Adrenergic and noradrenergic systems in panic/anxiety
The adrenergic and noradrenergic systems have long been studied in relation to physical and psychological stress. Together with glucocorticoids, catecholamines are implicated in the mobilization of forces in the case of threat. In such a situation, the body goes through a fight or flight reaction which is accompanied by peripheral secretion of catecholamines and glucocorticoids (Carlson, 1992). These hormones increase the availability of the body energy by glycogenolysis in liver and skeletal muscles thus raising the blood glucose and lactate, lipolysis in adipose tissue, mobilization of free fatty acids, and by increasing temperature. Both epinephrine and norepinephrine also dilate coronary blood vessels. While norepinephrine produces vasoconstriction in skin, mucosa, skeletal muscles and most other organs, epinephrine dilates veins in skeletal muscles. These effects result in hypertension and consequently in reflex bradycardia. Other symptoms of a sympatho-adrenergic stimulation involve modifications of breathing, increased temperature, localized sweating, decreased motility and tone of stomach and intestine, constrictions of sphincters in stomach and intestine as well as piloerection (Ganong, 1969). As mentioned above, many symptoms of the sympathetic activation are parts of the panic attack experience. This similarity makes the aminergic systems, especially noradrenergic and adrenergic functions, the most obvious paths to follow in the study of panic disorder. Indeed, numerous studies have explored them using human models of anxiety and panic or their animal parallels. Various positive or negative emotions, and anxiety, stress and fear among them, are accompanied by an increased release of catecholamines into the blood stream (Kopin, 1984). Breggin (1964) reported a study with healthy subjects in whom emotional stress resulted in increased concentrations of epinephrine and norepinephrine in urine and plasma. Both animal and human studies show that norepinephrine and epinephrine turnover is increased by stress.