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10.1161/HYPERTENSIONAHA.114.03863 http://scihub22266oqcxt.onion/10.1161/HYPERTENSIONAHA.114.03863 C4339088!4339088!25185128     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Hypertension 2014 ; 64 (6): 1275-81 Nephropedia Template TP {{tp|p=25185128|t=2014. TNF-alpha Produced in the Kidney Contributes to Angiotensin II-dependent Hypertension |pdf=|usr=}}{{25185128}} gab.com Text TNF-alpha Produced in the Kidney Contributes to Angiotensin II-dependent Hypertension JO: Hypertension http://www.kidney.de/pget.php?&tw=1&pmid=25185128 #FOAvip Immune system activation contributes to the pathogenesis of hypertension and the resulting progression of chronic kidney disease (CKD). In this regard, we recently identified a role for pro-inflammatory Th1 T lymphocyte responses in hypertensive kidney injury. As Th1 cells generate IFN-? and TNF-?, we hypothesized that IFN-? and TNF-? propagate renal damage during hypertension induced by activation of the renin-angiotensin system (RAS). Therefore, after confirming that mice genetically deficient of Th1 immunity were protected from kidney glomerular injury despite a preserved hypertensive response, we subjected mice lacking IFN-? or TNF-? to our model of hypertensive CKD. IFN-deficiency had no impact on blood pressure elevation or urinary albumin excretion during chronic angiotensin II infusion. By contrast, TNF-deficient (KO) mice had blunted hypertensive responses and reduced end-organ damage in our model. As Ang II-infused TNF KO mice had exaggerated eNOS expression in the kidney and enhanced nitric oxide (NO) bioavailability, we examined the actions of TNF-? generated from renal parenchymal cells in hypertension by transplanting wild-type or TNF KO kidneys into wild-type recipients prior to the induction of hypertension. Transplant recipients lacking TNF solely in the kidney had blunted hypertensive responses to Ang II and augmented renal eNOS expression, confirming a role for kidney-derived TNF-? to promote Ang II-induced blood pressure elevation by limiting renal NO generation. Twit Text FOAVip TNF-alpha Produced in the Kidney Contributes to Angiotensin II-dependent Hypertension ????Hypertension http://www.kidney.de/pget.php?&tw=1&pmid=25185128 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25185128 #FOAvip English Wikipedia <ref>{{Cite pmid|25185128}}</ref> TNF-alpha Produced in the Kidney Contributes to Angiotensin II-dependent Hypertension #MMPMID25185128 Zhang J; Patel MB; Griffiths R; Mao A; Song Ys; Karlovich NS; Sparks MA; Jin H; Wu M; Lin EE; Crowley SD Hypertension 2014[Dec]; 64 (6): 1275-81 PMID25185128show ga Immune system activation contributes to the pathogenesis of hypertension and the resulting progression of chronic kidney disease (CKD). In this regard, we recently identified a role for pro-inflammatory Th1 T lymphocyte responses in hypertensive kidney injury. As Th1 cells generate IFN-? and TNF-?, we hypothesized that IFN-? and TNF-? propagate renal damage during hypertension induced by activation of the renin-angiotensin system (RAS). Therefore, after confirming that mice genetically deficient of Th1 immunity were protected from kidney glomerular injury despite a preserved hypertensive response, we subjected mice lacking IFN-? or TNF-? to our model of hypertensive CKD. IFN-deficiency had no impact on blood pressure elevation or urinary albumin excretion during chronic angiotensin II infusion. By contrast, TNF-deficient (KO) mice had blunted hypertensive responses and reduced end-organ damage in our model. As Ang II-infused TNF KO mice had exaggerated eNOS expression in the kidney and enhanced nitric oxide (NO) bioavailability, we examined the actions of TNF-? generated from renal parenchymal cells in hypertension by transplanting wild-type or TNF KO kidneys into wild-type recipients prior to the induction of hypertension. Transplant recipients lacking TNF solely in the kidney had blunted hypertensive responses to Ang II and augmented renal eNOS expression, confirming a role for kidney-derived TNF-? to promote Ang II-induced blood pressure elevation by limiting renal NO generation. äTNF-alpha Produced in the Kidney Contributes to Angiotensin II-depende(epmc).pdf DeepDyve Pubget Overpricing