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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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Cholinergic vasodilation of the mouse ophthalmic artery in the presence of potassium ion channels and Na⁺/K⁺-ATPase blockers. Incubation of the vessels with (a) glibenclamide and (b) ouabain elicited no significant inhibitory effects on ACh-mediated vasodilation. However, the inhibition of the (c) Kir channels with BaCl₂ and, (d) combination blockade of Kir channels and LOX pathway with BaCl₂ and baicalein caused a significant inhibition of dilation. Values are expressed as mean ± s.e.m (n = 4–6 per group; ***P < 0.001, L-NAME and indomethacin vs L-NAME and indomethacin and BaCl₂, **P < 0.01, L-NAME and indomethacin vs L-NAME and indomethacin and BaCl₂ and baicalein).