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. 2017 Aug 2;7:7111. doi: 10.1038/s41598-017-07768-7

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Endothelium-dependent relaxation of the ophthalmic artery attributed to EDHF via arachidonic acid metabolites. Concentration-response curves to ACh (10⁻⁹–10⁻⁴ M) in the presence of (a) CYP₄₅₀ inhibitor, 17-ODYA and (b) LOX inhibitor, baicalein. Blocking of the CYP₄₅₀ pathway conferred a negligible inhibitory effect on ACh-induced vasodilation, whereas, inhibition of the LOX pathway elicited significant attenuation of vasodilation. Values are expressed as mean ± s.e.m (n = 6 per group; ***P < 0.001, L-NAME and indomethacin vs L-NAME and indomethacin and baicalein).