Key result
Paf receptor antagonists WEB 2086 and CV 6209 inhibited bradykinin-, A23187-, and ATP-induced PGI2 generation in bovine cultured aortic endothelial cells, suggesting a role for intracellular Paf.
Why the study?
Do platelet-activating factor receptor antagonists inhibit prostacyclin generation in bovine cultured aortic endothelial cells?
Do platelet-activating factor receptor antagonists inhibit prostacyclin generation in bovine cultured aortic endothelial cells?
Intracellular platelet-activating factor appears to play a role in signal transduction for prostacyclin generation in bovine aortic endothelial cells.
Answers are grounded in this paper and cite their sources.
No clinical implications from bovine cell data; leaves open intracellular Paf's role in endothelial PGI2 signaling.
Bovine culture endothelial cells (BAECs) generate platelet-activating factor (Paf) following activation by bradykinin (Bk 0.1 nM), the ionophore, A23187 (3 microM), and ATP (10 microM), but Paf is not released from the cells. These stimuli also elicit generation of prostacyclin (PGI2). The specific and competitive Paf receptor antagonists, WEB 2086 (0.1-1.0 microM) and CV 6209 (0.01-0.1 microM), inhibited Bk-, A23187- and, to a lesser extent, ATP-induced PGI2 generation but had no effect on basal PGI2 generation. These data suggest a role for intracellular Paf in signal transduction.
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Stewart et al. (1989) studied this question. Paf receptor antagonists (WEB 2086 and CV 6209) was evaluated on PGI2 generation. Paf receptor antagonists WEB 2086 and CV 6209 inhibited bradykinin-, A23187-, and ATP-induced PGI2 generation in bovine cultured aortic endothelial cells, suggesting a role for intracellular Paf.
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