Platelet-activating factor (PAF-acether): Present status

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Abstract
PAF-acether, first discovered in 1971–72, is now recognized as a 1-O-alkyl-2-acetyl-sn-glyceryl-3-phosphorylcholine released from various cells and organs, including macrophages, neutrophils, platelets, the kidney and heart. In this review, we will concentrate on the newest aspects of PAF-acether biochemistry and pathophysiology: (1) PAF-acether is probably formed by murine macrophages through a two-step process inplicating successively a phospholipase A2-like enzyme and an acetyltransferase; (2) study of phospholipids structurally related to PAF-acether indicates that the ether linkage at position 1, the short acyl chain at position 2 and the natural optical configuration are critical for biological activity; (3) besides platelet aggregation, PAF-acether induces a platelet-dependent, aspirin-independent bronchoconstriction in the guinea-pig and the monkey. It exhibits also a potent antihypertensive action in the rat, and triggers platelet-independent hemodynamic changes in perfused guinea-pig heart. Thus, this class of phospholipids is gaining increasing importance in pathophysiology.