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Influence of Thromboxane A2 on the Regulation of Adenosine Triphosphate-Sensitive Potassium Channels in Mouse Ventricular Myocytes

  • Jeong, In Seok (Department of Thoracic and Cardiovascular Surgery, Chonnam National University Medical School) ;
  • Cho, Hwa Jin (Department of Pediatrics, Chonnam National University Medical School) ;
  • Cho, Jeong Gwan (Department of Internal Medicine, Chonnam National University Medical School) ;
  • Kim, Sang Hyung (Department of Thoracic and Cardiovascular Surgery, Chonnam National University Medical School) ;
  • Na, Kook Joo (Department of Thoracic and Cardiovascular Surgery, Chonnam National University Medical School) ;
  • Kim, Jong-Keun (Department of Pharmacology, Chonnam National University Medical School)
  • Received : 2015.03.20
  • Accepted : 2015.11.05
  • Published : 2016.07.30

Abstract

Background and Objectives: Adenosine triphosphate (ATP)-sensitive potassium ($K_{ATP}$) channels play an important role in myocardial protection. We examined the effects of thromboxane $A_2$ on the regulation of $K_{ATP}$ channel activity in single ventricular myocytes. Materials and Methods: Single ventricular myocytes were isolated from the hearts of adult Institute of Cancer Research (ICR) mice by enzymatic digestion. Single channel activity was recorded by excised inside-out and cell-attached patch clamp configurations at -60 mV holding potential during the perfusion of an ATP-free K-5 solution. Results: In the excised inside-out patches, the thromboxane $A_2$ analog, U46619, decreased the $K_{ATP}$ channel activity in a dose-dependent manner; however, the thromboxane $A_2$ receptor antagonist, SQ29548, did not significantly attenuate the inhibitory effect of U46619. In the cell-attached patches, U46619 inhibited dinitrophenol (DNP)-induced $K_{ATP}$ channel activity in a dose-dependent manner, and SQ29548 attenuated the inhibitory effects of U46619 on DNP-induced $K_{ATP}$ channel activity. Conclusion: Thromboxane $A_2$ may inhibit $K_{ATP}$ channel activity, and may have a harmful effect on ischemic myocardium.

Keywords

References

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