The Sympatho AdrenalMedullary System

The adrenal medulla is an ontogenetic peculiarity: Being derived from the embryonic neural crest, it consists of modified postganglionic neurons belonging to the sympathetic branch of the autonomic nervous system. Its chromaffin cells, innervated by the splanchnic nerve, secrete the catecholamines epinephrine and norepinephrine directly into the blood stream. However, the major part of plasma norepinephrine, i.e., approx. 65%, is not of adrenal origin, but secreted by sympathetic nerve endings. As catecholamines do not cross the blood-brain barrier, their effects are mostly peripheral (Kvetnansky and McCarthy, 2007; Tentolouris et al, 2006).

The seminal role of adrenal hormones during stress was first reviewed by Cannon (1914), who summarized their actions as the "fight-or-flight reaction," with life-saving effects for the organism. Epinephrine and norepinephrine increase heart rate, the force of heart contraction and cardiac output, shift the blood supply to coronary arteries, skeletal muscle and the brain, while blood supply of skin, kidney, and mucosa is diminished. They reduce time for blood clotting through effects on blood platelets, reinforce glucagon-induced glycogenolysis, glucose production in the liver and lipolysis in adipose cells. Thus, through their actions, organ systems critical to survival are provided with energy and, via bronchodilatation, supplied with additional oxygen (Pollard, 2000).

Epinephrine and norepinephrine blood levels increase rapidly in response to challenge (<1 min). Epinephrine is furthermore very reactive to novelty, which should be considered when studying stress effects under laboratory conditions. In emergency medicine, epinephrine is administered in life-threatening conditions such as shock and cardiac arrest. On the other hand, increased catecholamine secretion during chronic stress may burden organ systems and may be involved in the pathogenesis of stress-related health impairments, such as atherosclerosis, myocardial ischemia, hypertension, and coronary heart disease (Lundberg, 2000). Of note, while cortisol responses habituate in the face of repeated stress exposure, catecholamine responses do not (Schommer et al, 2003).

In hypertension, a role for elevated norepinephrine levels has been established (DeQuattro and Feng, 2002). Epinephrine may furthermore interact with immune functions. In HIV, stress may be involved in disease progression partly due to epinephrine effects on HIV-infected leucocytes (Cole, 2008). In psoriasis and atopic dermatitis, a hyperre-sponsive plasma catecholamine response to psychosocial stress may be involved in dysreg-ulations in Th1/Th2 mediated immune states (Buske-Kirschbaum et al, 2006). The sympatho-adrenal-medullary system may also play a role in the pathogenesis of obesity. Epinephrine affects resting metabolic rate, lipolysis, and thermogenesis SNS overactivity is associated to visceral obesity (Tentolouris et al, 2006). Through actions on ascending vagal afferents, elevated systemic levels of epinephrine may possibly affect cognitive processes, such as memory and attention. An inverted U shape of catecholamine actions has been proposed, with moderate levels being beneficial, while low or high levels impairing cognitive performance (Lundberg, 2000; Roozendaal et al, 2009).

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