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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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Effect of 18α-GA on EDHF-mediated relaxation of the ophthalmic artery from eNOS−/− mice to ACh. Incubation of the vessels with 18α-GA evoked no inhibitory effects on vasodilation, indicating null involvement of gap junctions in mediating EDHF-type responses in the ophthalmic artery. Values are expressed as mean ± s.e.m (n = 6 per group).