Stress exposure activates sympathoneural system resulting in noradrenaline release. The sympathoneural system plays an important role in regulating cardiac function in both health and disease. The activity of sympathoneural system is dependent on the synthesis of noradrenaline, as determined by the rate-limiting enzymes tyrosine hydroxylase (TH), its reuptake through the noradrenaline transporter (NET), synaptic release, degradation and vesicular transport mediated by the vesicular monoamine transporter 2 (VMAT2). Functional noradrenergic transmission consists of a balance between noradrenaline synthesis, release and reuptake. Depletion of cardiac noradrenaline stores contribute to the progressive deterioration of cardiac function and decrease myocardial contractility (Liang C, 2007). Therefore, we examined changes in noradrenaline stores and protein levels of TH, NET and VMAT 2 in the right and left ventricle of chronic individually housed Wistar male rats. Animals remained for 12 weeks in individual housing, during this period visual isolation was guaranteed by white paper walls surrounding the cage. Chronic social isolation reduced noradrenaline content in the left ventricle. The protein levels of TH and NET in both ventricles were unchanged. However, in the right ventricle protein levels of VMAT2 were increased (p<0.05), whereas in the left ventricle VMAT2 protein levels were significantly decreased (p<0.05). Guillot and Miller (2009) described protective actions of the VMAT 2 in monoaminergic neurons, so packaging of catecholamine into vesicle serves two purposes: neurotransmission and neuroprotection. Since VMAT2 provides neuroprotection from toxicant, it could be hypothesized that decreased VMAT2 protein in the left ventricle may enhance oxidative stress in sympathetic nerves which innervate heart. Kristen and coworkers (2006) reported that in volume-overloaded hypertrophic hearts depletion of cardiac noradrenaline stores is caused by reduction of the sympathetic nerve density. Adult sympathetic neurons whose axons have been damaged decrease expression of noradrenaergic genes and production of noradrenaline (Pellegrino et al., 2011). Our data indicate differential changes in the status of sympathetic nerves in the right and left ventricles. Thus, the finding of increased expression of VMAT2 in the right ventricle would be consistent with increased capacity of noradrenaline storage, as an important adaptation to chronic stress, whereas depletion of noradrenaline stores in the left ventricle may be due to reduced VMAT2.