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Overview
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Background
PAF (C16) is an endogenous platelet-activating factor (PAF) and ligand for PAF receptors. The platelet-activating factor receptor is a G-protein coupled receptor which binds platelet-activating factor.PAF is produced by inflammatory cells and polymorphonuclear neutrophils. It induces increased vascular permeability. To examine the loss of selective endothelial permeability, the extravasative effect of PAF was assessed by monitoring the plasma loss of 125I-albumin (6.7 nm), 125I-low density lipoproteins (22.0 nm) and 125I-very low density lipoproteins (62.1 nm). There was no selective plasma retention of the labeled plasma tracers, which suggest that PAF-induced extravasation is dose-dependent, with increases in vascular permeability [1].Given into the renal arterial circulation of male Wistar rats, PAF (C16) increased in renal blood flow (6-15%) in a dose-dependent way. The PAF-induced systemic hypotension and renal vasodilation are independent of renal innervation and are PAF-receptor mediated [2].
[1]. Handley DA, Arbeeny CM, Lee ML, et al. Effect of platelet activating factor on endothelial permeability to plasma macromolecules. Immunopharmacology, 1984, 8(3-4): 137-142.
[2]. Handa RK, Strandhoy JW, Buckalew VM Jr. Platelet-activating factor is a renal vasodilator in the anesthetized rat. Am J Physiol, 1990, 258(6 Pt 2): F1504-1509.
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