Takotsubo syndrome (also known as stress-induced cardiomyopathy or takotsubo cardiomyopathy) is an acute, reversible left ventricular dysfunction typically triggered by emotional or physical stress. TS is a rare but dangerous disease. In-hospital mortality in patients with TS is identical to mortality of patients with ST-segment elevation myocardial infarction. There is no obstructive coronary plaque or thrombosis in patients with TS, but there is injury of both cardiomyocytes and endothelial cells. The main manifestations of TS are apical akinesia and apical ballooning. The main cause of death in patients with TS is cardiogenic shock. The excessive release of endogenous catecholamines is a trigger of TS. There is evidence that TS is a consequence of ß1-adrenergic receptor (ß1-AR) overstimulation by catecholamines. The protein kinase A inhibitor H-89 partially reversed stress-induced cardiac injury in rats with TS model (TSM).The ß2-AR antagonist ICI-118,551 exacerbated cardiac injury in TSM. The ß2-AR agonist formoterol partially reversed cardiac injury in TSM. The ß3-AR antagonist L-748337 had no effect on TSM. These findings indicate that the activation of ß1-AR plays a key role in the pathogenesis of cardiac injury in TSM. In contrast, ß2-AR stimulation protects the heart against stress-induced damage. However, there is evidence that ß2-AR overstimulation can cause a negative inotropic effect. It remains unclear why ß1-AR antagonists protect the heart against cardiac injury in TSM, but ß1-AR antagonists do not demonstrate a significant clinical effect in patients with TS. Administration of isoproterenol and immobilization stress can be used for TSM, because both impacts induce apical akinesia, but only immobilization causes apical ballooning. There is indirect evidence on the involvement of progesterone in cardiac injury in TSM. Kulcsszavak: The ß2-AR antagonist ICI-118,551 exacerbated cardiac injury in TSM. The ß2-AR agonist formoterol partially reversed cardiac injury in TSM. The ß3-AR antagonist L-748337 had no effect on TSM. These findings indicate that the activation of ß1-AR plays a key role in the pathogenesis of cardiac injury in TSM. In contrast, ß2-AR stimulation protects the heart against stress-induced damage. However, there is evidence that ß2-AR overstimulation can cause a negative inotropic effect. It remains unclear why ß1-AR antagonists protect the heart against cardiac injury in TSM, but ß1-AR antagonists do not demonstrate a significant clinical effect in patients with TS. Administration of isoproterenol and immobilization stress can be used for TSM, because both impacts induce apical akinesia, but only immobilization causes apical ballooning. There is indirect evidence on the involvement of progesterone in cardiac injury in TSM.  Kulcsszavak: stress-induced cardiac injury, takotsubo syndrome, adrenergic receptors, microvascular obstruction, microvascular injury