Epinephrine stimulates α, β1 and β2 receptors in vascular smooth muscle cells. It leads to an increase in systolic blood pressure, ventricular contractility, and heart rate, and it causes vasoconstriction in the arterioles of the skin, mucosa, and splanchnic areas, however, dose-dependently vasodilation in skeletal muscle arterioles as a first-line response to stress. Endothelial cells emerge to be target cells as well (26;27). Coactivation of the sympathetic nervous system may lead to indistinguishable coeffects together with norepinephrine. In addition to well characterized chronotropic and inotropic effects on the heart, epinephrine bears a certain antioxidant potential by increasing both the intra- and extracellular superoxide dismutase as a major oxidant-stress defense. Although hydrogen peroxide, the product of the reaction catalyzed by superoxide dismutase still is a reactive oxygen species, it is readily disposed of by both catalase and reduced glutathione. The induction of superoxide dismutase by epinephrine, e.g. during vigorous exercise, increases the amount of hydrogen peroxide that, in turn, is a known activator of eNOS, the endothelial isoform of nitric oxide synthase. Increased amounts of NO may attenuate epinephrine-induced vasoconstriction or promote vasodilation, thereby increasing blood flow, tissue oxygenation and blood-based antioxidative stress responses (28) (Figure 1). In addition, epinephrine increases C-reactive protein (CrP) in a dose-dependent manner, probably via a receptor mechanism (29).

Figure 1. Consequences of disease-related oxidative - stress regarding arteriolar tone. (Solid arrow: stimulation, non-solid arrow: inhibition.)