Key result
Mechanical stimulation via a fluid stream induced an increase in intracellular Ca2+ concentration and activated an inward Cl- current in cultured human aortic endothelial cells.
Mechanical stress from fluid flow induces a Cl- current in human aortic endothelial cells, which may modulate Ca2+ influx by altering membrane potential.
Cell culture results warrant no clinical action; leaves open flow-activated Cl- currents' role in native human endothelium.
A fluid stream through a microtube was applied to cultured human aortic endothelial cells to investigate the endothelial responses of both the ionic currents and intracellular Ca2+ concentration ([Ca2+]i) to mechanical stimulation. The fluid stream induced an increase in [Ca2+]i that was dependent on both the flow rate and the extracellular Ca2+ concentration. Gd3+ and niflumic acid inhibited the fluid stream-induced increase in [Ca2+]i, whereas Ba2+ and tetraethylammonium ion exhibited no effect. The fluid stream-induced [Ca2+]i increase was accompanied by the activation of an inward current at -52.8 mV. The reversal potential of the fluid stream-induced current shifted to positive potentials when the external Cl- concentration was reduced but was not affected by variation of the external Na+ concentration. During the exposure to the fluid stream, [Ca2+]i was voltage dependent, i.e., depolarization decreased [Ca2+]i. We therefore conclude that the fluid stream-induced current is largely carried by Cl- and that the Cl- current may thus play a role in modulating the Ca2+ influx by altering the membrane potential of endothelial cells.
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Nakao et al. (1999) studied this question. Mechanical stimulation (fluid stream) was evaluated on Endothelial responses of ionic currents and intracellular Ca2+ concentration. Mechanical stimulation via a fluid stream induced an increase in intracellular Ca2+ concentration and activated an inward Cl- current in cultured human aortic endothelial cells.
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