Objectives: 

In our study we used two inhibitors of NO- synthase, inhibitor of nNOS, 7-nitroindazole (7-NI) and nonspecific inhibitor of nitric oxide, NG-nitro-L-arginine-methyl ester (L-NAME). Despite many experimental studies effect of NOS inhibitors on radical and antioxidant signaling in the heart of young rats is not fully elucidated. The aim of study was to investigate changes in oxidative stress and antioxidant response in NO- deficiency in left ventricle (LV) of young rat heart.

Materials: 

Young male Wistar rats (4 - weeks old) were treated with 7-NI (10 mg/kg/day), L-NAME (50 mg/kg/day) or Control obtained only tap water ad libidum for 6 weeks. Basal blood pressure was measured by tail-cuff method. Gene expression of NADPHox subunit p22phox was determined by real time PCR. The superoxide production was evaluated using Lucigenin - Enhanced Chemiluminiscence. Gene expression of superoxide dismutases (SOD) and nitric oxide synthases (NOS) isoforms was determined using real-time PCR. NOS activity was detected by conversion of [3H]-L-arginine to [3H]-L-citrulline and SOD activity was measured spectrophotometrically by inhibition rate of WST-1 formazan production.

Results: 

Blood pressure was significantly increased only in L-NAME group and only L-NAME administration significantly decreased NOS activity. Expression of p22phox subunit was not change after treatment either with 7-NI or L-NAME and superoxide level was unchanged or decreased only in LV of 7-NI group. However, expression of SOD1 was increased and SOD3 was decreased in L-NAME group, no differences in SOD activity was observed among treated and control groups.

Conclusions: 

Treatment with NOS inhibitors L-NAME or 7-NI in LV of young Wistar heart did not influenced p22phox expression as well as final antioxidant response of SOD activity, however was effective in NOS blockade.

Supported by SAS-NSC JRP 2010/1