Rat pulmonary artery responses to some mediators of anaphylaxis: modifications by indomethacin.
Rat extralobar pulmonary artery responses to some anaphylactic mediators and arachidonic acid metabolites were studied on "in vitro". Histamine (H), serotonin (5HT), bradykinin (Bk) and norepinephrine (NE) contract the pulmonary arteries; all the arachidonic acid metabolites tested (PGE2 - PGF2 alpha - PGI2 - LTC4) also exert a vasocontractile activity and among these PGF2 alpha is the most active whereas LTC4 exerts only a weak effect. Isoproterenol, papaverine and adenosine weakly relax the vascular preparation, while acetylcholine and PAF-acether have no effect. The interference of indomethacin on NE-5HT-H-induced contractions has been investigated. Indomethacin reduced the contractile activity of H while the cyclo-oxygenase inhibitor did not significantly interfere with the effect of NE and 5HT. The possible relationships between some anaphylactic mediators and the arachidonic acid metabolites have been discussed.
D000707:Anaphylaxis / Q000209:etiology*; D000818:Animals; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000378:metabolism; D011464:Epoprostenol / Q000502:physiology; D006632:Histamine / Q000494:pharmacology; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology*; D008297:Male; D009638:Norepinephrine / Q000494:pharmacology; D011651:Pulmonary Artery / Q000187:drug effects*; D051381:Rats; D011919:Rats, Inbred Strains; D012701:Serotonin / Q000494:pharmacology; D014661:Vasoconstriction / Q000187:drug effects
D001095:Arachidonic Acids; D016718:Arachidonic Acid; D012701:Serotonin; D006632:Histamine; D011464:Epoprostenol; D009638:Norepinephrine; D007213:Indomethacin