Norepinephrine is an agonist of α and β1 adrenergic receptors, and causes vasoconstriction. Sympathetic nervous system activation leads to norepinephrine spillover from sympathetic nerve terminals and from adrenal medullary cells. Norepinephrine exerts direct positive inotropic and chronotropic effects in the heart as well as thermogenesis in adipocytes (30). However, increases in blood pressure may attenuate chronotropy and, in turn, result in reflex bradycardia via a baroreflex mechanism. Hypertension is caused by increasing peripheral vascular resistance. Norepinephrine increases oxidative stress (31). Sympathetic denervation worsens a lipopolysaccharide-induced rise of interleukin-6 and, consecutively, CRP. Therefore, one can conclude that the sympathetic nervous system including its main transmitter, norepinephrine, helps inhibit pro-inflammatory stimuli (32).