Potassium Supplementation Offsets the Effects of a High Sodium Diet on Endothelial Function but Not Blood Pressure Reactivity in Healthy, Normotensive Adults

High sodium diets are linked to endothelial dysfunction and increased blood pressure reactivity (BPR) to physiological stimuli, which are both notable cardiovascular disease (CVD) risk factors. High potassium diets are shown to lower blood pressure (BP) and improve endothelial function; however, previous interventions often increased potassium intake using food, making it diffcult to attribute these effects to potassium alone. The interactive effects of sodium and potassium on pre-clinical CVD risk factors remains unclear. The objective of this study was to determine if potassium can independently counteract the effects of a high sodium diet on endothelial function and BPR in healthy, normotensive adults. We hypothesized that endothelial function and BPR would be impaired with a high sodium diet compared to a low sodium diet but would improve with the addition of potassium supplements. Nineteen participants (13W/6M, age 26±4 y, BP 108±11/71±9 mmHg, BMI 25.1±2.7 kg/m 2 ) completed three 10-day controlled diets in random order: a moderate potassium/low sodium (MK/LS; 55 mmol K/50 mmol Na) diet, a moderate potassium/high sodium (MK/HS; 55 mmol K/300 mmol Na) diet, and a high potassium/high sodium (HK/HS; 120 mmol K/300 mmol Na) diet. Potassium intake was increased using potassium chloride supplements. Dietary compliance was confirmed by urinalysis. On day 10, endothelial function was assessed by brachial artery flow-mediated dilation (FMD), and BPR was assessed by measuring ΔMAP in response to an isometric handgrip exercise (IHG) with post-exercise ischemia (PEI) and the cold pressor test (CPT). Differences across diets were assessed by repeated-measures ANOVA. Twenty-four-hour ambulatory mean arterial pressure (MAP), which was measured on day 9, was not different across diets (MK/LS: 81±5 mmHg; MK/HS: 79±4 mmHg; HK/HS: 80±6 mmHg; p=0.15), indicating our participants were salt-resistant. FMD was significantly lower on the MK/HS diet compared to the MK/LS diet (MK/HS: 5.8±2.8% vs. MK/LS: 8.2±3.7%; p=0.004) and was rescued with the addition of potassium supplements (HK/HS: 8.9±3.2; p=0.009 compared to MK/HS). FMD on MK/LS and HK/HS diets were similar (p>0.05). There were no differences across diets in ΔMAP in response to the IHG (p=0.73), the PEI (p=0.67), or the CPT (p=0.94). Our findings suggest that, while sodium and potassium may not affect BPR, potassium supplementation effectively counteracts sodium-induced endothelial dysfunction in healthy, normotensive, salt-resistant adults. AHA/VIVA 23POST1009835; NHLBI R01 HL145055. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.