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. 2019 Dec 20;9:19540. doi: 10.1038/s41598-019-55995-x

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© The Author(s) 2019

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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Proposed mechanism of CAP2/Tmprss4-mediated water balance in wildtypes during LK diet. During dietary K⁺ depletion in wildtype mice, levels of corticosterone and progesterone normally rise and activity of the 11βHSD2 decreases. In distal tubules, upregulation of CAP2/Tmprss4 acts negatively on the final expression of NKCC2, AQP2 and HKA2. This may arise through a suppressive function of CAP2/Tmprss4 on AC6, thereby affecting cAMP-mediated signalling and its downstream effects on NKCC2 and AQP2. The rise is cAMP might also be responsible for increased HKA2 expression, and urinary calcium excretion^38,46. The GR seems to act positively on these mechanisms, thereby participating in the dysregulated water balance observed in CAP2/Tmprss4 knockout mice following LK diet.