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<p>Stress-induced cardiac injury (SICI) was modeled on female Wistar rats using a 24-h immobilization. SICI was quantified by <sup>99m</sup>Tc-pyrophosphate accumulation in the myocardium. Blockade of β<sub>1</sub>- and β<sub>2</sub>-adrenergic receptors (AR) led to a decrease in SICI. β<sub>1</sub>-AR antagonists nebivolol and atenolol almost completely prevented SICI. The selective β<sub>2</sub>-AR antagonist ICI 118,551 increased SICI, while the selective β<sub>3</sub>-AR antagonist L-748337 did not affect heart damage. The selective β<sub>2</sub>-AR agonist formoterol increased cardiac tolerance to stress. These findings suggest that β<sub>1</sub>-AR play a key role in the pathogenesis of SICI. Stimulation of β<sub>2</sub>-AR enhances cardiac tolerance to stress. β<sub>3</sub>-AR are not involved in the pathogenesis of SICI.</p>

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Role of β-Adrenergic Receptors in Stress-Induced Cardiac Injury

  • 期刊论文

  • 发表日期：

    2025年1月1日

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  • A. A. Boshchenko,
  • B. K. Kurbatov,
  • M. Kilin,
  • L. N. Maslov,
  • N. V. Naryzhnaya,
  • V. V. Saushkin,
  • K. V. Zavadovsky,
  • I. V. Stepanov,
  • S. V. Gusakova,
  • Yu. G. Birulina,
  • T. N. Zaitseva,
  • L. V. Smagliy

摘要

Stress-induced cardiac injury (SICI) was modeled on female Wistar rats using a 24-h immobilization. SICI was quantified by 99mTc-pyrophosphate accumulation in the myocardium. Blockade of β1- and β2-adrenergic receptors (AR) led to a decrease in SICI. β1-AR antagonists nebivolol and atenolol almost completely prevented SICI. The selective β2-AR antagonist ICI 118,551 increased SICI, while the selective β3-AR antagonist L-748337 did not affect heart damage. The selective β2-AR agonist formoterol increased cardiac tolerance to stress. These findings suggest that β1-AR play a key role in the pathogenesis of SICI. Stimulation of β2-AR enhances cardiac tolerance to stress. β3-AR are not involved in the pathogenesis of SICI.