Erythrocyte sodium buffering capacity status correlates with self-reported salt intake in a population from Livingstone, Zambia

Abstract

Background Salt impairs endothelial function and increases arterial stiffness independent of blood pressure. The mechanisms are unknown. Recent evidence suggests that there is a possible link between salt consumption and sodium buffering capacity and cardiovascular disease but there is limited evidence in the populations living in Sub-Saharan Africa. The aim of our study was to explore the relationship between erythrocyte sodium buffering capacity and sociodemographic, clinical factors, and self-reported salt consumption at Livingstone Central Hospital. Methods We conducted a cross sectional study at Livingstone Central hospital among 242 volunteers accessing routine medical checkups. Sociodemographic and dietary characteristics were obtained along with clinical measurements to evaluate their health status. Sodium buffering capacity was estimated by erythrocyte sodium sensitivity (ESS) test. We used descriptive and inferential statistics to describe and examine associations between erythrocyte sodium sensitivity and independent variables. Results The median age (interquartile range) of the study sample was 27 (22, 42) years. 54% (n = 202) and 46% (n = 169) were males and females, respectively. The majority (n = 150, 62%) had an ESS of >120%. High salt intake correlated positively with ESS or negatively with vascular sodium buffering capacity. Conclusions Self-reported high salt intake was associated with poor vascular sodium buffering capacity or high ESS in the majority of middle-aged Zambians living in Livingstone. The poor vascular sodium buffering capacity implies a damaged vascular glycocalyx which may potentially lead to a leakage of sodium into the interstitium. This alone is a risk factor for the future development of hypertension and cardiovascular disease. However, future studies need to validate vascular function status when using ESS testing by including established vascular function assessments to determine its pathophysiological and clinical implications.

Determination of blood group antigens using electrophoresis of erythrocytes incubated with specific antibodies

“…Nevertheless, hemolytic reactions still occur despite the accurate performance of standard methods of blood group detection [2]. The analysis of electrophoretic mobility (EM) of red blood cells (RBCs) reflects the presence of a negative charge on erythrocyte [3, 4] and is reduced after the treatment with the antibody, as was first demonstrated by Coulter [5] and after the addition of Coomb's reagent [6]. The first antibody is unable to project beyond the glycocalyx of the cell and causes a significant decrease in the negative charge [7].…”

Hypertensive heart disease: risk factors, complications and mechanisms

“…From the insterstitium sodium diffuses into the intestinal capillaries for transport. In the vasculature, excess dietary salt diminishes the buffering capacity of the negatively charged glycocalyx lining the endothelium and the red blood cells leading to extravasation of sodium and accumulation of salt in the interstitial tissues ( 140 , 155 , 156 ). Accumulation of salt in the skin increases the density and hyperplasia of the lymph-capillary network and this effect is mediated by activation of tonicity-responsive enhancer binding protein (TonEBP) in mononuclear phagocyte system (MPS) cells ( 140 ).…”

Therapeutic strategies targeting the endothelial glycocalyx

“…It is not clear how much sodium is required to degrade the glycocalyx. However, a recent study indicates that high sodium consumption was accompanied by poor red blood cell sodium sensitivity, which implies a deteriorated glycocalyx [11]. Recently, our laboratory demonstrated that 12-weeks of high-sodium diet in mice deteriorates the endothelial glycocalyx [12 && ] and induces arterial dysfunction, indicated by elevated systolic blood pressure, aortic stiffening, and endothelial dysfunction [13].…”