Journal
KIDNEY INTERNATIONAL
Volume 79, Issue 1, Pages 57-65Publisher
ELSEVIER SCIENCE INC
DOI: 10.1038/ki.2010.377
Keywords
acute kidney injury; eicosanoids; ischemia/reperfusion
Categories
Funding
- Werner Jackstadt-Stiftung, Wuppertal, Germany
- BMWi, Germany [KF0568201UL7]
- WHS
- USPHS NIH [GM31278]
- Robert A. Welch Foundation
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P01DK038226] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM031278] Funding Source: NIH RePORTER
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20-Hydroxyeicosatetraenoic acid (20-HETE) production is increased in ischemic kidney tissue and may contribute to ischemia/reperfusion (I/R) injury by mediating vasoconstriction and inflammation. To test this hypothesis, uninephrectomized male Lewis rats were exposed to warm ischemia following pretreatment with either an inhibitor of 20-HETE synthesis (HET0016), an antagonist (20-hydroxyeicosa-6(Z), 15(Z)-dienoic acid), an agonist (20-hydroxyeicosa-5(Z), 14(Z)-dienoic acid), or vehicle via the renal artery and the kidneys were examined 2 days after reperfusion. Pretreatment with either the inhibitor or the antagonist attenuated I/R-induced renal dysfunction as shown by improved creatinine clearance and decreased plasma urea levels, compared to controls. The inhibitor and antagonist also markedly reduced tubular lesion scores, inflammatory cell infiltration, and tubular epithelial cell apoptosis. Administering the antagonist accelerated the recovery of medullary perfusion, as well as renal medullary and cortical re-oxygenation, during the early reperfusion phase. In contrast, the agonist did not improve renal injury and reversed the beneficial effect of the inhibitor. Thus, 20-HETE generation and its action mediated kidney injury due to I/R. Whether or not these effects are clinically important will need to be tested in appropriate human studies. Kidney International (2011) 79, 57-65; doi: 10.1038/ki.2010.377; published online 20 October 2010
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