Platelet-activating factor-induced vasoconstriction in rat isolated, perfused hearts: contribution of cyclo-oxygenase and lipoxygenase arachidonic acid metabolites

Pharmacological Research Communications
A G Stewart, P J Piper

Abstract

The mechanism of the coronary vasoconstrictor action of platelet-activating factor (PAF) has been investigated in rat isolated, perfused hearts. PAF elicited an increase in coronary perfusion pressure which was attenuated by indomethacin- or diethylcarbamazine- pretreatment, whereas FPL55712 had a marked inhibitory effect. Accompanying the coronary vasoconstrictor response to PAF was an increase in the release of PGE2, PGF2 alpha, 6-keto-PGF1 alpha and TxB2 and the appearance of biologically-active concentrations of LTB4 and LTC4 in the cardiac effluent. Indomethacin-pretreatment prevented the increase in release of the measured cyclo-oxygenase metabolites without significantly altering the generation of either LTB4 or LTC4. Diethylcarbamazine markedly inhibited the PAF-induced release of both cyclo-oxygenase and lipoxygenase products. These findings suggest a causal role for vasoconstrictor arachidonic acid metabolites in the acute cardiac effects of PAF with the quantitatively most important contribution to the vasoconstriction made by LTC4.

References

Aug 1, 1982·Prostaglandins·J A SalmonR M Palmer

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Citations

Sep 1, 1992·Prostaglandins, Leukotrienes, and Essential Fatty Acids·P MentzH J Mest
Dec 1, 1991·Lipids·R E GoldsteinN J Davenport
Jan 1, 1991·Research in Experimental Medicine. Zeitschrift Für Die Gesamte Experimentelle Medizin Einschliesslich Experimenteller Chirurgie·S B FelixW E Berdel
Sep 1, 1995·Prostaglandins, Leukotrienes, and Essential Fatty Acids·K BeckerO E Brodde

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