The role of adrenergic and muscarinic receptors in stress-induced cardiac injury

Takotsubo syndrome (TS) is a rare but dangerous disease that can be fatal. The pathogenesis of TS is not well understood because there is no animal model of TS that fully mimics TS. It has now been documented that stress exposure (24 h) of rats induced the state which is similar TS in human: contracture damage of myofibrils, elevation of the serum creatine kinase MB level, increased Tc-99m-pyrophosphate (Tc-99m-PYP) accumulation in the heart, QTc interval prolongation, and contractility dysfunction of the heart. Immobilization stress resulted in an increase in coronary blood flow. Emotional stress increased the serum catecholamine level. Blockade of beta(1)-adrenergic receptor (AR) prevented stress-induced cardiac injury (SICI). Blockade of beta(2)-AR aggravated stress-induced cardiac injury. Stimulation of beta(2)-AR increased cardiac tolerance to stress. Inhibition of beta(3)-AR, alpha(1)-AR had no effect on SICI. Blockade of peripheral muscarinic receptors or alpha(2)-AR aggravated SICI. Pretreatment with the selective beta(1)-AR antagonist atenolol attenuates stress-induced cardiac contractility dysfunction, but recovery of cardiac contractility is not complete. There is indirect evidence that circulating catecholamines play an important role in SICI. Consequently, the activation of beta(1)-AR plays a significant role in SICI. However, there are other receptors which are also involved in SICI and require further investigation.

Automated summary

Takotsubo syndrome (TS) is a rare and dangerous disease with unclear pathogenesis related to stress exposure, characterized by heart damage and elevated serum creatine kinase MB levels. Research has found that activation of beta(1)-adrenergic receptor (AR) plays a significant role in stress-induced cardiac injury (SICI).