There is evidence that aldosterone/salt causes vascular inflammation which is characterized by endothelial dysfunction and recruitment of monocytes. A target of inflammatory processes is the endothelial glycocalyx (eGC) which is located on the cell membrane surface functioning as a sodium buffer with protective effects on the endothelium. The hypothesis was tested that salt “per se” influences both monocyte adhesion and the function of the eGC.

Human endothelial cells (EA.hy 926) were grown for 24 hours in low (130mM) and high (150mM) salt concentrations. For adhesion assays fluorescently labeled monocytes (CD14) were seeded onto confluent endothelial monolayers for 5h and quantified afterwards. Changes in the conformation of the eGC, in response to sodium, were monitored by using quantum dot (QD)-mediated immunofluorescence staining for heparan sulfates (HS) on the endothelial cell surface. The mineralocorticoid receptor (MR) and the epithelial sodium channel (ENaC) were specifically blocked by spironolactone and benzamil, respectively.

In the presence of aldosterone the number of adherent monocytes on the endothelial cells was significantly increased by 34% under high sodium conditions. Furthermore, high sodium diminished the number of HS, the major component of the eGC, by 34%. This can be prevented by treatment with spironolactone and benzamil (increased number of HS by 36% and 20%, respectively).

The data indicate that salt triggers inflammatory processes in vascular endothelium. It could be demonstrated that both spironolactone and benzamil have protective effects on the eGC. Thus, MR- and ENaC-blockade could be useful strategies in the prevention of salt/aldosterone-mediated inflammatory processes of the vasculature.