Possible involvement of adenine nucleotides in sympathetic neuroeffector mechanisms of dog basilar artery.

The transmission mechanism of sympathetic neuroeffector was studied in the isolated dog basilar artery. Electrical transmural stimulation produced an initial contractile response which was followed by a transient relaxation or a late contraction, or both relaxation and contraction. These arteries showed a marked uptake of [3H]norepinephrine ([3H]NE) or [3H]adenosine after incubation with these compounds, and electrical stimulation increased the release of [3H]NE or 3H-purine compounds. After treatment with tetrodotoxin or bretylium or in the sympathetically denervated arteries, the mechanical response to electrical stimulation and the release of 3H-compounds were attenuated; however, the mechanical response was not affected by treatment with reserpine. These results suggest that transmural stimulation releases not only [3H]NE but also 3H-purine compounds predominantly from the sympathetic nerve terminals and produces sympathetic contractile and relaxing responses. Phentolamine enhanced these sympathetic responses and augmented the release of [3H]NE and 3H-purine compounds. Exogenously applied NE produced a slowly developing contractile response and inhibited the release of 3H-purine compounds upon electrical transmural stimulation. Exogenously applied ATP produced responses which were similar in pattern to the sympathetic response and the release of [3H]NE was inhibited. Other adenine nucleotides and adenosine produced only relaxation. Theophylline attenuated the relaxing response to sympathetic nerve stimulation or to exogenously applied nucleotides. These results suggest that ATP or related nucleotides are released, concomitant with NE, from the sympathetic nerve terminals in the dog basilar artery and may act as neurotransmitters and/or modulators on presynaptic and postsynaptic membranes.