Adenosine-induced dilation of coronary resistance vessels is impaired in rats with type 2 diabetes mellitus: possible role of ATP-sensitive potassium channels and nitric oxide

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  • Yoshida Ikko
    Department of Cardiology, Respiratory Medicine and Nephrology, Hirosaki University Graduate School of Medicine,
  • Ishizaka Hiroshi
    Department of Cardiology, Respiratory Medicine and Nephrology, Hirosaki University Graduate School of Medicine,
  • Hasegawa Kazushi
    Department of Cardiology, Respiratory Medicine and Nephrology, Hirosaki University Graduate School of Medicine,
  • Satoh Kiyohiko
    Department of Cardiology, Respiratory Medicine and Nephrology, Hirosaki University Graduate School of Medicine,
  • Osanai Tomohiro
    Department of Cardiology, Respiratory Medicine and Nephrology, Hirosaki University Graduate School of Medicine,
  • Motomura Shigeru
    Department of Pharmacology, Hirosaki University Graduate School of Medicine
  • Okumura Ken
    Department of Cardiology, Respiratory Medicine and Nephrology, Hirosaki University Graduate School of Medicine,

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Other Title
  • アデノシン誘発性冠抵抗血管の拡張は２型糖尿病ラットで障害されている： ATP感受性Kチャネルと一酸化窒素の役割

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Abstract

Objectives: The purpose of this study was to test the hypothesis that adenosine-induced coronary microvascular dilation is blunted in the animals with diabetes mellitus (DM) through the impairment of KATP channel function.<br> Background: Adenosine-induced coronary vasodilation is demonstrated to be mediated by activation of ATP-sensitive potassium (KATP) channels and nitric oxide (NO).<br> Methods: The hearts of Otsuka Long-Evans Tokushima fatty rats (OLETF, type 2 DM rats), and control Long-Evans Tokushima fatty rats (LETO) at the ages of 32 and 8 weeks were perfused using a Langendorff system with constant perfusion pressure (80 mmHg). Changes in coronary flow to adenosine, pinacidil and sodium nitroprusside (SNP) were examined before and after administration of glibenclamide (10⁻⁷ M), or NG-nitro-L-arginine methyl ester (L-NAME, 10⁻⁴ M).<br> Results: At the age of 32 weeks, adenosine- and pinacidil-induced increases in coronary flow were blunted in OLETF as compared with those in LETO (both p<0.05). Glibenclamide attenuated adenosine-induced increase in coronary flow in LETO (p<0.05), but not in OLETF. In contrast, L-NAME attenuated adenosine-induced increase in coronary flow in OLETF (p<0.05), but not in LETO. SNP-induced increases in coronary flow in LETO and OLETF were comparable and were not affected by glibenclamide. In 8-week-old OLETF and LETO, no difference was observed in adenosine-, pinacidil- and SNP-induced increases in coronary flow between OLETF and LETO.<br> Conclusions: In this type 2 DM model, KATP channel function in coronary microcirculation is impaired. Adenosine-induced increase in coronary flow is mediated mainly by NO mechanism.

Journal

  • Hirosaki Medical Journal

    Hirosaki Medical Journal 61 (1), 8-18, 2010

    Hirosaki University Graduate School of Medicine,Hirosaki Medical Society

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