Postprandial Vascular Effects of a High Potassium Meal in Patients with Treated Hypertension

There is compelling evidence of an inverse association between potassium intake and blood pressure (BP). A potential mechanism for this effect may be dietary potassium-mediated augmentation of endothelium-dependent relaxation. To date, studies have investigated potassium intake supplementation over several weeks in healthy volunteers with variable results on vascular function. There is no assessment of the acute vascular effects of potassium supplementation achieved by the ingestion of potassium-rich food in a hypertensive population.

The purpose of this study was to investigate the effect of a high potassium meal on postprandial endothelial function as measured by flow-mediated dilatation (FMD).

We performed an investigator-blinded randomized crossover trial in 33 treated hypertensive individuals. Participants consumed both a high (~2400 mg) and low (~543 mg) K⁺ meal, separated by a one-week washout period. The primary endpoint was endothelial function as assessed by FMD pre-meal and postprandially at 60 and 120 min. Meals were compared at each time point using the Hills-Armitage approach.

33 individuals were included in the study (48% male, mean age 68). In the fasting state (Baseline), and at 60 min postprandial, radial artery FMD was not significantly different between the participants after consumption of either meal (baseline: high K⁺ 4.2 ± 2% versus Low K⁺ 2.6 ± 3%, p = 0.93; 60 min: high K⁺ 3.8 ± 4% versus Low K⁺ 4.1 ± 3%, p = 0.69). However, at 120 min, FMD tended to be higher in participants after the high K⁺ meal (5.2 ± 4.1%) than after the low K⁺ meal (3.9 ± 4.1%) (p = 0.07). There were no differences in participants' radial artery diameter and blood flow between meals.

This study does not support our hypothesis that a single high K⁺ meal improves vascular function in individuals with treated hypertension. This does not contradict the clinical evidence relating greater K⁺ intake with lower BP, but suggests that mechanistic investigations of increased K⁺ intake through diet alone and its impact on endothelial function as a mediator to reducing BP are complex and not simply due to single nutrient-mediated improvement in vascular function.