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. 2021 Feb 23;11:4387. doi: 10.1038/s41598-021-82972-0

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© The Author(s) 2021

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 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/.

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Endothelin-1-induced contraction in sFlt1 and vehicle-treated on syndecan-1 deficient mice and wild type controls. Syndecan-1 deficient mice and wild type controls were treated with sFlt1 or vehicle during two weeks. Carotid arteries were isolated for comparison of contractile responses, vasoconstriction is expressed in milliNewton per millimeter (mN/mm). (A) In wild types (WT), sFlt1 infusion augments maximal endothelin-1-induced vasoconstriction compared to vehicle (N = 6 vs. 6, p = 0.03). In sydencan-1 -/- mice, endothelin-1-induces vasoconstriction similar after sFlt1 and vehicle treatment (N = 5–4, p = 0.68). (B) In wild types, maximal methacholine-induced vasodilatation (after preconstriction with phenylephrine) is decreased in sFlt1-treated compared to vehicle-treated mice (N = 14 vs 14, p = 0.04). In sydecan-1 -/- mice, maximal methacholine-induced vasodilatation is similar after sFlt1 and vehicle treatment (N = 5–4). Bars represent mean ± SEM, ns indicates not-significant.