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. 2014 Sep 16;5:209. doi: 10.3389/fphar.2014.00209

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Copyright © 2014 Rodríguez and González.

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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Proposal model for regulation of FMV in placental vasculature in response to exercise. Moderate exercise during pregnancy could improve the placental vascular response to shear stress in a mechanism that involves mechano-transduction induced by extracellular signals by a complex mechanism that includes activity of voltage (K_v), ATP (K_ATP) and K_Ca, GPCRs, tyrosine-kinase receptors (TKRs) and VEGFR. Activation of this mechanism induces a signaling pathway that causes high phosphorylation (p-Ser1177) and activity in eNOS mediated by Ca²⁺/calmodulin (Ca²⁺/CAM) and protein kinase B (PKB/Akt). Decreased synthesis as well as reduced accumulation of ROS contributes to improve the bioavailability of NO. Activity of eNOS involves activity of hCAT-1, a protein co-expressed with cav-1 in caveolae (not shown), which is essential for NO synthesis. Diffusion of NO to smooth muscle cell (SMC) induces the activation of sGC and vascular smooth muscle relaxation.