The inhibitory action of pgf2α on release of [3H]noradrenaline enhanced by α2-adrenoceptor blockade,sodium-pump inhibition and 4-aminopyridine in the main pulmonary artery of the rabbit

Large concentrations of prostaglandin PGF_2α inhibited the stimulation (2 Hz) evoked release of ³H]noradrenaline from the isolated main pulmonary artery of the rabbit (the inhibition caused by 3 × 10^?5 M PGF_2α was 62%). Furthermore, PGF_2α inhibited the release evoked by stimulation when it was enhanced by different procedures. During blockade of presynaptic α₂-adrenoceptors by 3 × 10^?7 M yohimbine, which by itself enhanced the overflow of ³H]NA in response to stimulation, the inhibitory action of PGF_2α was more pronounced (78.2%). In tissue in which the Na⁺-pump was inhibited (K⁺-free treatment) where the overflow of ³H was markedly increased, PGF_2α exerted nearly equal inhibition of transmitter release to that observed in control experiments (64.3%). The inhibitory effect of PGF_2α on the stimulation-evoked release of ³H]NA was less pronounced (32.1%) in the presence of 10^?4M 4-aminopyridine (a blocker of K⁺ -channels).