The role of β-adrenergic receptors in stress-induced cardiac injury in a rat model of Takotsubo syndrome

Abstract

Introduction. The pathophysiological mechanisms of cardiac injury in Takotsubo syndrome are currently poorly understood. The role of adrenergic receptor (AR) subtypes in the development of stress-induced myocardial injury (SIMI) remains unclear.Aim. To assess the role of β-ARs in the development of SIMI.Material and Methods. The study was performed using female Wistar rats (n = 84). Rats were subject to 24-hour immobilization in the supine position to simulate SIMI. 99mTc-pyrophosphate radiopharmaceutical was used to determine the degree of cardiac injury.Results. The study showed that β-AR blockade with propranolol reduced the degree of cardiac injury by 38.4%. Selective β1- AR antagonists, atenolol and nebivolol, led to 2.00- and 2.55-fold decreases in 99mTc pyrophosphate accumulation in the heart, respectively. Blockade of β2-ARs by a selective antagonist ICI-118.551 caused an increase in the degree of 99mTc-pyrophosphate accumulation in the heart by 34.6%. A selective β3-AR antagonist L-748337 did not affect 99mTc pyrophosphate accumulation in the heart.Conclusions. The study showed that β1-ARs are involved in the damaging effects of stress on the heart during immobilization stress. β2-AR had a cardioprotective effect in immobilization. β3-AP did not play a significant role in the stress-induced cardiac injury with a single exposure to the stressor.