Eicosanoids of platelets and vascular wall in chronic renal insufficiency.
There is good evidence that retention products accumulating in chronic renal insufficiency influence prostaglandin (PG) synthesis, thus affecting platelet-vascular wall interaction. The vascular PGI2 synthesis is increased and prolonged in vitro, the plasma factor activity enhanced. A defective platelet function is frequently observed; it is completely restored by peritoneal dialysis, but only partially by hemodialysis. The sensitivity of platelets to PGI2 and its plasmatic degradation are unchanged. There is evidence of a shift of arachidonic acid metabolism from cyclooxygenase to lipoxygenase. These changes may be attributed to undialyzable plasma constituents, the 'middle molecules'.
D001095:Arachidonic Acids / Q000378:metabolism; D001792:Blood Platelets / Q000378:metabolism*; D011464:Epoprostenol / Q000378:metabolism*; D006801:Humans; D007676:Kidney Failure, Chronic / Q000378:metabolism*; D008084:Lipoxygenase / Q000378:metabolism; D009131:Muscle, Smooth, Vascular / Q000378:metabolism*; D010979:Platelet Function Tests; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism
D001095:Arachidonic Acids; D011464:Epoprostenol; D008084:Lipoxygenase; D011451:Prostaglandin-Endoperoxide Synthases