KATP channel current increases in postinfarction remodeled cardiomyocytes

R. Surber, C. Bollensdorff, S. Betge, T. Zimmer, K. Benndorf

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Adenosintriphosphate-sensitive potassium channels (KATP channels) are an important linkage between the metabolic state of a cell and electrophysiological membrane properties. In this study, KATP channels were studied in myocytes of normal and remodeled myocardium of the rat. Myocardial infarction was induced by ligature of the left anterior descending artery. Remodeled myocytes were obtained from the hypertrophied posterior left ventricular wall and interventricular septum 3 months after infarction. The current through KATP channels was measured in whole-cell and inside-out patches by using the patch-clamp technique. After myocardial infarction, the heart weight/body weight ratio was doubled and the myocytes were hypertrophied yielding a cell capacitance of 266±16 pF compared to 122±12 pF in control cells. The amount of Kir6.2 protein was indistinguishable in corresponding regions of control and remodeled hearts. The ATP sensitivity of KATP channels in remodeled cells was significantly lower than in control cells (half maximum block at 115 μmol/l ATP in remodeled and at 71 μmol/l ATP in control cells). The maximum I KATP density induced by metabolic inhibition was higher in small remodeled (176±15 pA/pF) than in control cells (127±11 pA/pF), but was unchanged in large remodeled cells. Both, the higher I KATP density and the lower sensitivity of the KATP channels to ATP suggest that remodeled cardiomyocytes develop an improved tolerance to ischemia by stabilizing the resting potential and decreasing excitability.

Original languageEnglish
Pages (from-to)428-434
Number of pages7
JournalPflugers Archiv European Journal of Physiology
Issue number4
Publication statusPublished - 1 Jul 2006
Externally publishedYes



  • Arrhythmogenesis
  • ATP sensitivity
  • K channels
  • Myocardial infarction
  • Remodeling

ASJC Scopus subject areas

  • Physiology

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