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. 2016 Jun 28;7:256. doi: 10.3389/fphys.2016.00256

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Copyright © 2016 Shah, Martin, Yan, Shapiro and Liu.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Schematic illustration of CTS and ROS mediated sodium handling in RPT and its relation to salt sensitivity. CTS induced intracellular ROS generation and extracellularly generated ROS stimulates Na/K-ATPase/c-Src signaling, protein carbonylation, and transporter redistribution. Pretreatment with NAC blocks this process. ROS1, CTS induced intracellular ROS generation through Na/K-ATPase signaling; ROS2, extracellular ROS generated by glucose oxidase or other stimuli. Please also see Figure 2. RPT, renal proximal tubule; NAC, N-acetyl-L-cysteine.