Dissociation of sodium-chloride cotransporter expression and blood pressure during chronic high dietary potassium supplementation

Robert Little, Sathish K. Murali, Søren B. Poulsen, Paul R. Grimm, Adrienne Assmus, Lei Cheng, Jessica R. Ivy, Ewout J. Hoorn, Vladimir Matchkov, Paul A. Welling, Robert A. Fenton*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

13 Citations (Scopus)
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Abstract

Dietary potassium (K+) supplementation is associated with a lowering effect in blood pressure (BP), but not all studies agree. Here, we examined the effects of short- and long-term K+ supplementation on BP in mice, whether differences depend on the accompanying anion or the sodium (Na+) intake and molecular alterations in the kidney that may underlie BP changes. Relative to the control diet, BP was higher in mice fed a high NaCl (1.57% Na+) diet for 7 weeks or fed a K+free diet for 2 weeks. BP was highest on a K+-free/high NaCl diet. Commensurate with increased abundance and phosphorylation of the thiazide sensitive sodium-chloride-cotransporter (NCC) on the K+-free/high NaCl diet, BP returned to normal with thiazides. Three weeks of a high K+ diet (5% K+) increased BP (predominantly during the night) independently of dietary Na+ or anion intake. Conversely, 4 days of KCl feeding reduced BP. Both feeding periods resulted in lower NCC levels but in increased levels of cleaved (active) α and γ subunits of the epithelial Na+ channel ENaC. The elevated BP after chronic K+ feeding was reduced by amiloride but not thiazide. Our results suggest that dietary K+ has an optimal threshold where it may be most effective for cardiovascular health.

Original languageEnglish
Article numbere156437
JournalJCI insight
Volume8
Issue number5
DOIs
Publication statusPublished - 8 Mar 2023

Bibliographical note

Funding Information:
We thank Tina Myhre Pedersen, Inger-Merete Paulsen, Christian Westberg (all from the Department of Biomedicine, Aarhus University) and Ingrid van den Berg (Erasmus Medical Center, the Netherlands) for technical support. We thank Cristina Esteva Font (Department of Biomedicine, Aarhus University) for slide scanning. The project was funded by the Leducq Foundation (17CVD05), the Novo Nor-disk Foundation (NNF21OC0067647, NNF17OC0029724, NNF19OC0058439), and the Independent Research Fund Denmark.

Funding Information:
We thank Tina Myhre Pedersen, Inger-Merete Paulsen, Christian Westberg (all from the Department of Biomedicine, Aarhus University) and Ingrid van den Berg (Erasmus Medical Center, the Netherlands) for technical support. We thank Cristina Esteva Font (Department of Biomedicine, Aarhus University) for slide scanning. The project was funded by the Leducq Foundation (17CVD05), the Novo Nordisk Foundation (NNF21OC0067647, NNF17OC0029724, NNF19OC0058439), and the Independent Research Fund Denmark.

Publisher Copyright:
© 2023, Little et al.

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