Fluid flow modulates calcium entry and activates membrane currents in cultured human aortic endothelial cells.
Human aortic endothelial cells (HAEC) respond to flow with Ca2+ entry, activation of a nonselective cation channel, activation of a chloride channel, and activation of a calcium-activated potassium channel. Conversely, human capillary endothelial cells were unaffected by similar flow rates. In HAEC the flow induced cytosolic free calcium increase ([Ca2+]i) and the ionic currents associated with it were sustained for up to 15 min after perfusion was stopped. In the absence of extracellular Ca2+, fluid flow was unable to evoke the [Ca2+]i increase or the increase in membrane currents but the response could be restored by addition of extracellular Ca2+. Surprisingly, the flow response was inhibited in 50% of the cells by inhibitors of nitric oxide production. The results suggest that the sustained flow response in HAEC may be partially mediated by nitric oxide production and release.
Jow
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F
Cardiovascular and Metabolic Diseases, Wyeth-Ayerst Research, CN 8000, Princeton, NJ 08543, USA.
Numann
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R
D001011:Aorta; D002118:Calcium / Q000502:physiology*; D002462:Cell Membrane / Q000502:physiology*; D002463:Cell Membrane Permeability; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000502:physiology*; D006801:Humans; D017136:Ion Transport / Q000502:physiology; D018408:Patch-Clamp Techniques; D013314:Stress, Mechanical
D002118:Calcium