title: Leptin modulates electrophysiological characteristics and isoproterenol-induced arrhythmogenesis in atrial myocytes.
abstract: BACKGROUND
  Obesity 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.
  
  
  RESULTS
  Whole 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).
  
  
  CONCLUSIONS
  Leptin regulates the LA electrophysiological characteristics and attenuates isoproterenol-induced arrhythmogenesis.
authors.forename: Yung-Kuo
authors.initials: YK
authors.lastname: Lin
authors.forename: Yao-Chang
authors.initials: YC
authors.lastname: Chen
authors.forename: Jen-Hung
authors.initials: JH
authors.lastname: Huang
authors.forename: Yenn-Jiang
authors.initials: YJ
authors.lastname: Lin
authors.forename: Shiang-Suo
authors.initials: SS
authors.lastname: Huang
authors.forename: Shih-Ann
authors.initials: SA
authors.lastname: Chen
authors.affiliation: Division of Cardiovascular Medicine, Department of Internal Medicine, Wan Fang Hospital, Taipei Medical University, 111, Hsin-Lung Road, Sec, 3, Taipei, Taiwan. a9900112@ms15.hinet.net.
authors.forename: Yi-Jen
authors.initials: YJ
authors.lastname: Chen
mesh_terms: D000200:Action Potentials / Q000187:drug effects*; D000818:Animals; D001281:Atrial Fibrillation / Q000209:etiology*; D006325:Heart Atria / Q000166:cytology / Q000503:physiopathology*; D020738:Leptin / Q000494:pharmacology*; D008297:Male; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000502:physiology; D009765:Obesity / Q000209:etiology; D011817:Rabbits
chemical_list: D020738:Leptin