Distinct role of intrarenal cyclooxygenase-1/2 in chronic XXXX .

@entity10964 @entity8 @entity63 @entity235 @entity1421 @entity15632 @entity2918 @entity1372 @entity9077 @entity4873 @entity9694 @entity8228
AIMS: The role of @entity9694 /2-induced @entity2918 (PG) in unilateral chronic @entity8 of anesthetized @entity235 was examined. METHODS: @entity63 kidneys were established by reducing renal blood flow of left renal artery to 10% of baseline with an adjustable clip. After 4 weeks, changes in intrarenal contents of @entity1421 /PGI2 and angiotensin (Ang) II were evaluated with renal microdialysis and biopsy. Furthermore, the effect of a non-specific COX inhibitor ( @entity10964 ), a @entity4873 -specific inhibitor ( @entity8228 ), and an Ang receptor antagonist ( @entity15632 ) on renal function and renal PG contents were evaluated. RESULTS: Unilateral renal artery clipping reduced renal plasma flow (RPF) in clipped (from 59 +/- 2 to 17 +/- 1 ml/min, n = 18) and nonclipped kidneys (from 59 +/- 2 to 44 +/- 2 ml/min) and natriuresis. Intrarenal @entity1421 increased only in clipped kidneys (from 114 +/- 7 to 375 +/- 25 pg/ml), whereas @entity9077 increased in both kidneys. @entity10964 reduced intrarenal PG contents, and decreased RPF, GFR, and urinary @entity1372 excretion (UNaV), whereas @entity8228 reduced UNaV in clipped (from 4.0 +/- 0.9 to 1.7 +/- 0.2 microEq/min) and nonclipped kidneys (from 5.4 +/- 0.5 to 2.9 +/- 0.3 microEq/min), without affecting renal hemodynamics. Intrarenal Ang II contents increased in clipped (from 0.70 +/- 0.06 to 2.32 +/- 0.33 pg/mg, n = 18) and nonclipped kidneys (from 0.65 +/- 0.06 to 2.45 +/- 0.33 pg/mg, n = 18), and @entity15632 improved renal hemodynamics and natriuresis. The elevated intrarenal Ang II content was suppressed by @entity8228 only in clipped kidneys. CONCLUSION: Unilateral @entity8 elevates intrarenal @entity1421 contents in clipped kidneys, which serves to countervail the aggravation of renal function. Furthermore, intrarenal COX isoforms may play differential roles, with @entity9694 participating in modulation of renal hemodynamics, and @entity4873 contributing to @entity1372 excretion and Ang II formation.
