Fig. 1. Phospholipase A2 action phospholipids (I) and 1-0-alkyl-2-acyl-glycero-3-phosphocoline (II). Abbreviations: R1, fatty acid esterified at the sn-1 position, usually saturated; R2, fatty acid esterified at the sn-2 position, usually unsaturated (eg arachidonic acid); X, polar head group (eg choline, ethanolamine, serine, inositol); and PAF, platelet activating factor. in the liberation of AA. Alternatively, diglyceride kinase can phosphorylate diacylglycerol to phosphatidic acid (PA), and arachidonic acid can be liberated from PA to PLA2. In vascular endothelial cells, thrombin, A23187 bradykinin, and histamine, directly or indirectly, appear to activate both PLC and PLA2 [4, 5]. Hong and coworkers [4, 5] noted an interesting species difference in the phospholipid pools from which the arachidonic acid was released following stimulation. In human endothelial cells, the major sources of AA were phosphatidy! choline and PI, whereas in porcine aortic endothelial cells the major sources were PI and phosphatidylethanolamine. It is difficult to evaluate the significance of these observations, but an additional metabolic pathway should be considered. In most solvent systems, the 1-0-alkyl-2-acyl-3-glycerophosphatidylcholine (Gro-PCHO) comigrates with phosphatidylcholine. Gro-PCHO is also substrate for PLA2, resulting in the formation of lyso-platelet activating factor (lyso-PAF). Lyso-PAF can be acetylated by an acetyltransferase [6] giving rise to PAF. The recent reports that human vascular endothelial cells can synthesize PAF in response to the same stimuli that evoke PGI2 production and with a similar time course suggest that there may be some coupling mechanism between prostaglandin synthesis and

PAF production [7, 8]. Stimulation of PLA2-mediated liberation of AA from Gro-PCHO might be such a mechanism. Thus, apparent differences in phospholipid turnover upon challenge with various stimuli may suggest an additional area of endothelial variability, ie variation in the capacity to synthesize PAF.