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Cardiovascular Research 2007 73(1):8-9; doi:10.1016/j.cardiores.2006.11.009
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Copyright © 2006, European Society of Cardiology

Endothelial nitric oxide synthase uncoupling: Is it a physiological mechanism of endothelium-dependent relaxation in cerebral artery?

Mitsuhiro Yokoyama* and Ken-ichi Hirata

Cardiovascular Division, Department of Internal Medicine, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan

* Corresponding author. Tel.: +81 78 382 5840; fax: +81 78 382 5858. Email address: yokoyama@med.kobe-u.ac.jp

Received 31 October 2006; accepted 8 November 2006

The first 10% of the full text of this article appears below.

See article by Drouin et al. [8] (pages 73–81) in this issue.

Nitric oxide (NO) is generated from the conversion of L -arginine to L-citrulline by endothelial nitric oxide synthase (eNOS), which requires Ca2+/calmodulin, FAD, FMN, and tetrahydrobiopterin (BH4) as cofactors. Chemical studies in vitro demonstrated that the catalytic mechanisms of NOS involve flavin-mediated electron transport from a flavin-containing reductase domain to a heme-containing oxygenase domain. Here, oxygen is reduced and incorporated into the guanidine group of L-arginine, giving rise to NO and L-citrulline. Calcium/calmodulin binding to NOS increases the rate of reduction . . . [Full Text of this Article]


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