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10.1161/HYPERTENSIONAHA.114.04975 http://scihub22266oqcxt.onion/10.1161/HYPERTENSIONAHA.114.04975 C4326622!4326622!25601932     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 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Hypertension 2015 ; 65 (3): 569-76 Nephropedia Template TP {{tp|p=25601932|t=2015. RENAL TRANSPORTER ACTIVATION DURING ANGIOTENSIN II HYPERTENSION IS BLUNTED IN IFN-??/? AND IL-17A ?/? MICE |pdf=|usr=}}{{25601932}} gab.com Text RENAL TRANSPORTER ACTIVATION DURING ANGIOTENSIN II HYPERTENSION IS BLUNTED IN IFN- / AND IL-17A / MICE JO: Hypertension http://www.kidney.de/pget.php?&tw=1&pmid=25601932 #FOAvip Ample genetic and physiological evidence establishes that renal salt handling is a critical regulator of blood pressure. Studies also establish a role for the immune system, T-cell infiltration and immune cytokines in hypertension. This study aimed to connect immune cytokines, specifically IFN-? and IL-17A, to sodium transporter regulation in the kidney during angiotensin II (AngII) hypertension. C57BL/6J (wild type, WT) mice, responded to AngII infusion (490 ng/kg/min, 2 weeks) with a rise in blood pressure (to 170 mmHg) and a significant decrease in the rate of excretion of a saline challenge. In comparison, mice that lacked the ability to produce either IFN-? (IFN-??/?) or IL-17A (IL-17A?/?) exhibited a blunted rise in blood pressure (to <150 mmHg), and both genotypes maintained baseline diuretic and natriuretic responses to a saline challenge. Along the distal nephron, AngII infusion increased abundance of the phosphorylated forms of the Na-K-2Cl cotransporter, Na-Cl cotransporter and Ste20/SPS-1 related proline-alanine rich kinase, in both the WT and IL-17A?/? but not in IFN-??/? mice; epithelial Na channel abundance increased similarly in all three genotypes. In the proximal nephron, AngII infusion significantly decreased abundance of Na/H-exchanger isoform 3 and the motor myosin VI in IL-17A?/? and IFN-??/? , but not WT; the Na-phosphate cotransporter decreased in all three genotypes. Our results suggest that during AngII hypertension both IFN-? and IL-17A production interfere with the pressure natriuretic decrease in proximal tubule sodium transport and that IFN-? production is necessary to activate distal sodium reabsorption. Twit Text FOAVip RENAL TRANSPORTER ACTIVATION DURING ANGIOTENSIN II HYPERTENSION IS BLUNTED IN IFN- / AND IL-17A / MICE ????Hypertension http://www.kidney.de/pget.php?&tw=1&pmid=25601932 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25601932 #FOAvip English Wikipedia <ref>{{Cite pmid|25601932}}</ref> RENAL TRANSPORTER ACTIVATION DURING ANGIOTENSIN II HYPERTENSION IS BLUNTED IN IFN-??/? AND IL-17A ?/? MICE #MMPMID25601932 Kamat NV; Thabet SR; Xiao L; Saleh MA; Kirabo A; Madhur MS; Delpire E; Harrison DG; McDonough AA Hypertension 2015[Mar]; 65 (3): 569-76 PMID25601932show ga Ample genetic and physiological evidence establishes that renal salt handling is a critical regulator of blood pressure. Studies also establish a role for the immune system, T-cell infiltration and immune cytokines in hypertension. This study aimed to connect immune cytokines, specifically IFN-? and IL-17A, to sodium transporter regulation in the kidney during angiotensin II (AngII) hypertension. C57BL/6J (wild type, WT) mice, responded to AngII infusion (490 ng/kg/min, 2 weeks) with a rise in blood pressure (to 170 mmHg) and a significant decrease in the rate of excretion of a saline challenge. In comparison, mice that lacked the ability to produce either IFN-? (IFN-??/?) or IL-17A (IL-17A?/?) exhibited a blunted rise in blood pressure (to <150 mmHg), and both genotypes maintained baseline diuretic and natriuretic responses to a saline challenge. Along the distal nephron, AngII infusion increased abundance of the phosphorylated forms of the Na-K-2Cl cotransporter, Na-Cl cotransporter and Ste20/SPS-1 related proline-alanine rich kinase, in both the WT and IL-17A?/? but not in IFN-??/? mice; epithelial Na channel abundance increased similarly in all three genotypes. In the proximal nephron, AngII infusion significantly decreased abundance of Na/H-exchanger isoform 3 and the motor myosin VI in IL-17A?/? and IFN-??/? , but not WT; the Na-phosphate cotransporter decreased in all three genotypes. Our results suggest that during AngII hypertension both IFN-? and IL-17A production interfere with the pressure natriuretic decrease in proximal tubule sodium transport and that IFN-? production is necessary to activate distal sodium reabsorption. äRENAL TRANSPORTER ACTIVATION DURING ANGIOTENSIN II HYPERTENSION IS BLU(epmc).pdf DeepDyve Pubget Overpricing