M) increased both the resting and the nerve stimulation-evoked release of [3H]noradrenaline from the isolated main pulmonary artery of the rabbit in the presence of uptake blockers (cocaine, 3 X 10(-5) M; corticosterone, 5 X 10(-5) M), and inhibited the nerve stimulation-evoked postsynaptic response. The resting transmitter releasing action of vinpocetine increased in the absence of cocaine. Exogenously applied (-)noradrenaline [(-)NA] (10(-6) M) or clonidine (10(-6) M) inhibited the vinpocetine (3 X 10(-5) M)-potentiated [3H]NA release and contracted the circular muscle. The clonidine-induced contraction was abolished by 10(-7) M prazosin. The inhibitory action of (-)-NA on vinpocetine-potentiated [3H]NA release was partly antagonized by 3 X 10(-7) M yohimbine, a preferential alpha 2-adrenoceptor blocker. In Ca-free Krebs solution containing 1 mM EGTA the neurotransmitter releasing action of vinpocetine was abolished, however, its stimulating action on the resting [3H]NA outflow was not changed. In Na-pump-inhibited arteries (K-free solution), where both the resting and the nerve stimulation-evoked release of neurotransmitter had already been increased, vinpocetine further enhanced the nerve stimulation-evoked release of [3H]NA. It is concluded that vinpocetine may have alpha 2- and alpha 1-adrenoceptor blocking action, as well as a tyramine-like effect. The presynaptic neurotransmitter releasing action of vinpocetine is presumably the consequence of its inhibitory action on the Ca-pump which is suggested by the finding that in K-free solution vinpocetine was able to enhance further the release of neurotransmitter.
