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

フォーマット:

論文

責任表示:

Yoshida, Ikko ; Ishizaka, Hiroshi ; Hasegawa, Kazushi ; Satoh, Kiyohiko ; Osanai, Tomohiro ; Motomura, Shigeru ; Okumura, Ken

言語:

英語

出版情報:

弘前大学出版会, 2010-03-25

著者名:

Yoshida, Ikko

Ishizaka, Hiroshi

Hasegawa, Kazushi

Satoh, Kiyohiko

Osanai, Tomohiro

Motomura, Shigeru

Okumura, Ken

続きを見る

掲載情報:

弘前医学

ISSN:

0439-1721      

巻:

61

通号:

1

開始ページ:

8

終了ページ:

18

バージョン:

publisher

概要:

Objectives The purpose of this study was to test the hypothesis that adenosine-induced coronarymicrovascular dilation is blunted in the animals with diabetes mellitus（ DM） through the impairment of KATP channelfunction.　 Background Adenosin … e-induced coronary vasodilation is demonstrated to be mediated by activation of ATPsensitivepotassium（ 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 withconstant 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 OLETFas compared with those in LETO （both p<0.05）. Glibenclamide attenuated adenosine-induced increase in coronaryfl ow in LETO （p<0.05）, but not in OLETF. In contrast, L-NAME attenuated adenosine-induced increase in coronaryflow in OLETF （p<0.05）, but not in LETO. SNP-induced increases in coronary flow in LETO and OLETF werecomparable and were not aff ected by glibenclamide. In 8-week-old OLETF and LETO, no diff erence was observed inadenosine-, 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. Adenosineinducedincrease in coronary fl ow is mediated mainly by NO mechanism. 続きを見る

URL:

http://hdl.handle.net/10129/3275