Although the modern lifestyle in industrial cities with a high population density is a risk factor in the development of lifestyle-related diseases, including cardiovascular and mental disorders, the causal role of stress in the aetiology of cardiovascular diseases is not understood satisfactorily. Furthermore age, sex and family history of hypertension represent important issues that may interact with environmental factors and participate in development of cardiovascular disorders.The aim of this study was to investigate the influence of chronic social stress produced by crowding on blood pressure (BP), vascular function and nitric oxide (NO) production in young normotensive Wistar-Kyoto (WKY), borderline hypertensive (BHR) and spontaneously hypertensive (SHR) rats of both sexes. Five-week males and females of WKY, BHR (F1 offspring of SHR dames and WKY sires) and SHR were exposed to stress produced by crowding (5 rats/cage, 70 cm2/100g, n=10) for two weeks as described previously (1). Controls were kept 4 rats/cage (200 cm2/100g, n=8). Blood pressure (BP) was determined by tail-cuff method. Vascular function (endothelium-dependent acetylcholine (ACh)-induced relaxation and its components) of the femoral artery was investigated using wire myograph. NO synthase activity was determined by conversion of [3H]-L-arginine in the aorta and brainstem. Results were analysed by ANOVA and Bonferroni post-hoc test and they are presented as mean±SEM.Basal BP of 5-week-old male and female WKY, BHR and SHR was 104±2 and 103±2 mmHg, 127±3 and 115±4 mmHg and 140±3 and 137±2 mmHg, respectively (p<0.001 among strains). Two-week crowding accelerated BP increase in both BHR males and females (p<0.01) vs. basal which was not seen in WKY and SHR. In SHR similar time-related elevation of BP was observed in control and stressed groups at the end of experiment. However, a significant BP elevation was seen in SHR males after the 1st week of stress (vs. control), which was not observed in females. There was significantly higher BP in males vs. females during the experiment (131±2 vs. 125±2 mmHg, p<0.0001). Stress significantly reduced body weight gain (p<0.0001) and elevated plasma corticosterone (p<0.01) and BP (p<0.001) vs. control rats, however these effects were the most pronounced in BHR strain. Blood glucose was reduced in stressed males while no changes were observed in females vs. non-stressed rats. NO synthase activity in the aorta of control BHR and SHR females was significantly higher vs. WKY (p<0.05) and stress elevated NOS activity in females of all strains investigated vs. control. In males, aortic NO production was elevated only in control SHR vs. WKY and interestingly no effect of stress was seen in young males. However, stress reduced NO production in the brainstem of both males and females of WKY and BHR while no effect was observed in SHR of both sexes. Endothelial dysfunction was observed in SHR strain vs. both WKY and BHR. Stress did not affect vascular function in females significantly in any strain despite quantitative alterations of its NO-dependent and NO-independent components. However, in males stress paradoxically improved endothelium-dependent ACh-induced relaxation in SHR vs. control, which was associated with an elevation of NO-independent component of relaxation without changes in NO-dependent relaxation. In conclusion, results showed that the influence of chronic social stress produced by crowding in young rats depends on the genetic predisposition to hypertension (in both males and females). WKY rats were able to adapt to stress while BHR were the most vulnerable to stress-induced elevation of BP. In contrast, genetic predisposition to hypertension is a dominant factor in hypertension development in SHR. Finally, differences in stress-induced time course of BP increase, mechanism of vascular function and NO production were observed in young males and females.