Role of nitric oxide in the development of glomerular ischemia reperfusion injury in rats

AIM:To investigate the effects of nitric oxide on ultrastructure and anionic sites of glomerular in renal ischemia reperfusion injured (I-RI) rats. METHODS:Animals were divided randomly into five groups:(1) sham group (n=6);(2) I-RI group (n=6), 0.3 mL normal saline was injected via venae lingualis 20 min before ischemia;(3) SNP+I-RI group (n=6), 2.5 μg/kg sodium nitroprusside (SNP) was injected via venae lingualis 20 min before ischemia;(4) AG+I-RI group (n=6), 10 mg/kg aminoguanidine (AG) was injected via venae lingualis 20 min before ischemia;(5) L-NNA+I-RI group (n=6), 10 mg/kg Nω-nitro-L-arginine (L-NNA) was injected via venae lingualis 20 min before ischemia. Anionic sites of glomerular were studied with a cationic probe-polyethyleneimine (PEI) and ultrastructure was observed under electron microscope in renal I-RI rats. RESULTS:(1) Ultrastructure of glomerular was normal and anionic sites (AS) was located clearly in lamina rare externa of GBM in sham rats. The PEI particles arranged regularly in line (19.3±1.7/1 000 nm) under electronic microscope. Obvious foot processes derangement and effacement were observed and the AS number in GBM of I-RI group was fewer (16.6±1.0/1 000 nm, P<0.05) and the particle was smaller than that in sham group. (2) Compared with I-RI group, the foot process effacement was aggravated in SNP+I-RI group and L-NNA+I-RI group. SNP caused the numbers of anionic sites reduced after renal I-RI (11.7±3.2/1 000 nm, P<0.05), and the electronic density of the PEI granule was also reduced. AG lead a increase in anionic site number (17.8±1.0/1 000 nm, P<0.05), but still fewer than that in sham group (P<0.05). The numbers of anionic sites was not changed in L-NNA+I-RI group (14.7±0.9/1 000 nm, P>0.05). CONCLUSION:Foot process effacement and reduction of anionic sites were present in glomerular filtration membrane in renal I-RI rats. NO aggravated those injuries, indicating that NO plays a role in the ultrastructure damages of glomerular filtration membrane in I-RI rats.