Chronic social stress increases nitric oxide-dependent vasorelaxation in normotensive rats

Abstract

The aim of this study was to examine oxidative load and endothelium-dependent vasorelaxation in the serotonin pre-constricted femoral artery (FA) of Wistar-Kyoto (WKY) rats exposed to chronic social stress produced by crowding in the presence or absence of ascorbic acid (AsA) in working solution. Adult male rats were randomly divided into control (living space: 480 cm(2)/rat) or stressed (living space: 200 cm(2)/rat) groups for 8 weeks. Blood pressure and heart rate, determined using tail-cuff plethysmography, were not influenced by stress vs. control. Conjugated dienes (CD) and concentrations of thiobarbituric acid-reactive substances (TBARS) were measured in the left ventricle and liver (for assessment of oxidative load) and were found unchanged by chronic crowding. The nitric oxide (NO)-dependent component of endothelium-dependent relaxation was investigated in the FA using a wire myograph. In both the presence and absence of AsA, acetylcholine-induced relaxation of the FA of stressed rats significantly exceeded that of the controls, which was associated with an increase of the NO-dependent component. In conclusion, the data showed that chronic crowding did not produce oxidative stress in the organs investigated and indicate that elevation of NO production during chronic stress is an important way of adaptation, which may prevent normotensive rats from the development of stress-induced hypertension.

Keywords: ascorbic acid; crowding; endothelium; social stress; vasoconstriction.

Figure 1

Effect of chronic social stress on acetylcholine (ACh)-induced relaxations in absence of ascorbic acid. Endothelium-dependent relaxations before (A,D) and after (B,E) incubation with the nitric oxide (NO) synthase inhibitor N^G-nitro-L-arginine methyl ester (L-NAME); Sodium nitroprusside (SNP) – induced endothelium-independent relaxation (C); NO-dependent component of absolute ACh-induced relaxations (F). Values represent mean ± SEM of 5–7 rats. Abbreviations: AUC-area under the curve; *p<0.05, compared to respective value in control rats; ^††† p<0.001, ^†† p<0.01, ^† p<0.05, compared to respective value in control or stressed rats without L-NAME.

Figure 2

Effect of chronic social stress on acetylcholine (ACh)-induced relaxations in presence of ascorbic acid. Endothelium-dependent relaxations before (A,D) and after (B,E) incubation with the nitric oxide (NO) synthase inhibitor N^G-nitro-L-arginine methyl ester (L-NAME); Sodium nitroprusside (SNP) – induced endothelium-independent relaxation (C); NO-dependent component of absolute ACh-induced relaxations (F). Values represent mean ± SEM of 5–7 rats. Abbreviations: AUC-area under the curve; ***p<0.001, **p<0.01, *p<0.05, compared to respective value in control rats; ^††† p<0.001, ^†† p<0.01, ^† p<0.05, compared to respective value in control or stressed rats without L-NAME.