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1 The Hatter Institute, UCL Hospitals and Medical School, London, United Kingdom
2 Institute for Pathophysiology, Universitatsklinikum Essen, Essen, Germany
3 Department of Biochemistry, University of Szeged, Szeged, Hungary
4 Department of Basic Sciences, The Royal Veterinary College, London, United Kingdom
* To whom correspondence should be addressed. E-mail: gfbaxter{at}rvc.ac.uk.
BNP has been reported to be released from myocardium during ischemia. We hypothesised that BNP mediates cardioprotection during ischemia-reperfusion and examined if exogenous BNP limits myocardial infarction and the potential role of KATP channel opening. Langendorff-perfused rat hearts underwent 35 min left coronary artery occlusion and 120 min reperfusion. Control infarct/risk ratio (I/R) was 44.8 ± 4.4% (mean + SE). BNP perfused 10 min before ischemia limited infarct size in a concentration-dependent manner, with maximal protection observed at 10-8 M (I/R 20.1 ± 5.2%, P < 0.01 v control), associated with a 2.5-fold elevation of myocardial cGMP above control value. To examine the role of KATP channel opening, glibenclamide (10-6 M), 5-hydroxydecanoate (5-HD 10-4 M), or HMR1098 (10-5 M), were co-perfused with BNP 10-8 M. Protection afforded by BNP was abolished by glibenclamide or 5-HD but not by HMR 1098, suggesting involvement of the putative mitochondrial but not sarcolemmal KATP channel opening. We conclude that natriuretic peptide/cGMP/KATP channel signaling may constitute an important injury-limiting mechanism in myocardium.
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