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Research Article Free access | 10.1172/JCI119860

Myocardial ischemia induces differential regulation of KATP channel gene expression in rat hearts.

M Akao, H Otani, M Horie, M Takano, A Kuniyasu, H Nakayama, I Kouchi, T Murakami, and S Sasayama

Cardiovascular Division of Internal Medicine, Kyoto University Hospital, Kyoto 606, Japan.

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Cardiovascular Division of Internal Medicine, Kyoto University Hospital, Kyoto 606, Japan.

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Cardiovascular Division of Internal Medicine, Kyoto University Hospital, Kyoto 606, Japan.

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Cardiovascular Division of Internal Medicine, Kyoto University Hospital, Kyoto 606, Japan.

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Cardiovascular Division of Internal Medicine, Kyoto University Hospital, Kyoto 606, Japan.

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Cardiovascular Division of Internal Medicine, Kyoto University Hospital, Kyoto 606, Japan.

Find articles by Nakayama, H. in: JCI | PubMed | Google Scholar

Cardiovascular Division of Internal Medicine, Kyoto University Hospital, Kyoto 606, Japan.

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Cardiovascular Division of Internal Medicine, Kyoto University Hospital, Kyoto 606, Japan.

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Cardiovascular Division of Internal Medicine, Kyoto University Hospital, Kyoto 606, Japan.

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Published December 15, 1997 - More info

Published in Volume 100, Issue 12 on December 15, 1997
J Clin Invest. 1997;100(12):3053–3059. https://doi.org/10.1172/JCI119860.
© 1997 The American Society for Clinical Investigation
Published December 15, 1997 - Version history
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Abstract

The cardiac ATP-sensitive potassium (KATP) channel is thought to be a complex composed of an inward rectifier potassium channel (Kir6.1 and/or Kir6.2) subunit and the sulfonylurea receptor (SUR2). This channel is activated during myocardial ischemia and protects the heart from ischemic injury. We examined the transcriptional expression of these genes in rats with myocardial ischemia. 60 min of myocardial regional ischemia followed by 24-72 h, but not 3-6 h, of reperfusion specifically upregulated Kir6.1 mRNA not only in the ischemic (approximately 2.7-3.1-fold) but also in the nonischemic (approximately 2.0-2.6-fold) region of the left ventricle. 24 h of continuous ischemia without reperfusion also induced an increase in Kir6.1 mRNA in both regions, whereas 15-30 min of ischemia followed by 24 h of reperfusion did not induce such expression. In contrast, mRNAs for Kir6.2 and SUR2 remained unchanged under these ischemic procedures. Western blotting demonstrated similar increases in the Kir6.1 protein level both in the ischemic (2.4-fold) and the nonischemic (2.2-fold) region of rat hearts subjected to 60 min of ischemia followed by 24 h of reperfusion. Thus, prolonged myocardial ischemia rather than reperfusion induces delayed and differential regulation of cardiac KATP channel gene expression.

Version history
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