BACKGROUND: The role of @entity35313 and @entity35314 in the saluretic and @entity30750 -angiotensin responses to loop diuretics in the cat is unknown. We propose in vivo characterisation of isoform roles in a @entity1483 model by administering non-steroidal anti-inflammatory drugs (NSAIDs) with differing selectivity profiles: @entity29774 ( @entity35314 selective) and @entity7988 ( @entity35313 selective). RESULTS: In this four period crossover study, we compared the effect of four treatments: placebo, @entity29774 once or twice daily and @entity7988 once daily concomitantly with @entity1483 in seven healthy @entity468 . For each period, urine and blood samples were collected at baseline and within 48  h of treatment starting. Plasma @entity30750 activity (PRA), plasma and urinary @entity1369 concentrations, glomerular filtration rate (GFR) and 24  h urinary volumes, electrolytes and @entity1813 ( @entity1421 , @entity33449 , @entity3448 ), @entity8 biomarker excretions [N-acetyl-beta-D-glucosaminidase (NAG) and Gamma-Glutamyltransferase] were measured. Urine volume (24  h) and urinary @entity1372 , @entity2865 and @entity460 excretions increased from baseline with all treatments. Plasma @entity1011 increased with all treatments except placebo, whereas GFR was significantly decreased from baseline only with @entity7988 . PRA increased significantly with placebo and once daily @entity29774 and the increase was significantly higher with placebo compared to @entity7988 (10.5        4.4 vs 4.9        5.0  ng  ml(-1) h(-1)). Urinary @entity1369 excretion increased with all treatments but this increase was inhibited by 75  % with @entity7988 and 65  % with once daily @entity29774 compared to placebo. Urinary @entity1421 excretion decreased with all treatments and excretion was significantly lower with @entity7988 compared to placebo. Urinary @entity3448 excretion was significantly increased from baseline only with placebo. NAG increased from baseline with all treatments. Immunohistochemistry on post-mortem renal specimens, obtained from a different group of @entity468 that died naturally of non-renal causes, suggested constitutive @entity35313 and @entity35314 co-localization in many renal structures including the @entity1020 ( @entity1020 ). CONCLUSIONS: These data suggest that both @entity35313 and @entity35314 could generate the signal from the @entity1020 to the @entity30750 secreting cells in @entity468 exposed to @entity1483 . Co-localization of COX isoenzymes in @entity1020 cells supports the functional data reported here.

Effect of XXXX and @entity35314 inhibition on @entity1483 -induced renal responses and isoform immunolocalization in the healthy cat kidney.

@entity7988 :: ('MESH:D007660', 'Chemical') :: ['ketoprofen'] @entity8 :: ('MESH:D007674', 'Disease') :: ['renal injury'] @entity1369 :: ('MESH:D000450', 'Chemical') :: ['aldosterone'] @entity35314 :: ('807936(Tax:9685)', 'Gene') :: ['COX-2'] @entity1421 :: ('MESH:D015232', 'Chemical') :: ['PGE2'] @entity2865 :: ('CHEBI:17996', 'Chemical') :: ['chloride'] @entity33449 :: ('CHEBI:28158', 'Chemical') :: ['6-keto-PGF1a'] @entity1483 :: ('MESH:D005665', 'Chemical') :: ['furosemide'] @entity1372 :: ('MESH:D012964', 'Chemical') :: ['sodium'] @entity3448 :: ('CHEBI:28728', 'Chemical') :: ['TxB2'] @entity460 :: ('MESH:D002118', 'Chemical') :: ['calcium'] @entity29774 :: ('MESH:C551524', 'Chemical') :: ['robenacoxib'] @entity1011 :: ('MESH:D003404', 'Chemical') :: ['creatinine'] @entity35313 :: ('807934(Tax:9685)', 'Gene') :: ['cyclooxygenase(COX)-1', 'COX-1'] @entity468 :: ('9685', 'Species') :: ['cats'] @entity1020 :: ('MESH:D008268', 'Disease') :: ['macula densa', 'MD'] @entity1813 :: ('MESH:D015777', 'Chemical') :: ['eicosanoids'] @entity30750 :: ('101081695', 'Gene') :: ['renin']
@entity35313 :: (807934(Tax:9685),Gene) :: ['Cyclooxygenase(COX)-1']
