A high potassium intake protects endothelial function and reduces pro-inflammatory markers under high-sodium conditions in salt-resistant adults

High sodium (HS) intake is related to endothelial dysfunction (ED) and the development of cardiovascular disease. ED is a key factor in high blood pressure (BP), and a HS intake can promote ED mainly through the production of reactive oxygen species (ROS). Data shows that the effectiveness of therapeutic strategies to reduce ROS does not fully restore endothelial function suggesting that the contribution of an alternative cellular pathway for HS-induced ED, such as inflammation, may be involved. In contrast, a high potassium (HK) intake has protective effects on cardiovascular health by decreasing blood pressure (BP). The objective of this work was to determine if a HK diet could attenuate the deleterious effect of a HS diet on endothelial function and inflammatory markers in healthy, normotensive adults. Nineteen salt-resistant (SR) participants (9M/10F, age 28.4±7.4 years, BMI 24.1±2.4 Kg/m2, BP 106±8/68±7 mmHg) completed three 10-day diets: moderate potassium/low sodium (MK/LS, 65/50 mmol), moderate potassium/high sodium (MK/HS, 65/300 mmol), high potassium/high sodium (HK/HS 120 mmol/300 mmol). Participants wore an ambulatory BP monitor for 24 hours to determine SR. On day 10, endothelial function was assessed by brachial artery flow-mediated dilation (FMD), and a blood draw was performed. Interleukin-6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1) were quantified in the plasma using an ELISA kit (RayBiotech, GA). Differences across diets were assessed by ANOVA. There was no difference in 24-hour mean arterial pressure between the MK/LS and MK/HS diets (p=0.46), confirming that all participants were SR. FMD was lower on MK/HS diet (4.65±2.4%) compared to MK/LS (7.62±3.12%, p =0.0006) and HS/HK (7.64±2.48%, p =0.0007) diets. IL-6 was increased on MK/HS diet (45.7±12.8 pg/mL) compared to MK/LS (25.7±11.56 pg/mL, p =0.0005) and HK/HS (36.7±12.3 pg/mL, p =0.0044). Similarly, MCP-1 was also increased on MK/HS (78.8±58.3 pg/mL) compared to MK/LS (57.43±53.67 pg/mL, p =0.006) and HK/HS (60.32±56.3 pg/mL, p =0.001). Our current data demonstrate a protective role of increased potassium intake against HS-induced endothelial dysfunction. Moreover, HK intake mitigates the pro-inflammatory effects triggered by a HS diet in healthy SR adults. Supported by 1R01HL145055 This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

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Journal
Physiology
Published
2025-05-01
DOI
https://doi.org/10.1152/physiol.2025.40.s1.1627
Primary Topic
Sodium Intake and Health
Type
article
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article

A high potassium intake protects endothelial function and reduces pro-inflammatory markers under high-sodium conditions in salt-resistant adults

Shannon L. Lennon, Kathryn E. Kaseman, Jessica L. Irwin, César Eduardo Jacintho Moritz et al.
Physiology
Sodium Intake and Health
article

A high potassium intake protects endothelial function and reduces pro-inflammatory markers under high-sodium conditions in salt-resistant adults

Shannon L. Lennon, Kathryn E. Kaseman, Jessica L. Irwin, César Eduardo Jacintho Moritz, Andrea J. Lobene
article en

Abstract

High sodium (HS) intake is related to endothelial dysfunction (ED) and the development of cardiovascular disease. ED is a key factor in high blood pressure (BP), and a HS intake can promote ED mainly through the production of reactive oxygen species (ROS). Data shows that the effectiveness of therapeutic strategies to reduce ROS does not fully restore endothelial function suggesting that the contribution of an alternative cellular pathway for HS-induced ED, such as inflammation, may be involved. In contrast, a high potassium (HK) intake has protective effects on cardiovascular health by decreasing blood pressure (BP). The objective of this work was to determine if a HK diet could attenuate the deleterious effect of a HS diet on endothelial function and inflammatory markers in healthy, normotensive adults. Nineteen salt-resistant (SR) participants (9M/10F, age 28.4±7.4 years, BMI 24.1±2.4 Kg/m2, BP 106±8/68±7 mmHg) completed three 10-day diets: moderate potassium/low sodium (MK/LS, 65/50 mmol), moderate potassium/high sodium (MK/HS, 65/300 mmol), high potassium/high sodium (HK/HS 120 mmol/300 mmol). Participants wore an ambulatory BP monitor for 24 hours to determine SR. On day 10, endothelial function was assessed by brachial artery flow-mediated dilation (FMD), and a blood draw was performed. Interleukin-6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1) were quantified in the plasma using an ELISA kit (RayBiotech, GA). Differences across diets were assessed by ANOVA. There was no difference in 24-hour mean arterial pressure between the MK/LS and MK/HS diets (p=0.46), confirming that all participants were SR. FMD was lower on MK/HS diet (4.65±2.4%) compared to MK/LS (7.62±3.12%, p =0.0006) and HS/HK (7.64±2.48%, p =0.0007) diets. IL-6 was increased on MK/HS diet (45.7±12.8 pg/mL) compared to MK/LS (25.7±11.56 pg/mL, p =0.0005) and HK/HS (36.7±12.3 pg/mL, p =0.0044). Similarly, MCP-1 was also increased on MK/HS (78.8±58.3 pg/mL) compared to MK/LS (57.43±53.67 pg/mL, p =0.006) and HK/HS (60.32±56.3 pg/mL, p =0.001). Our current data demonstrate a protective role of increased potassium intake against HS-induced endothelial dysfunction. Moreover, HK intake mitigates the pro-inflammatory effects triggered by a HS diet in healthy SR adults. Supported by 1R01HL145055 This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

PhysiologyVol. 40(S1)
University of Delaware (US)
Openalex Percentile: Top 81%
Sodium Intake and Health
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