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Two barriers for sodium in vascular endothelium?
1Institute of Physiology II, University of Münster, Münster, Germany. oberlei@uni-muenster.de
Annals of Medicine
|April 5, 2012
Summary
Sodium excess stiffens endothelial cells and damages the endothelial glycocalyx, increasing vascular permeability. This leads to sodium overload and organismal damage, impacting blood pressure regulation.
Area of Science:
- Cardiovascular Biology
- Cellular Physiology
- Renal Physiology
Background:
- The vascular endothelium is crucial for regulating blood pressure.
- Elevated plasma sodium concentration (sodium excess) stiffens endothelial cells and impairs function.
- The endothelial glycocalyx (eGC), an anionic biopolymer, is known to deteriorate under high sodium conditions.
Purpose of the Study:
- To investigate the impact of sodium excess on endothelial cell function and vascular permeability.
- To elucidate the role of the endothelial glycocalyx (eGC) as a sodium barrier.
- To propose a two-barrier model for sodium transport across the endothelium.
Main Methods:
- Surface measurements to assess endothelial glycocalyx integrity.
- Analysis of endothelial cell stiffening in response to increased sodium concentration.
- Investigating the interplay between aldosterone, sodium excess, and sodium channel expression.
Main Results:
- A 5% increase in plasma sodium concentration stiffened endothelial cells by approximately 25%.
- Sodium excess led to the deterioration of the endothelial glycocalyx (eGC).
- Aldosterone in the presence of sodium excess caused eGC breakdown and increased plasma membrane sodium channels.
Conclusions:
- A two-barrier model is proposed, with the eGC and endothelial plasma membrane acting as sequential sodium barriers.
- Sodium excess increases vascular sodium permeability by damaging the eGC and upregulating sodium channels.
- Chronic sodium overload, exacerbated by impaired eGC buffering, can lead to systemic damage and affect blood pressure regulation.
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