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1 The Hatter Institute, University College London Hospitals and Medical School, London WC1E 6BT, United Kingdom; 2 Institute for Pathophysiology, Universitatsklinikum Essen, Essen 45122, Germany; 3 Department of Biochemistry, University of Szeged, Szeged H-6720, Hungary; and 4 The Royal Veterinary College, London NW1 0TU, United Kingdom
B-type natriuretic
peptide (BNP) has been reported to be released from the myocardium
during ischemia. We hypothesized that BNP mediates
cardioprotection during ischemia-reperfusion and examined
whether exogenous BNP limits myocardial infarction and the potential
role of ATP-sensitive potassium (KATP) channel opening. Langendorff-perfused rat hearts underwent 35 min of left coronary artery occlusion and 120 min of reperfusion. The control
infarct-to-risk ratio was 44.8 ± 4.4% (means ± SE). BNP
perfused 10 min before ischemia limited infarct size in a
concentration-dependent manner, with maximal protection observed at
10
8 M (infarct-to-risk ratio: 20.1 ± 5.2%,
P < 0.01 vs. control), associated with a 2.5-fold
elevation of myocardial cGMP above the control value. To examine
the role of KATP channel opening, glibenclamide
(106 M), 5-hydroxydecanoate (5-HD; 104 M),
or HMR-1098 (105 M) was coperfused with BNP
(108 M). Protection afforded by BNP was abolished by
glibenclamide or 5-HD but not by HMR-1098, suggesting the involvement
of 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.
cGMP; ischemia-reperfusion; infarct size; preconditioning
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