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. 2021 Nov 15;11:22278. doi: 10.1038/s41598-021-01735-z

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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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Apelin deficiency induction of arterial hypertension (AHT) in Apelin-knockout mice (KO-APL mice, grey bars, n = 8) as compared to wild-type mice (WT, white bar, n = 8). (A) Diastolic and systolic pressure measured using the tail cuff method, with all measurements obtained once per day for 4 consecutive days. (B) Mean arterial pressure (MAP) calculated from diastolic and systolic pressure. (C) Pulse pressure corresponds to the difference between diastolic and systolic pressure. (D) Mean pressure (systole and diastole) obtained on day 4 of the measurements (see panel A). (E) Mean MAP obtained on day 4 of the measurements (see panel B). (F) Mean pulse pressure obtained on day 4 of the measurements (see panel C). (G) Velocity of propagation of the aorta measured by the pulse wave speed (PVW). (H) Heart rate expressed in beat per minutes. (I) mRNA expression of smooth muscle contraction markers include alpha smooth muscle actin (αSMA), smooth muscle 22 alpha (SM22α), h-caldesmon. (J) Plasma nitrogen oxide (NO) assay. The results are the mean ± SEM. Statistically significant differences (Mann–Whitney).