renal/urinary system
N |
• unlike mice homozygous for Ptgs2tm1.1Fun, no signs of perivascular to interstitial inflammation are seen
|
• decrease in the urine level of 2,3-dinor-6-keto-PGF1alpha, the major urinary metabolite of prostacyclin metabolism
|
• moderate multifocal hypoplasia of glomerular tufts within the superficial renal cortex
• mild, multifocal glomerular hyperplasia within the deeper cortex
|
• mild to moderate, multifocal tubular degeneration and regeneration particularly within the superficial cortex
|
homeostasis/metabolism
• following vessel injury with FeCl3 the overall formation of platelet aggregates is increased compared to wild-type controls
|
• mild increase
|
• increase in the propensity for thrombogenesis in response to FeCl3 induced injury
|
• decrease in the urine level of 2,3-dinor-6-keto-PGF1alpha, the major urinary metabolite of prostacyclin metabolism
|
cardiovascular system
N |
• despite association of PTGS2 inhibition with moderate risk of hypertension, blood pressure is not significantly different from wild-type controls
|
hematopoietic system
• following vessel injury with FeCl3 the overall formation of platelet aggregates is increased compared to wild-type controls
|