@article{oai:hirosaki.repo.nii.ac.jp:00003667,
 author = {Yoshida, Ikko and Ishizaka, Hiroshi and Hasegawa, Kazushi and Satoh, Kiyohiko and Osanai, Tomohiro and Motomura, Shigeru and Okumura, Ken},
 issue = {1},
 journal = {弘前医学},
 month = {Mar},
 note = {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.
　 Background Adenosine-induced coronary vasodilation is demonstrated to be mediated by activation of ATPsensitive
potassium（ KATP） channels and nitric oxide（ NO）.
　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 fl ow 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）.
　 Results At the age of 32 weeks, adenosine- and pinacidil-induced increases in coronary fl ow were blunted in OLETF
as compared with those in LETO （both p<0.05）. Glibenclamide attenuated adenosine-induced increase in coronary
fl ow 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 aff ected by glibenclamide. In 8-week-old OLETF and LETO, no diff erence was observed in
adenosine-, pinacidil- and SNP-induced increases in coronary fl ow between OLETF and LETO.
　Conclusions In this type 2 DM model, KATP channel function in coronary microcirculation is impaired. Adenosineinduced
increase in coronary fl ow is mediated mainly by NO mechanism., 弘前医学. 61(1), 2010, p.8-18},
 pages = {8--18},
 title = {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},
 volume = {61},
 year = {2010}
}