IMR Press / RCM / Volume 19 / Issue 3 / DOI: 10.31083/j.rcm.2018.03.3181
Open Access Original Research
Activation of β1-adrenoceptors may not be involved in arrhythmogenesis in ischemic heart disease
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1 Department of Pharmacology and Toxicology, Faculty of Pharmacy, Comenius University, Bratislava, Slovak Republic, 832 32
2 2Department of Physiology & Pathophysiology and Institute of Cardiovascular Sciences, Max Rady College of Medicine, St.Boniface Hospital Albrechtsen Research Centre, University of Manitoba, Winnipeg, R2H 2A6, Canada

*Correspondence: (Naranjan S. Dhalla)

Rev. Cardiovasc. Med. 2018, 19(3), 97–101;
Published: 30 September 2018

Although ischemic heart disease is invariably associated with marked activation of sympathetic nervous system, elevated levels of circulating catecholamines and lethal ventricular arrhythmias, the mechanisms of arrhythmogenesis due to myocardial ischemia are not fully understood. Since catecholamines are known to produce stimulatory effects in the heart mainly by acting on β1-adrenoceptors, this study was undertaken to test the involvement of these receptors in the development of arrhythmias due to myocardial infarction (MI) induced upon occluding the left coronary artery in rats for a period of 2 h. The animals were treated with or without atenolol (20 mg/kg; daily), a selective β1-adrenoceptors blocker, for 14 days before inducing MI. No alterations in the number of MIinduced episodes and incidence or duration of different types of arrhythmias were observed. In fact, the incidence of trigemines and reversible ventricular fibrillation due to MI were significantly increased in the atenolol-treated animals. These observations support the view that the activation of β1-adrenoceptors may not be exclusively involved in the development of arrhythmias during the occurrence of ischemic heart disease and other mechanisms can underlie the electric instability of such damaged heart.

myocardial ischemia
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