Protein Kinase C Activates ATP-sensitive Potassium Channels in Rabbit Ventricular Myocytes

  • Kim, Na-Ri (Mitochondrial Signaling Laboratory, Department of Physiology and Biophysics, College of Medicine, Cardiovascular & Metabolic Disease Center, Biohealth Products Research Center, Inje University) ;
  • Youm, Jae-Boum (Mitochondrial Signaling Laboratory, Department of Physiology and Biophysics, College of Medicine, Cardiovascular & Metabolic Disease Center, Biohealth Products Research Center, Inje University) ;
  • Joo, Hyun (Mitochondrial Signaling Laboratory, Department of Physiology and Biophysics, College of Medicine, Cardiovascular & Metabolic Disease Center, Biohealth Products Research Center, Inje University) ;
  • Kim, Hyung-Kyu (Mitochondrial Signaling Laboratory, Department of Physiology and Biophysics, College of Medicine, Cardiovascular & Metabolic Disease Center, Biohealth Products Research Center, Inje University) ;
  • Kim, Eui-Yong (Mitochondrial Signaling Laboratory, Department of Physiology and Biophysics, College of Medicine, Cardiovascular & Metabolic Disease Center, Biohealth Products Research Center, Inje University) ;
  • Han, Jin (Mitochondrial Signaling Laboratory, Department of Physiology and Biophysics, College of Medicine, Cardiovascular & Metabolic Disease Center, Biohealth Products Research Center, Inje University)
  • Published : 2005.08.21

Abstract

Several signal transduction pathways have been implicated in ischemic preconditioning induced by the activation of ATP-sensitive $K^+$ $(K_{ATP})$ channels. We examined whether protein kinase C (PKC) modulated the activity of $K_{ATP}$ channels by recording $K_{ATP}$ channel currents in rabbit ventricular myocytes using patch-clamp technique and found that phorbol 12,13-didecanoate (PDD) enhanced pinacidil-induced $K_{ATP}$ channel activity in the cell-attached configuration; and this effect was prevented by bisindolylmaleimide (BIM). $K_{ATP}$ channel activity was not increased by $4{\alpha}-PDD$. In excised insideout patches, PKC stimulated $K_{ATP}$ channels in the presence of 1 mM ATP, and this effect was abolished in the presence of BIM. Heat-inactivated PKC had no effect on channel activity. PKC-induced activation of $K_{ATP}$ channels was reversed by PP2A, and this effect was not detected in the presence of okadaic acid. These results suggest that PKC activates $K_{ATP}$ channels in rabbit ventricular myocytes.

Keywords

References

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