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The KATP channel is an important component of flow sensing in the pulmonary endothelium

We have reported earlier that loss of flow or shear in the pulmonary endothelium in situ leads to an immediate endothelial cell membrane depolarization that was attributed to the closure of a KATP channel, based on studies with inhibitors. Here the effects of stop of flow were studied in vitro using a fluorescent potentiometric dye and whole cell patch clamp measurements under real time flow conditions in pulmonary microvascular endothelial cells derived from wild type and KATP channel knockout (KIR6.2 gene targeted) mice. Cells were cultured under the usual static conditions or under flow to give 10 dynes/cm2 shear stress for 24 h (flow adapted). In wild type flow adapted cells, stop of flow induced endothelial membrane depolarization, as monitored by the fluorescent dye bis‐oxonol. However minimal change in membrane potential was seen in non flow adapted (statically cultured) or flow adapted and non flow adapted KIR6.2−/ − cells with stop of flow. Whole cell inwardly rectifying K+ current (KIR) in wild type flow adapted cells was reduced ~40% with cessation of flow, but was unchanged in static and KIR6.2−/ − cells. The response of the endothelial membrane to stop of flow in wild type cells and the lack thereof in KATP knockout cells indicate that the KATP channel is an important component of the pulmonary endothelial shear stress response mechanism.