科研之友
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摘要
Cardiac electrophysiological function is under the regulatory control of the sympathetic nervous system. In addition to classical beta-adrenoceptors (beta-AR, including beta(1)- and beta(2)- subtypes), beta(3)-AR is also expressed in human heart and shows its distinctive functions. This study is aimed to elucidate the role of beta(3)-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 beta(3)-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 beta(3)-AR agonist, leading to the increase of AF inducibility and duration. Similarly, beta(3)-AR activation induced time-dependent shortening of action potential duration (APD), together with decrease of L-type calcium current (I-Ca,I-L) and increase of inward rectifier potassium current (I-K1) and transient outward potassium current (I-to) in rapid pacing atrial myocytes. Meanwhile, all the effects were abolished by specific beta(3)-AR antagonist, SR59230A. In summary, our study represents that activation of beta(3)-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 beta(3)-AR in heart diseases.
- 出版日期2011
- 单位哈尔滨医科大学
