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. 2022 Apr 25;36(11):952–959. doi: 10.1038/s41371-022-00698-6

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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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Fig. 3 — Microbiota metabolites SCFAs modulate distinct GPCRs and thereby affect blood pressure. For example, activation of Gpr43 and 41 results in vasodilation and blood pressure attenuation. In contrast, activation of olfr78 increases SNA and renin secretion resulting in blood pressure elevation. Moreover, high salt depletes lactobacillus spp. causing dysbiosis and activation of inflammatory immune response by releasing IL-17 and other inflammatory signaling molecules consequently causing blood pressure elevation. FMT is strong evidence to show that gut microbiota plays an indispensable role in the contribution of high blood pressure. SCFAs short-chain fatty acids, GPCRs G protein-coupled receptors, SNA sympathetic nerve activity, FMT fecal microbiota transplantation, GF germ free.