Purinergic and cyclic AMP modulation of noradrenaline release in cat femoral arteries.

1. Adenosine, AMP, ATP (5 x 10(-4) M), 5'-N-ethylcarboxamide adenosine (NECA) and N6-L-phenylisopropyl adenosine (L-PIA) (10(-4) M) decreased tritium release elicited by electrical stimulation (ES) or 50 mM K+ in cat femoral arteries preincubated with [3H]noradrenaline (NA). 2. This effect was antagonized by 1-methyl-3-isobutylxanthine (MIX, 5 x 10(-5) M). 3. The release induced by ionophore X-537A (10(-5) M) was unaffected by adenosine and AMP. 4. The increase of intracellular cAMP levels caused by dibutyryl cAMP (5 x 10(-4) M), Ro-20 1724 (10(-4) M), forskolin (5 x 10(-6) M), NaF (2 x 10(-3) M) reduced, but MIX (5 x 10(-5) M) increased tritium release elicited by ES and K+. 5. Dipyridamole (5 x 10(-5) M) and erythro-9-2-hydroxy-3 nonyl adenosine (EHNA) (10(-4) M) also reduced tritium release. 6. Dipyridamole decreased both the uptake of [3H]NA and [3H]adenosine. 7. These data indicate: (a) the existence of A1 and A2 subtypes of purinoceptors situated presynaptically, which modulates NA release, (b) the intracellular increase of cAMP negatively modulates this secretion, and (c) these arteries possess an active system for incorporating and degrading adenosine.