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. 2020 Jan 21;10:889. doi: 10.1038/s41598-020-57803-3

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© The Author(s) 2020

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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Diagram illustrating the main findings of the study and the proposed mechanism involved in the observed alterations. The ascending aorta of complete deletion (CD) mice shows stenosis and attenuated phenylephrine-induced contractions compared to wild-type mice. The present study suggests that phenylephrine, besides activating α1_A/D-adrenoceptors located in smooth muscle cells (SMC) to induce contraction, could also stimulate endothelial cell (EC) α1_A-adrenoceptors that could trigger the release of nitric oxide (NO) by endothelial neuronal nitric oxide synthase (nNOS)²⁴, whose expression is increased in CD mice. This increased release of NO could be responsible for the impairment of α1-adrenoceptor-mediated contractions in the ascending aorta of CD mice. WBS, Williams-Beuren syndrome.