Endogenous catecholamines noradrenaline, adrenaline and dopamine have a significant role in the functioning of several organ systems including the cardiovascular one. Noradrenaline is the principal neurotransmitter in the post-ganglionic neurons of the sympathetic nerve system, while adrenaline and, to a lesser extent, noradrenaline are secreted from the adrenal medulla. All these mechanisms are involved in the stressful reaction to various stimuli as part of the fight-or-flight reaction. There are a number of pathological conditions where excessive production of catecholamines results in overstimulation of the adrenergic receptors, which are responsible for hypertension, tachycardia, coronary vasospasm and cardiac ischaemia, resulting in myocardial injury. Such conditions include Pheochromocytoma and takotsubo syndrome. Xenobiotics can also damage the cardiovascular system via the adrenergic receptors and they can be divided into direct adrenoceptor agonists (eg, isoprenaline), indirect sympathomimetics, acting via the excessively liberated noradrenaline (eg, amphetamines, cocaine), and mixed-action sympathomimetics that act in both manners (eg, ephedrine). The main recognised mechanisms of catecholamine-induced myocardial injury are myocardial ischemia, coronary insufficiency, intracellular calcium (Ca2+) overload, mitochondrial dysfunction, depletion of high-energy phosphate stores, increased membrane permeability, electrolyte content changes, alterations in metabolism and oxidative stress. Oxidation products of catecholamines—adrenochromes—can also be the cause of myocardial necrosis.