Objectives: 

This study investigated the influence of chronic social stress produced by crowding on vascular function and nitric oxide (NO) bioavailability in young normotensive and borderline hypertensive (BHR) female rats.

Materials: 

Five-week females of BHR and Wistar-Kyoto (WKY) rats were exposed to crowding for two weeks. Crowding was induced by placement of 5 rats per cage (about 70cm2/100g). Controls were kept 4 rats per cage (about 160cm2/100g). Vascular studies were conducted in the femoral artery by wire myograph. The superoxide production was evaluated using lucigenin enhanced chemiluminiscence and NO synthase activity was determined by conversion of [3H]-L-Arginine to [3H]-L-citrulline in the aorta.

Results: 

Blood pressure (determined by tail-cuff) of 5-week WKY and BHR was 107±2 and 130± 2 mmHg, respectively (p<0.01) and crowding failed to affect it significantly. NO production was significantly higher in the aorta of control BHR vs. WKY (p<0.05) and stress significantly increased NOS activity in both strains vs. the control group. Superoxide level was elevated and NO-dependent component of relaxation was reduced significantly in control BHR vs.WKY. Crowding stress elevated superoxide production and reduced NO-dependent component of relaxation only in WKY while no changes in these parameters were seen in BHR vs. control. There were no differences in overall endothelium-dependent ACh-induced relaxation among the groups investigated.

Conclusions: 

Chronic social stress accelerated oxidative stress and reduced vascular NO bioavailability only in WKY. In BHR, despite reduced basal NO bioavailability, crowding did not modify their oxidative stress and vascular function. Data suggest effective, but qualitatively different, adaptation to crowding stress in young females of both strains. Supported by the grants No. APVV-0523-10 and VEGA 2/0084/10.