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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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Effects of NOS and COX blockers on ACh-mediated vasodilatation. Endothelium-dependent responses of ophthalmic artery of eNOS−/− mice to ACh in the presence of (a) non-isoform-selective NOS inhibitor, L-NAME (10⁻⁴ M, n = 6) and (b) non-isoform-selective COX inhibitor, indomethacin (10⁻⁵ M, n = 6) exhibited no significant attenuation of dilation. (c) Similarly, combination blockade of both NOS and COX did not inhibit ACh-induced vasodilation. However, combined inhibition with L-NAME, indomethacin and a depolarizing concentration of potassium chloride solution (30 mM KCl) abolished non-NO, non-prostanoid-mediated relaxation to ACh (***P < 0.001, L-NAME and indomethacin vs L-NAME and indomethacin and KCl). Values are expressed as mean ± s.e.m.