Increasing Nitric Oxide Synthase in Human Renal Graft Rejection after Kidney Transplantation

Nitric oxide (NO) is a potent endothelial-drived vasorelaxing factor and may involved in salt sensitive hypertension and renal damage. Nitric oxide is produced from L-arginine by activation of nitric oxide synthase (NOS). Three NOS has been identified which are brain NOS (bNOS), inducible NOS (iNOS) and endothelial NOS (eNOS). On the other hand, renal graft rejection is major problem after kidney transplantation with severe renal damage and renal vasoconstriction. While NOS has been reported localized in human and animal kidney, the status of three NOS in human renal tissue with rejection remains poorly defined. Therefore, the present study was designed to determine the expression of bNOS, iNOS and eNOS by immunohistochemical staining (IHCS) in human renal tissue with rejection and compared with that in normal human renal tissue.Human renal biopsy (n=5) were obtained after kidney transplantation with mild and moderate renal rejection. Normal kidney biopsy was obtained during nephrectomy.