Fluid flow modulates calcium entry and activates membrane currents in cultured human aortic endothelial cells.

Abstract

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.