Abstract
BackgroundObesity is an important risk factor for atrial fibrillation (AF). Leptin is an important adipokine. However, it is not clear whether leptin directly modulates the electrophysiological characteristics of atrial myocytes.ResultsWhole cell patch clamp and indo-1 fluorescence were used to record the action potentials (APs) and ionic currents in isolated rabbit left atrial (LA) myocytes incubated with and without (control) leptin (100 nM) for 1 h to investigate the role of leptin on atrial electrophysiology. Leptin-treated LA myocytes (n = 19) had longer 20% of AP duration (28 ± 3 vs. 21 ± 2 ms, p < 0.05), but similar 50% of AP duration (51 ± 4 vs. 50 ± 3 ms, p > 0.05), and 90% of AP duration (89 ± 5 vs. 94 ± 4 ms, p > 0.05), as compared to the control (n = 22). In the presence of isoproterenol (10 nM), leptin-treated LA myocytes (n = 21) showed a lower incidence (19% vs. 54.2%, p < 0.05) of delayed afterdepolarization (DAD) than the control (n = 24). Leptin-treated LA myocytes showed a larger sodium current, but a smaller ultra-rapid delayed rectifier potassium current, and sodium-calcium exchanger current than the control. Leptin-treated and control LA myocytes exhibited a similar late sodium current, inward rectifier potassium current, transient outward current and L-type calcium current. In addition, the leptin-treated LA myocytes (n = 38) exhibited a smaller intracellular Ca2+ transient (0.21 ± 0.01 vs. 0.26 ± 0.01 R410/485, p < 0.05) and sarcoplasmic reticulum Ca2+ content (0.35 ± 0.02 vs. 0.43 ± 0.03 R410/485, p < 0.05) than the control LA myocytes (n = 42).ConclusionsLeptin regulates the LA electrophysiological characteristics and attenuates isoproterenol-induced arrhythmogenesis.
Highlights
Obesity is an important risk factor for atrial fibrillation (AF)
Obesity increase the prevalence of hypertension, ischemic heart disease, congestive heart failure, and ventricular dysfunction, which can contribute to the development of AF [6,7,8,9]
In the presence of isoproterenol (10 nM), leptin- treated left atrial (LA) myocytes exhibited a lower incidence of delayed afterdepolarization (DAD) than the control myocytes (Figure 1B)
Summary
Obesity is an important risk factor for atrial fibrillation (AF). It is not clear whether leptin directly modulates the electrophysiological characteristics of atrial myocytes. Obesity increase the prevalence of hypertension, ischemic heart disease, congestive heart failure, and ventricular dysfunction, which can contribute to the development of AF [6,7,8,9]. Leptin signaling has been shown to contribute to atrial fibrosis and angiotensin II-evoked AF [29]. These findings suggest that leptin may play a critical role in cardiac electrophysiology. The purpose of this study was to investigate the effect of leptin on the electrophysiological characteristics of atria myocytes and its role in atrial arrhythmogenesis
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