EFFECTS OF 4-AMINOPYRIDINE ON THE ADRENERGIC-NERVE TERMINALS OF RABBIT ARTERIES

  • 1 January 1981
    • journal article
    • research article
    • Vol. 219  (3) , 792-797
Abstract
Adrenergic nerves of the rabbit pulmonary artery and aorta were stimulated by electrical pulses (0.3 or 5 ms duration) and also by nicotine. The effects of 4-aminopyridine (4-AP), a K+ channel inhibitor, were investigated on contractile responses of these arteries or on 3H-efflux from [3H]norepinephrine-treated pulmonary artery in response to these stimuli. Tetrodotoxin (0.1-0.3 .mu.M) abolished the contractions and the 3H-efflux induced by an electrical pulse of 0.3 ms duration, but not the adrenergic responses induced by a pulse of 5 ms duration or by nicotine. The adrenergic responses to an electrical pulse of 5 ms (with tetrodotoxin) or nicotine were inhibited by guanethidine (10 .mu.M) or removal of the extracellular Ca. A short electrical pulse indirectly stimulates the adrenergic nerve terminals through conducted action potentials; a long pulse or nicotine directly stimulates the terminals. 4-AP in concentrations over 10 .mu.M markedly augmented the adrenergic responses to these 2 electrical stimuli. The adrenergic response induced by nicotine was little affected by 4-AP in concentrations up to 100 .mu.M. At 300 .mu.M, the concentration-contraction curve of nicotine shifted to the right and 3H-efflux was markedly reduced. This inhibitory effect of 4-AP on the contraction was not affected by alterations in the extracellular Ca concentration. 4-AP did not affect the responses to exogenously applied norepinephrine. 4-AP has inhibitory effects on nicotinic receptors of adrenergic nerve terminals and nicotine releases norepinephrine in a manner which differs from the release seen with electrical stimulation.