Mechanism for the stimulation of platelet-activating factor production by cyclooxygenase inhibitors. Analysis for the participation of prostaglandin E2 and cAMP.:—Analysis for the participation of prostaglandin E2 and cAMP—

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Stimulation of rat peritoneal macrophages by the endomembrane Ca2+-ATPase inhibitor thapsigargin, or by the protein kinase C activator 12-O-tetradecanoylphorbol 13-acetate (TPA), enhanced the production of cell-associated plateletactivating factor (PAF) and extracellular prostaglandin E2 (PGE2) . Both the thapsigargin-and the TPA-induced PAF production were further enhanced dose-dependently by the cyclooxygenase inhibitor indomethacin in accordance with the decrease of PGE2 production. The addition of exogenous PGE2 counteracted the enhancing effect on PAF production by the cyclooxygenase inhibitors indomethacin, naproxen, and ibuprofen. In addition, dibutylyl cAMP also lowered the indomethacin-induced increase of PAF production. On the other hand, PAF acetylhydrolase activity in the cells was not inhibited by indomethacin treatment. These findings suggest that the stimulation of PAF production by the cyclooxygenase inhibitor is due to the inhibition of PGE2 production, but not due to the inhibition of the degradation of PAF by PAF acetylhydrolase.
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