Activation of the SNS in response to stress results in increased secretions of catecholamines, epinephrine and norepinephrine, and higher levels of catecholamines lead to increase in blood pressure and heart rate and more oxygenated blood glucose is required (Cruess et al., 2004). There is evidence that increased SNS activity is a mechanism for atherogenesis, ventricular hypertrophy, and hypertension (Cruess et al., 2004). There is a large body of evidence that perceived stress, personality characteristics, and specific emotion states, including hostility and depression, are linked to decreases in the neurotransmitter serotonin in particular, and depression may have a link to coronary heart disease (CHD) through the serotonergic system (Cruess et al., 2004). Depressive symptoms are often associated with CHD and there are indications that proinflammatory cytokines mediate this relationship (Cruess et al., 2004).

Stress can also have an effect through over activation of the HPA axis. Psychological stressors elicit a physiological response by activating specific cognitive and affective processes and their central nervous system underpinnings (Dickerson and Kemeny, 2004). Sensory information is integrated and the significance of environmental stimuli is appraised through the thalamus and frontal lobes. These cognitive appraisals can elicit emotional responses through the connections from the prefrontal cortex to structures of the limbic system including the amygdala and hippocampus which connect to the hypothalamus and serve as a pathway for activating the HPA axis (Dickerson and Kemeny, 2004). Activation of the HPA axis is initiated by the paraventricular nucleus of the hypothalamus releasing corticotropin releasing hormone, which in turn stimulates the anterior pituitary to secrete adrenocorticotropin hormone (ACTH) which in turn triggers the adrenal cortex to release the glucocorticoid (GC) cortisol into the bloodstream (Dickerson and Kemeny, 2004). GCs act to restore homeostasis. Cortisol affects metabolism by mobilizing energy resources by elevating blood glucose levels; surpresses the immune system by inhibiting proteins that play a central role in regulating inflammation; and affects the cardiovascular system through the catecholamines and other sympathetic products that induce vasoconstriction (Dickerson and Kemeny, 2004; Herman et al., 2003). “Although the effects of catecholamines are almost immediate and transient, cortisol is slower acting and more likely to influence blood flow and glucose production during prolonged stress responses” (Cruess et al., 2004, p. 43). Prolonged cortisol activation brought about by failure to shut down this response after stressor termination or by frequent exposure to stressors is associated with a number of negative health consequences including