Abstract
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 α 2-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).
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
