Is endothelial-nitric-oxide-synthase-derived nitric oxide involved in cardiac hypoxia/reoxygenation-related damage.
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Date
2011-03
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Abstract
Nitric oxide (NO) has been reported to act both as a destructive and a protective agent in the pathogenesis of the
injuries that occur during hypoxia/reoxygenation (H/R). It has been suggested that this dual role of NO depends
directly on the isoform of NO synthase (NOS) involved. In this work, we investigate the role that NO derived from
endothelial NOS (eNOS) plays in cardiac H/R-induced injury.Wistar rats were submitted to H/R (hypoxia for 30 min;
reoxygenation of 0 h, 12 h and 5 days), with or without prior treatment using the selective eNOS inhibitor L-NIO
(20 mg/kg). Lipid peroxidation, apoptosis and protein nitration, as well as NO production (NOx), were analysed. The
results showed that L-NIO administration lowered NOx levels in all the experimental groups. However, no change
was found in the lipid peroxidation level, the percentage of apoptotic cells or nitrated protein expression, implying
that eNOS-derived NO may not be involved in the injuries occurring during H/R in the heart. We conclude that LNIO
would not be useful in alleviating the adverse effects of cardiac H/R.
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Keywords
Apoptosis, endothelial nitric oxide synthase, hypoxia, L-NIO, nitric oxide, reoxygenation
Citation
Rus A, Peinado MA, Blanco S, Moral ML del. Is endothelial-nitric-oxide-synthase-derived nitric oxide involved in cardiac hypoxia/reoxygenation-related damage. Journal of Biosciences. 2011 Mar; 36(1): 69-78.