The platelet-independent release of thromboxane A2 by Paf-acether from guinea-pig lungs involves mechanisms distinct from those for leukotriene

British Journal of Pharmacology
J LefortB B Vargaftig


Intra-arterial injections of platelet-activating factor (Paf-acether, 10-300 ng) to the perfused guinea-pig lung induced a dose-related bronchoconstriction, followed by contraction of the rat aorta superfused with the lung effluent, indicating the release of thromboxane A2 (TXA2) activity. These effects were matched with injections of bradykinin (Bk) at 100-1000 ng, leukotriene C4(LTC4) at 10-300 ng or arachidonic acid (AA) at 30-300 micrograms. Repeated doses of Paf-acether led to a specific desensitization of the release of TXA2, under conditions where Bk, LTC4 and arachidonic acid retained their ability to release TXA2. Bronchoconstriction and the release of TXA2 induced by Paf-acether were suppressed when the lungs were perfused with acetylsalicylic acid, but not with salicylic acid. The phospholipase A2 inhibitor, p-bromophenacyl bromide suppressed the release of TXA2 by Bk, but did not interfere with its formation from AA, nor with its release with Paf-acether and LTC4. The lipoxygenase inhibitor, nordihydroguaiaretic acid, inhibited to a similar extent the release of TXA2 by Bk, LTC4 and Paf-acether but also reduced directly the formation of TXA2 from arachidonic acid, invalidating its use as a specific antilipoxygenase ...Continue Reading


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