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

• Nojiri Michiko

  Department of Pharmacology, Tokyo University of Pharmacy and Life Science

• Tanonaka Kouichi

  Department of Pharmacology, Tokyo University of Pharmacy and Life Science

• Yabe Ken-ichi

  Department of Pharmacology, Tokyo University of Pharmacy and Life Science

• Kawana Ken-ichiro

  Department of Pharmacology, Tokyo University of Pharmacy and Life Science

• Iwai Takeshi

  Department of Pharmacology, Tokyo University of Pharmacy and Life Science

• Yamane Makiko

  Department of Pharmacology, Tokyo University of Pharmacy and Life Science

• Yoshida Hiroyuki

  Department of Pharmacology, Tokyo University of Pharmacy and Life Science

• Hayashi Jun-ichi

  Department of Gerontology, Kyorin University, School of Medicine

• Takeo Satoshi

  Department of Pharmacology, Tokyo University of Pharmacy and Life Science

抄録

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 A₁/A₂-antagonist sulfophenyl theophylline (SPT) nor the ATP-sensitive potassium channel (K_ATP 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_ATP-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_ATP channel, either of which is fully enough to exert the cytoprotective effects.

収録刊行物

• Jpn.J.Pharmacol.

  Jpn.J.Pharmacol. 80 (1), 15-23, 1999

  公益社団法人 日本薬理学会

キーワード

• Adenosine receptor
• Adult rat cardiomyocyte
• ATP-sensitive potassium channel
• Preconditioning
• Protein kinase C

詳細情報

• CRID: 1390001204285037440
• NII論文ID: 10008194449
• NII書誌ID: AA00691188
• DOI: 10.1254/jjp.80.15
• COI: 1:CAS:528:DyaK1MXjtlGisrk%3D
• ISSN: 13473506
• ISSN: 00215198
• NDL書誌ID: 4732987
• PubMed: 10446752
• Web Site: https://ndlsearch.ndl.go.jp/books/R000000004-I4732987
• Web Site: https://api.elsevier.com/content/article/PII:S0021519819308844?httpAccept=text/xml
• Web Site: https://api.elsevier.com/content/article/PII:S0021519819308844?httpAccept=text/plain
• Web Site: https://www.jstage.jst.go.jp/article/jjp/80/1/80_1_15/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/1999227215
• 本文言語コード: en
• データソース種別:
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