The inhibitory action of PGF2 alpha on release of [3H]noradrenaline enhanced by alpha 2-adrenoceptor blockade, sodium-pump inhibition and 4-aminopyridine in the main pulmonary artery of the rabbit

• Published in: Neuropharmacology Vol. 23; no. 1; p. 37
• Main Authors: Török, T L, Bunyevácz, Z, Nguyen, T T, Hadházy, P, Magyar, K, Vizi, E S
• Format: Journal Article
• Language: English
• Published: England 01-01-1984
• Subjects: 4-Aminopyridine; Aminopyridines - pharmacology; Animals; Dinoprost; Electric Stimulation; Female; Ion Channels - drug effects; Male; Norepinephrine - metabolism; Potassium - metabolism; Prostaglandins F - pharmacology; Pulmonary Artery - metabolism; Rabbits; Receptors, Adrenergic, alpha - drug effects; Sodium - metabolism; Yohimbine - pharmacology
• ISSN: 0028-3908
• DOI: 10.1016/0028-3908(84)90214-4

Large concentrations of prostaglandin PGF2 alpha inhibited the stimulation (2 Hz) evoked release of [3H]noradrenaline from the isolated main pulmonary artery of the rabbit (the inhibition caused by 3 X 10(-5) M PGF2 alpha was 62%). Furthermore, PGF2 alpha inhibited the release evoked by stimulation when it was enhanced by different procedures. During blockade of presynaptic alpha 2-adrenoceptors by 3 X 10(-7) M yohimbine, which by itself enhanced the overflow of [3H]NA in response to stimulation, the inhibitory action of PGF2 alpha 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, PGF2 alpha exerted nearly equal inhibition of transmitter release to that observed in control experiments (64.3%). The inhibitory effect of PGF2 alpha on the stimulation-evoked release of [3H]NA was less pronounced (32.1%) in the presence of 10(-4) M 4-aminopyridine (a blocker of K+-channels).