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. 2020 Nov 23;11:64. doi: 10.1186/s13293-020-00340-5

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© The Author(s) 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 3 — Sodium restriction impairs endothelial function in female mice only in an NO-dependent manner. Endothelial-dependent relaxation responses to acetylcholine (ACH) (a), endothelial-independent relaxation responses to sodium nitroprusside (SNP) (b), and relaxation responses to acetylcholine in the presence of nitric oxide synthase inhibitor Nω-Nitro-L-arginine methyl ester hydrochloride (LNAME) (c) in male and female mice on NSD or SRD. Two-way ANOVA of dose-response curves with repeated measures (*P < 0.05, male NSD N = 5, male SRD N = 8, female NSD N = 5, female SRD N = 11)