In contrast, endothelin exhibits mainly vasoconstrictor properties. High levels of endothelin can increase renal vascular resistance, reduce renal plasma flow, reduce coronary blood flow, and cause hypertension. It has been suggested that the elaboration of endothelin in the kidney may play a role in the pathophysiology of postischemic acute renal failure. Endothelial damage could therefore result from an imbalance between the vasodilatory properties of EDRF and prostacyclin and the vasoconstricting properties of endothelin. This imbalance provides the focus for nutritional manipulation.
Cellular Nutritional Approach
Eicosanoids of the 2-series prostaglandins (PGES, PGI,, TXA) and the 4-series leukotrienes (LTB4, LTD4, LTEJ are potent inflammatory mediators synthesized from arachido-nic acid (AA) (20:4o>6), an omega-6 polyunsaturated fatty acid (o>-6 PUFA) derived from linoleic acid (18:2a>6). Currently, the long-chain triglyceride (LOT) used in parenteral and enteral nutritional regimens is provided by soybean and safflower oils. These oils, which contain mainly linoleic acid, may induce additional elaboration of the eicosanoids. Consequently, reduced prostacyclin synthesis by the damaged endothelium* is of particular importance, since endothelial cell damage is enhanced by TXA^-induced platelet aggregation and by LTB4-enhanced leukocyte accumulation.
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