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10.1096/fj.14-250282 http://scihub22266oqcxt.onion/10.1096/fj.14-250282 24868010!5395730!24868010     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       FASEB+J 2014 ; 28 (9): 4015-25 Nephropedia Template TP {{tp|p=24868010|t=2014. Feedforward activation of endothelial ENaC by high sodium |pdf=|usr=}}{{24868010}} gab.com Text Feedforward activation of endothelial ENaC by high sodium JO: FASEB J http://www.kidney.de/pget.php?&tw=1&pmid=24868010 #FOAvip Kidney epithelial sodium channels (ENaCs) are known to be inactivated by high sodium concentrations (feedback inhibition). Recently, the endothelial sodium channel (EnNaC) was identified to control the nanomechanical properties of the endothelium. EnNaC-dependent endothelial stiffening reduces the release of nitric oxide, the hallmark of endothelial dysfunction. To study the regulatory impact of sodium on EnNaC, endothelial cells (EA.hy926 and ex vivo mouse endothelium) were incubated in aldosterone-free solutions containing either low (130 mM) or high (150 mM) sodium concentrations. By applying atomic force microscopy-based nanoindentation, an unexpected positive correlation between increasing sodium concentrations and cortical endothelial stiffness was observed, which can be attributed to functional EnNaC. In particular, an acute rise in sodium concentration (+20 mM) was sufficient to increase EnNaC membrane abundance by 90% and stiffening of the endothelial cortex by 18%. Despite the absence of exogenous aldosterone, these effects were prevented by the aldosterone synthase inhibitor FAD286 (100 nM) or the mineralocorticoid receptor (MR)-antagonist spironolactone (100 nM), indicating endogenous aldosterone synthesis and MR-dependent signaling. Interestingly, in the presence of high-sodium concentrations, FAD286 increased the transcription of the MR by 69%. Taken together, a novel feedforward activation of EnNaC by sodium is proposed that contrasts ENaC feedback inhibition in kidney. Twit Text FOAVip Feedforward activation of endothelial ENaC by high sodium ????FASEB J http://www.kidney.de/pget.php?&tw=1&pmid=24868010 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24868010 #FOAvip English Wikipedia <ref>{{Cite pmid|24868010}}</ref> Feedforward activation of endothelial ENaC by high sodium #MMPMID24868010 Korte S; Strater AS; Druppel V; Oberleithner H; Jeggle P; Grossmann C; Fobker M; Nofer JR; Brand E; Kusche-Vihrog K FASEB J 2014[Sep]; 28 (9): 4015-25 PMID24868010show ga Kidney epithelial sodium channels (ENaCs) are known to be inactivated by high sodium concentrations (feedback inhibition). Recently, the endothelial sodium channel (EnNaC) was identified to control the nanomechanical properties of the endothelium. EnNaC-dependent endothelial stiffening reduces the release of nitric oxide, the hallmark of endothelial dysfunction. To study the regulatory impact of sodium on EnNaC, endothelial cells (EA.hy926 and ex vivo mouse endothelium) were incubated in aldosterone-free solutions containing either low (130 mM) or high (150 mM) sodium concentrations. By applying atomic force microscopy-based nanoindentation, an unexpected positive correlation between increasing sodium concentrations and cortical endothelial stiffness was observed, which can be attributed to functional EnNaC. In particular, an acute rise in sodium concentration (+20 mM) was sufficient to increase EnNaC membrane abundance by 90% and stiffening of the endothelial cortex by 18%. Despite the absence of exogenous aldosterone, these effects were prevented by the aldosterone synthase inhibitor FAD286 (100 nM) or the mineralocorticoid receptor (MR)-antagonist spironolactone (100 nM), indicating endogenous aldosterone synthesis and MR-dependent signaling. Interestingly, in the presence of high-sodium concentrations, FAD286 increased the transcription of the MR by 69%. Taken together, a novel feedforward activation of EnNaC by sodium is proposed that contrasts ENaC feedback inhibition in kidney. |Animals[MESH] |Aorta/cytology/drug effects/*metabolism[MESH] |Blotting, Western[MESH] |Cell Membrane/drug effects/metabolism[MESH] |Cells, Cultured[MESH] |Cytochrome P-450 CYP11B2/antagonists & inhibitors/genetics/metabolism[MESH] |Endothelium, Vascular/cytology/drug effects/*metabolism[MESH] |Epithelial Sodium Channels/genetics/*metabolism[MESH] |Human Umbilical Vein Endothelial Cells/cytology/drug effects/*metabolism[MESH] |Humans[MESH] |Mice[MESH] |Microscopy, Atomic Force[MESH] |Microscopy, Fluorescence[MESH] |Mineralocorticoid Receptor Antagonists/*pharmacology[MESH] |RNA, Messenger/genetics[MESH] |Real-Time Polymerase Chain Reaction[MESH] |Reverse Transcriptase Polymerase Chain Reaction[MESH]Feedforward activation of endothelial ENaC by high sodium (epmc).pdf DeepDyve Pubget Overpricing