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Am J Physiol Heart Circ Physiol (February 21, 2003). doi:10.1152/ajpheart.00057.2003
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Submitted on January 21, 2003
Accepted on February 11, 2003

Knockout of the KATP channel subunit Kir6.2 negates ischemic preconditioning-induced protection of myocardial energetics

Richard J. Gumina1, Darko Pucar1, Peter Bast1, Denice M. Hodgson1, Christopher E. Kurtz1, Petras P. Dzeja1, Takashi Miki2, Susumu Seino2, and Andre Terzic1*

1 Department of Cardiovascular, Mayo Clinic, Rochester, MN, USA
2 Department of Cellular and Molecular Medicine, Chiba University, Chiba, Japan

* To whom correspondence should be addressed. E-mail: terzic.andre{at}mayo.edu.

While ischemic preconditioning induces bioenergetic tolerance, remodeling energy metabolism crucial for post-ischemic recovery of the heart, the molecular components associated with preservation of cellular energy production, transfer and utilization are not fully understood. Here, myocardial bioenergetic dynamics were assessed by 18O-assisted 31P NMR spectroscopy in control or preconditioned hearts from wild-type (WT) or Kir6.2-deficient mice, lacking metabolism-sensing sarcolemmal KATP channels (Kir6.2-KO). In WT versus Kir6.2-KO hearts, preconditioning induced a significantly higher total ATP turnover (232±20 versus 155±15 nmolxmg protein-1xmin-1), ATP synthesis rate (58±3% versus 46±3% 18O-labeling of {gamma}ATP), and ATP consumption rate (51±4% versus 31±4% 18O-labeling of inorganic phosphate) following ischemia-reperfusion. Moreover, preconditioning preserved cardiac creatine kinase-catalyzed phosphotransfer in WT (234±26 nmolxmg protein-1xmin-1), but not Kir6.2-KO hearts (133±18 nmolxmg protein-1xmin-1). In contrast to WT hearts, preconditioning failed to preserve contractile recovery in Kir6.2-KO hearts as tight coupling between post-ischemic performance and high-energy phosphoryl transfer was compromised in the KATP channel-deficient myocardium. Thus, intact KATP channels are integral in ischemic preconditioning-induced protection of cellular energetic dynamics and associated cardiac performance.




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