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1 Department of Human Nutritional Sciences, University of Manitoba, Winnipeg, Manitoba, Canada
2 Department of Human Nutritional Sciences, University of Manitoba, Winnipeg, Manitoba, Canada; Department of Pediatrics and Child Health, University of Manitoba, Winnipeg, Manitoba, Canada
* To whom correspondence should be addressed. E-mail: aukema{at}umanitoba.ca.
Renal prostanoids are important regulators of normal renal function and maintenance of renal homeostasis. In diseased kidneys renal cylooxygenase (COX) expression and prostanoid formation are altered. Using the Han:Sprague-Dawley-cy rat, the aim of this study was to determine the relative contribution of renal COX isoforms (protein, gene expression and activity) on renal prostanoid production [thromboxane B2 (TXB2, stable metabolite of TXA2), prostaglandin E2 (PGE2) and 6-keto-prostaglandin F1a (6-keto- PGF1a, stable metabolite of PGI2)] in normal and diseased kidneys. In diseased kidneys, COX-1 immunoreactive protein and mRNA levels were higher and COX-2 levels were lower when compared to normal kidneys. In contrast, COX activities were higher in diseased compared to normal kidneys for both COX-1 [0.05[[plusmn]0.02 vs. 0.45±0.11 ng prostanoids/min/mg protein (P<0.001)] and COX-2 [0.64±0.10 vs. 2.32±0.22 ng prostanoids/min/mg protein (P<0.001)]. As the relative difference in activity was greater for COX-1, the ratio of COX-1/COX-2 was higher in diseased compared to normal kidneys, although the predominant activity was still due to the COX-2 isoform in both genotypes. Endogenous and steady-state in vitro levels of prostanoids were ~2-10 times higher in diseased compared to normal kidneys. The differences between normal and diseased kidney prostanoids was in the order of TXB2 > 6-keto-PGF1a > PGE2, as determined by higher renal prostanoid levels and COX activity ratios of TXB2/6-keto- PGF1a, TXB2/PGE2 and 6-keto-PGF1a /PGE2 . This specificity in both the COX isoform type and for the prostanoids produced has implications for normal and diseased kidneys in treatments involving selective inhibition of COX isoforms.
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