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Dual modulation of nitric oxide production in the heart during ischaemia/reperfusion injury and inflammation
2010
Thrombosis and Haemostasis
SummaryNitric oxide (NO) homeostasis maintained by neuronal/endothelial nitric oxide (NO) synthase (n/eNOS) contributes to regulate cardiac function under physiological conditions. At the early stages of ischaemia, NO homeostasis is disturbed due to Ca2+-dependent e/nNOS activation. In endothelial cells, successive drop in NO concentration may occur due to both uncoupling of eNOS and/or successive inhibition of nNOS catalytic activity mediated by arachidonic acid-induced tyrosine
doi:10.1160/th09-08-0554
pmid:20508903
fatcat:jqaxdixc2nc33iwopc7mhdshzq