Exercise-induced cardioprotection: A role for eNOS uncoupling and NO metabolites

Journal article


Farah, C., Kleindienst, Adrien, Bolea, G., Meyer, G., Gayrard, Sandrine, Geny, B., Obert, Phillippe, Cazorla, O., Tanguy, Stephane and Reboul, Cyril. (2013). Exercise-induced cardioprotection: A role for eNOS uncoupling and NO metabolites. Basic Research in Cardiology. 108(6), pp. 1 - 13. https://doi.org/10.1007/s00395-013-0389-2
AuthorsFarah, C., Kleindienst, Adrien, Bolea, G., Meyer, G., Gayrard, Sandrine, Geny, B., Obert, Phillippe, Cazorla, O., Tanguy, Stephane and Reboul, Cyril
Abstract

Exercise is an efficient strategy for myocardial protection against ischemia–reperfusion (IR) injury. Although endothelial nitric oxide synthase (eNOS) is phosphorylated and activated during exercise, its role in exercise-induced cardioprotection remains unknown. This study investigated whether modulation of eNOS activation during IR could participate in the exercise-induced cardioprotection against IR injury. Hearts isolated from sedentary or exercised rats (5 weeks training) were perfused with a Langendorff apparatus and IR performed in the presence or absence of NOS inhibitors [N-nitro-l-arginine methyl ester, l-NAME or N5-(1-iminoethyl)-l-ornithine, l-NIO] or tetrahydrobiopterin (BH4). Exercise training protected hearts against IR injury and this effect was abolished by l-NAME or by l-NIO treatment, indicating that exercise-induced cardioprotection is eNOS dependent. However, a strong reduction of eNOS phosphorylation at Ser1177 (eNOS-PSer1177) and of eNOS coupling during early reperfusion was observed in hearts from exercised rats (which showed higher eNOS-PSer1177 and eNOS dimerization at baseline) in comparison to sedentary rats. Despite eNOS uncoupling, exercised hearts had more S-nitrosylated proteins after early reperfusion and also less nitro-oxidative stress, indexed by lower malondialdehyde content and protein nitrotyrosination compared to sedentary hearts. Moreover, in exercised hearts, stabilization of eNOS dimers by BH4 treatment increased nitro-oxidative stress and then abolished the exercise-induced cardioprotection, indicating that eNOS uncoupling during IR is required for exercise-induced myocardial cardioprotection. Based on these results, we hypothesize that in the hearts of exercised animals, eNOS uncoupling associated with the improved myocardial antioxidant capacity prevents excessive NO synthesis and limits the reaction between NO and O2·− to form peroxynitrite (ONOO−), which is cytotoxic.

Keywordsnitro-oxidative stress; training; myocardial infarction; enos monomerization
Year2013
JournalBasic Research in Cardiology
Journal citation108 (6), pp. 1 - 13
PublisherSpringer-Verlag
ISSN0300-8428
Digital Object Identifier (DOI)https://doi.org/10.1007/s00395-013-0389-2
Scopus EID2-s2.0-84890264223
Page range1 - 13
Research GroupSports Performance, Recovery, Injury and New Technologies (SPRINT) Research Centre
Publisher's version
File Access Level
Controlled
Place of publicationGermany
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