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Cardiovascular Research Advance Access originally published online on September 18, 2007
Cardiovascular Research 2008 77(2):380-386; doi:10.1093/cvr/cvm011
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2007. For permissions please email: journals.permissions@oxfordjournals.org

Exercise and tachycardia increase NADPH oxidase and ryanodine receptor-2 activity: possible role in cardioprotection

Gina Sánchez1, Matías Escobar2, Zully Pedrozo2, Pilar Macho1, Raúl Domenech1, Steffen Härtel3, Cecilia Hidalgo2 and Paulina Donoso2,*

1 Programa de Fisiopatología, Instituto de Ciencias Biomédicas y Centro FONDAP de Estudios Moleculares de la Célula, Facultad de Medicina, Universidad de Chile, Chile
2 Programa de Biología Celular y Molecular, Instituto de Ciencias Biomédicas y Centro FONDAP de Estudios Moleculares de la Célula, Facultad de Medicina, Universidad de Chile, Casilla 70005, Santiago 7, Chile
3 Programa de Anatomía y Biología del Desarrollo, Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Chile

* Corresponding author. Tel: +56 2 978 6602; fax: +56 2 777 6916. E-mail address: pdonoso{at}med.uchile.cl

Aim: Our objective was to investigate in cardiac muscle the contribution of NADPH oxidase to (a) ryanodine receptor-2 (RyR2) S-glutathionylation and (b) the preconditioning effects of exercise and tachycardia on infarct size following coronary artery occlusion.

Methods and results: We measured NADPH oxidase activity, RyR2 S-glutathionylation, and calcium release kinetics in sarcoplasmic reticulum (SR) vesicles isolated from dog ventricular muscle after exercise and tachycardia, plus or minus prior administration of the NADPH oxidase inhibitor apocynin. In ventricular muscle sections, we studied the colocalization of NADPH oxidase and RyR2 by confocal microscopy using fluorescent antibodies. We determined the effect of apocynin on the infarct size produced by occlusion of the descendent anterior coronary artery in animals preconditioned by exercise or tachycardia. Exercise and tachycardia increased NADPH oxidase activity, RyR2 S-glutathionylation, and calcium release rates in isolated SR vesicles. Cardiac muscle sections displayed significant colocalization of NADPH oxidase and RyR2, suggesting direct and specific effects of reactive oxygen species (ROS) produced by NADPH oxidase on RyR2 activation. The NADPH oxidase inhibitor apocynin prevented the increase in RyR2 S-glutathionylation, reduced calcium release activity, and completely prevented the protective effects of exercise and tachycardia on infarct size.

Conclusions: The loss of cardioprotection induced by the NADPH oxidase inhibitor suggests that ROS generated by this enzyme are important mediators of the preconditioning response, which presumably involves NADPH oxidase-induced RyR2 S-glutathionylation.

KEYWORDS ca-channels; oxygen radicals; redox signaling; preconditioning

Time for primary review: 30 days


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