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10.1111/apha.12397 http://scihub22266oqcxt.onion/10.1111/apha.12397 C4308436!4308436!25219340     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Acta+Physiol+(Oxf) 2015 ; 213 (3): 722-30 Nephropedia Template TP {{tp|p=25219340|t=2015. ET-1 increases reactive oxygen species following hypoxia and high salt diet in the mouse glomerulus |pdf=|usr=}}{{25219340}} gab.com Text ET-1 increases reactive oxygen species following hypoxia and high salt diet in the mouse glomerulus JO: Acta Physiol (Oxf) http://www.kidney.de/pget.php?&tw=1&pmid=25219340 #FOAvip Aim: The current study was designed to determine whether ET-1 derived from endothelial cells contributes to oxidative stress in the glomerulus of mice subjected to a high salt diet and/or hypoxia. Methods: C57BL6/J control mice or vascular endothelial cell ET-1 knockout (VEET KO) mice were subjected to three-hour exposure to hypoxia (8% O2) and or 2 weeks of high salt diet (4% NaCl) prior to metabolic cage assessment of renal function and isolation of glomeruli for determination of reactive oxygen species (ROS). Results: In control mice, hypoxia significantly increased urinary protein excretion during the initial 24 hrs, but only in animals on a high salt diet. Hypoxia increased glomerular ET-1 mRNA expression in control, but not in vascular endothelial cell ET-1 knockout (VEET KO) mice. Under normoxic conditions, mice on a high salt diet had approximately 150% higher glomerular ET-1 mRNA expression compared to a normal salt diet (p<0.05). High salt diet administration significantly increased glomerular ROS production in flox control, but not in glomeruli isolated from VEET KO mice. In C57BL6/J mice, the ETA receptor selective antagonist, ABT-627, significantly attenuated the increase in glomerular ROS production produced by high salt diet. In addition, chronic infusion of C57BL6/J mice with a sub-pressor dose of ET-1 (osmotic pumps) significantly increased levels of glomerular ROS that were prevented by ETA antagonist treatment. Conclusion: These data suggest that both hypoxia and a high salt diet increases glomerular ROS production via endothelial derived ET-1-ETA receptor activation and provide a potential mechanism for ET-1 induced nephropathy. Twit Text FOAVip ET-1 increases reactive oxygen species following hypoxia and high salt diet in the mouse glomerulus ????Acta Physiol (Oxf) http://www.kidney.de/pget.php?&tw=1&pmid=25219340 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25219340 #FOAvip English Wikipedia <ref>{{Cite pmid|25219340}}</ref> ET-1 increases reactive oxygen species following hypoxia and high salt diet in the mouse glomerulus #MMPMID25219340 Heimlich JB; Speed JS; Bloom CJ; O'Connor PM; Pollock JS; Pollock DM Acta Physiol (Oxf) 2015[Mar]; 213 (3): 722-30 PMID25219340show ga Aim: The current study was designed to determine whether ET-1 derived from endothelial cells contributes to oxidative stress in the glomerulus of mice subjected to a high salt diet and/or hypoxia. Methods: C57BL6/J control mice or vascular endothelial cell ET-1 knockout (VEET KO) mice were subjected to three-hour exposure to hypoxia (8% O2) and or 2 weeks of high salt diet (4% NaCl) prior to metabolic cage assessment of renal function and isolation of glomeruli for determination of reactive oxygen species (ROS). Results: In control mice, hypoxia significantly increased urinary protein excretion during the initial 24 hrs, but only in animals on a high salt diet. Hypoxia increased glomerular ET-1 mRNA expression in control, but not in vascular endothelial cell ET-1 knockout (VEET KO) mice. Under normoxic conditions, mice on a high salt diet had approximately 150% higher glomerular ET-1 mRNA expression compared to a normal salt diet (p<0.05). High salt diet administration significantly increased glomerular ROS production in flox control, but not in glomeruli isolated from VEET KO mice. In C57BL6/J mice, the ETA receptor selective antagonist, ABT-627, significantly attenuated the increase in glomerular ROS production produced by high salt diet. In addition, chronic infusion of C57BL6/J mice with a sub-pressor dose of ET-1 (osmotic pumps) significantly increased levels of glomerular ROS that were prevented by ETA antagonist treatment. Conclusion: These data suggest that both hypoxia and a high salt diet increases glomerular ROS production via endothelial derived ET-1-ETA receptor activation and provide a potential mechanism for ET-1 induced nephropathy. äET-1 increases reactive oxygen species following hypoxia and high salt(epmc).pdf DeepDyve Pubget Overpricing