NICOTINE-INDUCED RESPONSE IN GUINEA-PIG AORTA ENHANCED BY GONIOPORA TOXIN

  • 1 January 1982
    • journal article
    • research article
    • Vol. 223  (3) , 790-794
Abstract
The possible involvement of Na action potentials in sympathomimetic effects of nicotine was investigated in isolated guinea pig aortas. Goniopora toxin (GPT), a polypeptide isolated from coral, was used to increase the Na influx through the fast Na channel of the postganglionic sympathetic nerves; tetrodotoxin (TTX) was used to block this flux. Nicotine (10-300 .mu.M) produced sympathetic nerve-mediated contractions in a concentration-dependent manner. GPT (30 nM) enhanced the responses to nicotine over the entire range of concentrations tested, yet there was no effect on resting tension. Such an effect of GPT was concentration-dependent and was apparent in concentrations > 10 nM. GPT had no effect on the responses to exogenously applied norepinephrine. TTX (100 nM) abolished this potentiating effect of GPT but did not inhibit the usual nicotine-induced responses. The 3H-efflux induced by nicotine (100 .mu.M) in the preparations preincubated with [3H]norepinephrine was not significantly inhibited by TTX (100 nM). GPT (30 nM) markedly augmented nicotine-induced 3H-efflux and TTX prevented this effect of GPT. The augmentation of the nicotine-induced response by GPT in isolated guinea pig aortas may be due to a prolongation of the duration of the presynaptic action potential. The effects of nicotine on adrenergic nerve terminals may involve 2 mechanisms: one mediated by Na action potentials and one independent of these action potentials.