B-type natriuretic peptide limits infarct size in rat isolated heart via KATP channel opening

D'Souza, Savio P., Yellon, Derek M., Martin, Claus, Schulz, Rainer, Heusch, Gerd, Onody, Annamaria, Ferdinandy, Peter and Baxter, Gary Francis ORCID: https://orcid.org/0000-0002-7887-6841 2003. B-type natriuretic peptide limits infarct size in rat isolated heart via KATP channel opening. American Journal of Physiology - Heart and Circulatory Physiology 284 (5) , H1592-H1600. 10.1152/ajpheart.00902.2002

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Abstract

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 (10−6 M), 5-hydroxydecanoate (5-HD; 10−4 M), or HMR-1098 (10−5 M) was coperfused with BNP (10−8 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/KATPchannel signaling may constitute an important injury-limiting mechanism in myocardium.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Pharmacy
Uncontrolled Keywords:	cGMP; ischemia-reperfusion; infarct size; preconditioning
ISSN:	0363-6135
Last Modified:	17 Oct 2022 08:45
URI:	https://orca.cardiff.ac.uk/id/eprint/965

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