| Autor: |
Pauló, Tünde, Tóth, Péter T, Nguyen, Tinh Thi, Forgács, Lilla, TÖRÖK, TamáS L, Magyar, Kálmán |
| Zdroj: |
Journal of Pharmacy and Pharmacology; September 1986, Vol. 38 Issue: 9 p668-673, 6p |
| Abstrakt: |
Vinpocetine (10−6− 3 × 10−5M) 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 × 10−5M; corticosterone, 5 × 10−5M), 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] (10−6M) or clonidine (10−6M) inhibited the vinpocetine (3 × 10−5M)-potentiated [3H]NA release and contracted the circular muscle. The clonidine-induced contraction was abolished by 10−7M prazosin. The inhibitory action of (−)-NA on vinpocetine-potentiated [3H]NA release was partly antagonized by 3 × 10−7M yohimbine, a preferential α2-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 α2- and α1-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. |
| Databáze: |
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