Involvement of Adenosine Receptor, Potassium Channel and Protein Kinase C in Hypoxic Preconditioning of Isolated Cardiomyocytes of Adult Rat

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A possible mechanism for hypoxic preconditioning of adult rat cardiomyocytes was pharmacologically investigated. Isolated cardiomyocytes in all experimental groups were incubated for 120 min under hypoxic conditions followed by 15-min reoxygenation (sustained H/R). Sustained H/R decreased rod-shaped cells. Exposure of the cardiomyocytes to 20-min of hypoxia/30-min reoxygenation (hypoxic preconditioning) attenuated the sustained H/R-induced decrease in rod-shaped cells. The effects of hypoxic preconditioning were abolished by treatment with the protein kinase C (PKC) inhibitor polymyxin B, but abolished by neither the adenosine A<SUB>1</SUB>/A<SUB>2</SUB>-antagonist sulfophenyl theophylline (SPT) nor the ATP-sensitive potassium channel (K<SUB>ATP</SUB> channel) blocker glibenclamide. In another series of experiments, cardiomyocytes were incubated without hypoxic preconditioning in the presence of either the PKC activator PMA, adenosine or K<SUB>ATP</SUB>-channel opener nicorandil and then subjected to sustained H/R. Treatment of the cells with PMA, adenosine or nicorandil mimicked the effects of hypoxic preconditioning. The effects of treatment with adenosine and nicorandil were abolished by polymyxin B treatment. Combined treatment with both SPT and glibenclamide abolished the effects of hypoxic preconditioning, whereas it failed to abolish PMA-induced cytoprotection. These results suggest that the activation of PKC in hypoxic preconditioned cardiomyocytes coupled independently with stimulation of adenosine receptor or opening of K<SUB>ATP</SUB> channel, either of which is fully enough to exert the cytoprotective effects.


  • The Japanese Journal of Pharmacology

    The Japanese Journal of Pharmacology 80(1), 15-23, 1999-05-01

    The Japanese Pharmacological Society

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