Exaggerated renal pathology of partial ablation-induced chronic renal failure in eNOS deficient mice.
We investigated the role of endothelial nitric oxide synthase (eNOS) in the remnant kidney model of chronic renal failure, by using eNOS-deficient (eNOS-/-) and wild-type mice. There were significant increments of blood urea nitrogen level, plasma creatinine concentration and proteinuria in both wild-type and eNOS-/- mice at 8 weeks after 5/6 nephrectomy, but observed changes were more prominent in eNOS-/- mice. Only 7 out of 30 eNOS-/- mice were alive during 8-week experimental period, whereas survival rate in the wild-type mice was 69%. The glomerular size distribution indicated that the glomeruli of 5/6 nephrectomized eNOS-/- mice tended to be larger compared with cases of wild-type mice. It seems likely that eNOS-derived NO is protective against renal injuries in this disease model.
Yamashita
Chika
C
Laboratory of Pathological and Molecular Pharmacology, Osaka University of Pharmaceutical Sciences, 4-20-1 Nasahara, Takatsuki, Osaka 569-1094, Japan.
Tazawa
Naoko
N
Ohkita
Mamoru
M
Matsumura
Yasuo
Y
D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D001806:Blood Urea Nitrogen; D001835:Body Weight / Q000502:physiology; D003404:Creatinine / Q000097:blood / Q000652:urine; D007668:Kidney / Q000473:pathology*; D007676:Kidney Failure, Chronic / Q000235:genetics* / Q000473:pathology*; D007677:Kidney Function Tests; D007678:Kidney Glomerulus / Q000473:pathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009392:Nephrectomy; D052250:Nitric Oxide Synthase Type III / Q000172:deficiency* / Q000235:genetics*; D009929:Organ Size / Q000502:physiology; D011507:Proteinuria / Q000235:genetics; D013534:Survival
D003404:Creatinine; D052250:Nitric Oxide Synthase Type III