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Electrophysiological properties of human coronary endothelial cells
B J Zünkler1, B Henning, M Gräfe
1Federal Institute for Drugs and Medical Devices, Berlin, FRG.
Insights
Human coronary endothelial cells (HCEC) exhibit inwardly rectifying K+ currents and are depolarized by ATP/ADP via P2 purinoceptors. These electrophysiological properties are similar in macro- and microvascular HCEC.
Area of Science:
- Cardiovascular Physiology
- Cellular Electrophysiology
Background:
- Human coronary endothelial cells (HCEC) play a crucial role in vascular function.
- Understanding their electrophysiological properties is key to comprehending coronary circulation.
Purpose of the Study:
- To investigate and compare the electrophysiological properties of macro- and microvascular HCEC.
- To identify ion channel activity and responses to vasoactive agents in HCEC.
Main Methods:
- Whole-cell patch-clamp technique applied to isolated human coronary endothelial cells.
- Analysis of membrane potential, ion currents (K+, Ca2+), and responses to extracellular ions and nucleotides.
- Comparison of electrophysiological characteristics between macro- and microvascular HCEC.
Main Results:
- HCEC exhibit inwardly rectifying K+ currents and some outwardly directed K+ currents.
- No voltage-dependent Ca2+ currents were observed in isolated HCEC.
- Extracellular ATP and ADP caused significant depolarization via P2 purinoceptors, involving Ca2+ influx, with no major differences between macro- and microvascular cells.
Conclusions:
- HCEC possess distinct electrophysiological properties, including inwardly rectifying K+ currents.
- Nucleotide signaling via P2 purinoceptors significantly influences HCEC membrane potential.
- Electrophysiological characteristics of macro- and microvascular HCEC are largely comparable.
Abstract:
The electrophysiological properties of human coronary endothelial cells (HCEC) of macro- and microvascular origin were studied using the whole-cell configuration of the patch-clamp technique. The membrane potential of confluent HCEC (-41.9 +/- 3.9 mV (mean +/- SEM, n = 32) for macro- and -33.6 +/- 2.6 mV (n = 64) for microvascular cells, respectively) was less negative than the K+ equilibrium potential. Inward currents of isolated cells at potentials below the K+ equilibrium potential were blocked by external Ba2+ (1 mM), inactivated due to time- and voltage-dependent block caused by external Na+, and their amplitudes were enhanced by increasing extracellular [K+]; these currents were identified as inwardly rectifying K+ currents. Some isolated cells displayed outwardly directed K+ currents which were abolished after replacement of Cs+ for K+ on both sides of the membrane. Voltage-dependent Ca2+ currents could not be observed in isolated HCEC. Hyperpolarizations induced by vasoactive agonists have been observed in some endothelial cells from different species. In contrast, extracellularly applied ATP (adenosine-5'-triphosphate) and ADP (adenosine-5'-diphosphate) at micromolar concentrations depolarized confluent HCEC, whereas adenosine had no effect on resting potentials (RP), indicating that the nucleotide-induced depolarizations were mediated via P2- purinoceptors. These depolarizations occurred even after replacement of N-methyl-D-glucamine for extracellular Na+, indicating that Ca(2+)-influx was involved. There were no marked differences in the electrophysiological properties between cells of macro and microvascular origin.