β1-Adrenoceptor Autoantibodies Affect Action Potential Duration and Delayed Rectifier Potassium Currents in Guinea Pigs

详细信息    查看全文

• 作者：Yuhui Zhao ; Haixia Huang ; Yunhui Du ; Xiao Li ; Tingting Lv…
• 关键词：β1 ; Adrenoceptor ; Autoantibody ; Action potential ; Delayed rectifier potassium current
• 刊名：Cardiovascular Toxicology
• 出版年：2015
• 出版时间：January 2015
• 年：2015
• 卷：15
• 期：1
• 页码：1-9
• 全文大小：1,326 KB
• 参考文献：1. Herren, A. W., Bers, D. M., & Grandi, E. (2013). Post-translational modifications of the cardiac Na channel: Contribution of CaMKII-dependent phosphorylation to acquired arrhythmias. / American Journal of Physiology-heart and Circulatory Physiology, / 305, H431–H445. CrossRef
  2. Bozdogan, O., Kaya, S. T., Yasar, S., & Orallar, H. (2013). Effect of ATP-dependent channel modulators on ischemia-induced arrhythmia change depending on age and gender. / Experimental Biology and Medicine, / 238, 1170-179. CrossRef
  3. Le, Q. K., Benito, B., Naud, P., Qi, X. Y., Shi, Y. F., Tardif, J. C., et al. (2013). T-type calcium current contributes to escape automaticity and governs the occurrence of lethal arrhythmias after atrioventricular block in mice. / Circulation-arrhythmia and Electrophysiology, / 6, 799-08. CrossRef
  4. Snyder, D. J. (2000). Molecular biology of potassium channels. In D. P. Zipes & J. Jalife (Eds.), / Cardiac electrophysiology: From cell to bedside (pp. 21-1). Philadelphia: Saunders W. S.
  5. Cui, J., Melman, Y., Palma, E., Fishman, G. I., & McDonald, T. V. (2000). Cyclic AMP regulates the HERG K⁺ channel by dual pathways. / Current Biology, / 10, 671-74. CrossRef
  6. Marx, S. O., Kurokawa, J., Reiken, S., Motoike, H., D’Armiento, J., Marks, A. R., et al. (2002). Requirement of a macromolecular signaling complex for beta adrenergic receptor modulation of the KCNQ1–KCNE1 potassium channel. / Science, / 295, 496-99. CrossRef
  7. Brodde, O. E. (1991). Beta 1- and beta 2-adrenoceptors in the human heart: Properties, function, and alterations in chronic heart failure. / Pharmacological Reviews, / 43, 203-42.
  8. Harmati, G., Banyasz, T., Barandi, L., Saentandrassy, N., Horvath, B., Szabo, G., et al. (2011). Effects of & #x03B2;-adrenoceptor stimulation on delayed rectifier K(+) currents in canine ventricular cardiomyocytes. / British Journal of Pharmacology, / 162, 890-96. CrossRef
  9. Wallukat, G., & Wollenberger, A. (1987). Effects of serum gamma globulin fraction of patients with allergic asthma and dilated cardiomyopathy on chronotropic beta adrenoceptor function in cultured neonatal rat heart myocytes. / Biomedica Biochimica Acta, / 46, 634-39.
  10. Ma, X. R., Duan, J. L., Zuo, L., Wang, J., Yan, Z., Zheng, R. H., et al. (2010). The proarrhythmic effects of autoantibody against beta1 adrenergic receptor. / Zhongguo Ying Yong Sheng Li Xue Za Zhi, / 26, 257-60.
  11. Zipes, D. P. (1991). Sympathetic stimulation and arrhythmias. / New English Journal of Medicine, / 325, 656-57. CrossRef
  12. Christ, T., Wettwer, E., Dobrew, D., Adolph, E., Knaut, M., Wallukat, G., et al. (2001). Autoantibodies against the beta-1 adrenoceptor prolong action potential duration and enhance contractility in isolated cardiomyocytes. / Journal of Molecular and Cellular Cardiology, / 33, 1515-525. CrossRef
  13. Wang, Y. Y., Ma, Z. Y., Li, X. D., Wang, J. C., Zhang, W., Li, L., et al. (2012). Serum positive for the autoantibody against the β(1)-adrenoceptor from Chinese patients with congestive heart failure decreases I(ss) in mouse cardiac myocytes. / Clinical and Developmental Immunology, / 113, 3218-228.
  14. Medei, E. H., Nascimento, J. H., Pedrosa, R. C., Barcellos, L., Masuda, M. O., Sicouri, S., et al. (2008). Antibodies with beta-adrenergic activity from chronic chagasic patients modulate the QT interval and M cell action potential duration. / Europace, / 10, 868-76. CrossRef
  15. Katritsis, D. G., & Camm, A. J. (2004). Nonsustained ventricular tachycardia: Where do we stand? / European Heart Journal, / 25, 1093-099. CrossRef
  16. Gowdak, L. H., de Paula, F. J., Cesar, L. A., Bortolotto, L. A., & de Lima, J. J.
• 作者单位：Yuhui Zhao (1)
  Haixia Huang (1)
  Yunhui Du (1)
  Xiao Li (1)
  Tingting Lv (1)
  Suli Zhang (1)
  Hua Wei (2)
  Jianyu Shang (1)
  Ping Liu (1)
  Huirong Liu (1) (3)
  
  1. Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, 100069, China
  2. Medical Experiment and Test Center, Capital Medical University, Beijing, 100069, China
  3. Beijing Key Laboratory of Metabolic Disturbance Related Cardiovascular Disease, Beijing, 100069, China
  
• 刊物主题：Pharmacology/Toxicology; Cardiology;
• 出版者：Springer US
• ISSN：1559-0259

文摘

β1-Adrenoceptor autoantibodies (β1-AAs) affect the action potential duration (APD) in cardiomyocytes and are related to ventricular arrhythmias. The delayed rectifier potassium current (I K) plays a crucial role in APD, but the effects of β1-AAs on I K have not been completely illuminated. This work aimed to observe the effects of β1-AAs on I K and APD and further explore the mechanisms of β1-AA-mediated ventricular arrhythmias. β1-AAs were obtained from sera of patients with coronary heart disease (CHD) and nonsustained ventricular tachycardia. With whole-cell patch clamp technique, action potentials and I K were recorded. The results illustrated 0.1?μmol/L β1-AAs shortened APD at 50?% (APD50) and 90?% (APD90) of the repolarization. However, at 0.01?μmol/L, β1-AAs had no effects on either APD90 or APD50 (P?>?0.05). At 0.001?μmol/L, β1-AAs significantly prolonged APD90 and APD50. Moreover, β1-AAs (0.001, 0.01, 0.1?μmol/L) dose-dependently increased the rapidly activating delayed rectifier potassium current (I Kr), but similarly decreased the slowly activating delayed rectifier potassium current (I Ks) and increased L-type calcium currents at the different concentrations. Taken together, the IKr increase induced by high β1-AA concentrations is responsible for a significant APD reduction which would contribute to repolarization changes and trigger the malignant ventricular arrhythmias in CHD patients.