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.