Sodium Shows No Mercy on the Nanomechanics of Endothelial Cells
See related article, pp 391–396
Weinberger et al1 defined sodium sensitivity and sodium resistance of blood pressure in 576 women and men by 2 separate techniques. Sodium-sensitive individuals were older, had lower renin values, and were more commonly black. Follow-up of these subjects for ≤20 years was revealing. Initial baseline measurements were associated with subjects who had died compared with subjects known to be alive: age at study, blood pressure, hypertension, sodium sensitivity, baseline renin levels, and body mass index. When survival curves were examined, normotensive salt-sensitive subjects aged >25 years when initially studied were found to have a cumulative mortality similar to that of hypertensive subjects, whereas salt-resistant normotensive subjects had increased survival.2 Diagnosing sodium sensitivity is tedious, involving at least several days of volume expansion and contraction or observing blood pressure responses to a low-salt diet. Furthermore, the mechanisms of the phenomenon are imperfectly explained.
The Oberleithner laboratory offers some refreshing new views on the subject. Their focus is on endothelial cells, which harbor 4 mechanically distinct compartments, namely the glycocalyx, the cell cortex, the cytoplasm, and the nucleus.3 In addition, endothelial cells have a slightly modified version of the epithelial sodium channel (EnNaC) that has considerable regulatory importance in terms of endothelial cell behavior (Figure). The group has focused on nanomechanics of endothelial cells because stiffness of single cellular compartments has a crucial affect on endothelial cell function, subsequent vascular stiffness, and has direct implications for sodium-dependent effects.