Abstract
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.
