Impact of Salt Loading on Endothelial Dependent Vasodilation and Arterial Blood Pressure

Cardiovascular diseases are the leading cause of premature mortality. Hypertension, or high blood pressure, is the most prevalent risk factor, with high dietary sodium intake being a strong predictor. Some claim that sodium has a pathological role when intake is low or high and a physiological role when sodium intake is moderate, however the population groups these studies were performed in had underlying health conditions so they were not considered to be healthy. Recently, researchers indicated a 2-compartment model of sodium regulation and arterial dilation involving storage in the sugar molecules, glycosaminoglycans (GAGs), that are on the surface of epithelial/endothelial cells to form the glycocalyx. When the glycocalyx is disrupted, sodium enters endothelial cells and reduces their ability to cause dilation. Exercise can increase blood flow/shear stress and oxidative stress, which may cause the glycocalyx to be perturbed. In this study, participants were tested on four different occasions – twice at baseline and twice postsupplementation. Continuous ECG and blood pressure measurements were collected through each testing session. Participants underwent a flow mediated dilation (FMD) protocol to measure endothelial dependent dilation of the brachial artery using Doppler ultrasound as well as a 30- minute exercise bout using a handgrip dynamometer. Following the baseline testing session, participants were instructed to ingest 16 capsules per day of either salt or placebo (sugar), for a seven-day period that began on the day their baseline measurements were gathered. After a week of taking the capsules for a week, participants were tested following the same steps as the baseline session. They then underwent a “wash-out” period for a week and were tested again at the end of that week as a second baseline. Participants were then given the capsules that contained the other corresponding contents for another seven-day period and were then tested again at the end of the seven-day period. The data was analyzed using a within-subject repeated measures analysis of variance (ANOVA), with the software JASP. We hypothesized that when there is an increase in sodium levels, the endothelial function will be affected especially in vascular systems where the glycocalyx has been modified by increases in blood flow through exercise. We also hypothesized that arterial blood pressure will be increased systemically. We found significant changes in both absolute and relative FMD responses between the baseline and post testing for the salt condition. We did not find any significant differences from baseline to post testing for the placebo. We also did not find any significant differences between the shear rates, baseline brachial artery diameters, and blood flow for both the salt and placebo conditions and testing sessions. Exploratory post-hoc analyses also suggest that absolute dilation was reduced after sodium intake compared to their baseline and placebo conditions. Finally, we found no significant changes in systolic, diastolic, and mean arterial blood pressure in either condition or from baseline to post testing and there was no significant difference in heart rate. The methodology presented here lays a strong foundation for future work and has the potential to be further developed into a larger scale study. If future studies see significant differences in exercise-induced endothelial function post salt-loading and if other physiological mechanisms effect endothelial function and arterial blood pressure, individuals will then be able to adjust their dietary sodium intake to a level which reduces the risk of cardiovascular disease and hypertension.