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* To whom correspondence should be addressed. E-mail: anf{at}mail.med.upenn.edu.
Abstract We have shown previously that "ischemia" (abrupt cessation of flow) leads to rapid membrane depolarization and increased generation of reactive oxygen species (ROS) in lung microvascular endothelial cells. This response is not associated with anoxia but reflects loss of normal shear stress. This study evaluated whether a similar response occurs in aortic endothelium. Plasma membrane potential and production of ROS were determined by fluorescence microscopy and cytochrome c reduction in flow-adapted rat or mouse aorta or monolayer cultures of rat aortic endothelial cells (RAEC). Within 30 s after flow cessation, endothelial cells that had been flow-adapted showed plasma membrane depolarization that was inhibited by pretreatment with cromakalim, a KATP channel agonist. Flow cessation also led to ROS generation which was inhibited by cromakalim and the flavoprotein inhibitor, diphenyleneiodonium. Aortic endothelium from mice with "knock-out" of the KATP channel (KIR6.2) showed a markedly attenuated change in membrane potential and ROS generation with flow cessation. Aortic endothelium from mice with "knock-out" of NADPH oxidase (gp91phox) had similar membrane depolarization as wild-type mice but absent ROS generation. Thus, rat and mouse aortic endothelial cells respond to abrupt flow cessation by KATP channel-mediated membrane depolarization followed by NADPH oxidase-mediated ROS generation, possibly representing a cell signaling response to altered mechanotransduction.
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