Abstract
Cardiac electrophysiological function is under the regulatory control of the sympathetic nervous system. In addition to classical β-adrenoceptors (β-AR, including β<sub>1</sub>- and β<sub>2</sub>- subtypes), β<sub>3</sub>-AR is also expressed in human heart and shows its distinctive functions. This study is aimed to elucidate the role of β<sub>3</sub>-AR in the regulation of atrial fibrillation (AF), especially its role in rapid pacing-induced atrial electrical remodeling in rabbits. The rapid atrial pacing model was established by embedding electrodes in the right atrium pacing at a speed of 600 beats per minute. The protein level of β<sub>3</sub>-AR in the atria was found significantly upregulated by western blot. The atrial effective refractory period (AERP) and its rate adaptation were decreased after pacing which were further shortened by BRL37344, a selective β<sub>3</sub>-AR agonist, leading to the increase of AF inducibility and duration. Similarly, β<sub>3</sub>-AR activation induced time-dependent shortening of action potential duration (APD), together with decrease of L-type calcium current (I<sub>Ca,L</sub>) and increase of inward rectifier potassium current (I<sub>K1</sub>) and transient outward potassium current (I<sub>to</sub>) in rapid pacing atrial myocytes. Meanwhile, all the effects were abolished by specific β<sub>3</sub>-AR antagonist, SR59230A. In summary, our study represents that activation of β<sub>3</sub>-AR promotes the atrial electrical remodeling process by altering the balance of ion channels in atrial myocytes, which provides new insights into the pharmacological role of β<sub>3</sub>-AR in heart diseases.
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