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Microvascular endothelial cells from human omentum lack an inward rectifier K+ current
H M Himmel1, U Rauen, U Ravens
1Institute of Pharmacology and Toxicology, Faculty of Medicine Carl Gustav Carus, Technical University, Dresden, Germany.
Abstract:
In most macrovascular endothelial cell (EC) preparations, resting membrane potential is determined by the inwardly rectifying K+ current (I(K1)), whereas in microvascular EC the presence of I(K1) varies markedly. Cultured microvascular EC from small vessels of human omentum were examined by means of the voltage-clamp technique to elucidate the putative role of I(K1) in maintaining resting membrane potential. Macrovascular EC from human iliac artery and bovine aorta served as reference. Human omentum EC showed an outwardly rectifying current-voltage relation. Inward current was hardly sensitive to variations of extracellular [K+] and Ba2+ block suggesting lack of I(K1). However, substitution of extracellular [Na+] and/or [Cl-] affected the current-voltage relation indicating that Na+ and Cl- contribute to basal current. Furthermore, outward current was reduced by tetraethylammonium (10 mM), and cell-attached recordings suggested the presence of a Ca2+-activated K+ current. In contrast to human omentum EC, EC from human iliac artery and bovine aorta possessed inwardly rectifying currents which were sensitive to variations of extracellular [K+] and blocked by Ba2+. Thus, the lack of I(K1) in human omentum EC suggests that resting membrane potential is determined by Na+ and Cl- currents in addition to K+ outward currents.
Insights
Microvascular endothelial cells (EC) from human omentum lack the inwardly rectifying K+ current (I(K1)) typically found in macrovascular EC. Resting membrane potential in these cells is influenced by Na+ and Cl- currents, alongside K+ outward currents.
Area of Science:
- Endothelial cell physiology
- Ion channel function
- Cardiovascular research
Background:
- Resting membrane potential in macrovascular endothelial cells (EC) is primarily determined by the inwardly rectifying K+ current (I(K1)).
- The presence and role of I(K1) in microvascular EC are variable and not fully understood.
- Human omentum microvascular EC were investigated to clarify the contribution of I(K1) to their resting membrane potential.
Purpose of the Study:
- To investigate the presence and function of inwardly rectifying K+ current (I(K1)) in human omentum microvascular endothelial cells (EC).
- To determine the ion channel mechanisms underlying the resting membrane potential in these microvascular EC.
- To compare ion channel activity in microvascular EC with that of macrovascular EC.
Main Methods:
- Voltage-clamp technique applied to cultured microvascular EC from human omentum.
- Comparison with macrovascular EC from human iliac artery and bovine aorta.
- Assessment of current-voltage relations, ion sensitivity (K+, Ba2+, Na+, Cl-), and channel blockers (tetraethylammonium).
Main Results:
- Human omentum EC exhibited an outwardly rectifying current-voltage relation.
- Inward currents were insensitive to extracellular K+ and Ba2+ block, indicating a lack of I(K1).
- Extracellular Na+ and Cl- influenced the current-voltage relation, suggesting their contribution to basal current. Tetraethylammonium reduced outward current, and Ca2+-activated K+ current was suggested.
- In contrast, EC from human iliac artery and bovine aorta showed Ba2+-sensitive, inwardly rectifying currents dependent on extracellular K+.
Conclusions:
- Human omentum microvascular EC lack the inwardly rectifying K+ current (I(K1)) characteristic of macrovascular EC.
- Resting membrane potential in human omentum EC is likely determined by Na+ and Cl- currents, in addition to K+ outward currents.
- This study highlights distinct ion transport mechanisms in microvascular versus macrovascular endothelial cells.
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