Release of prostaglandins from the isolated perfused rabbit ear by bradykinin and acetylcholine.
(1) The isolated rabbit ear was perfused via its artery and the venous outflow superfused a PGE-sensitive rat stomach strip or a PGF-sensitive rat colon. (2) Injection of bradykinin intra-arterially into the ear produced a larger contraction of the rat stomach strip than the application of the same dose of bradykinin directly to the superfused muscle. (3) This difference is explained as a release of PGE-like material by bradykinin since indomethacin (infused i.a. into the ear) reduced the effect of the i.a. applied bradykinin. (4) PGF-like material could not be detected in the venous effluent. (5) ACh released only minimal amounts of PGE-like substance. (6) CONCLUSION: The amount of PGE-like material released by bradykinin is large enough to sensitize the paravascular pain receptors in the rabbit ear for the attack of bradykinin. Therefore, inhibition of PG-synthesis (i.e. by indomethacin) or inhibition of the sensitizing action of E-type PGs (i.e. by polyphloretin phosphate) reduces the pain producing effect of bradykinin. Since ACh releases only minimal amounts of E-type PGs, its effect is reduced only to a minimal extent by indomethacin or polyphloretin phosphate.
D000109:Acetylcholine / Q000494:pharmacology*; D000287:Administration, Topical; D000818:Animals; D001681:Biological Assay; D001920:Bradykinin / Q000008:administration & dosage / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D004423:Ear / Q000378:metabolism; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D007269:Injections, Intra-Arterial; D009119:Muscle Contraction / Q000187:drug effects; D009130:Muscle, Smooth / Q000187:drug effects; D011458:Prostaglandins E / Q000378:metabolism* / Q000502:physiology; D011817:Rabbits; D051381:Rats
D011458:Prostaglandins E; D000109:Acetylcholine; D001920:Bradykinin; D007213:Indomethacin