Biology Reference
In-Depth Information
In the past, the term “cell stiffness” has been used as a global description
of a mechanical cell property. More recently, cell stiffness could be split
into at least two components, one describing the stiffness of the plasma
membrane including the spiderweb-like submembranous actin network (cell
shell), the other describing the stiffness of the bulk cytoplasm. 16 By a further
reduction of the indentation velocity and indentation depth, a third stiffness
component can be separated from the other two, which is located above the
cell membrane and most likely relates to the glycocalyx. It is a very soft layer
(several 100 nm thick, stiffness is about 0.2 pN/nm) and neglected pending
further experiments.
6.2.3
Sodium: “Sffener” of Vascular Endothelial Cells
Hypertension, stroke, coronary heart disease and kidney ibrosis are related
to high sodium intake as shown in many studies.
Although the deleterious
action of high sodium intake is obvious, the underlying mechanisms how salt
(NaCl) acts at the organ, tissue and cellular levels are still unclear. High sodium
causes ibrosis in kidney and heart
17
When dietary salt intake exceeds renal excretion capacity, sodium is stored
in the space between cells bound to extracellular organic material.
18
and supports inlammatory processes.
19
A close
look at the plasma sodium concentration shows that there is a small but
signiicant rise in sodium concentration (3 to 4 mM) when dietary salt intake
is high.
20
Hence, it was postulated that changes in plasma sodium could
directly affect blood pressure.
Stimulated by this work, it was tested whether endothelial cells directly
respond to small changes in extracellular sodium. Indeed, cells stiffen within
minutes when extracellular sodium is elevated. This mechanical response
happens only when aldosterone, a sodium-saving steroid hormone, is present
in the culture media. Surprisingly, endothelial cells are highly sensitive to
sodium in a narrow physiological range ( Fig. 6.10 ) . Small increments of
extracellular sodium between 140 and 145 mM increase cell stiffness by
more than 20%, indicating a relevant physiological role in the control of
endothelial function.
Cells exposed to low sodium are more deformable by shear force than the
same cells exposed to high sodium as demonstrated in the two AFM images of
Fig. 6.11 . Endothelial cells scanned at constant force and constant frequency
in a solution of 135 mM sodium (=low sodium) are visibly lattened by the
scanning AFM tip. In contrast, in medium containing 150 mM sodium (=high
sodium), the same endothelial cells resist the “pressure” of the scanning AFM
tip and remain prominent.
21,22
23
 
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