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10.5301/jn.5000174 http://scihub22266oqcxt.onion/10.5301/jn.5000174 C4048819!4048819!22573529     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Nephrol 2012 ; 25 (3): 269-75 Nephropedia Template TP {{tp|p=22573529|t=2012. Pathogenesis of calcineurin inhibitor?induced hypertension |pdf=|usr=}}{{22573529}} gab.com Text Pathogenesis of calcineurin inhibitor induced hypertension JO: J Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=22573529 #FOAvip This article reviews the current understanding of the mechanisms of calcineurin inhibitor?induced hypertension. Already early after the introduction of cyclosporine in the 1980s, vasoconstriction, sympathetic excitation and sodium retention by the kidney had been shown to play a role in this form of hypertension. The vasoconstrictive effects of calcineurin inhibitors are related to interference with the balance of vasoactive substances, including endothelin and nitric oxide. Until recently, the renal site of the sodium-retaining effect of calcineurin inhibitors was unknown. We and others have shown that calcineurin inhibitors increase the activity of the thiazide-sensitive sodium chloride cotransporter through an effect on the kinases WNK and SPAK. Here, we review the pertinent literature on the hypertensinogenic effects of calcineurin inhibitors, including neural, vascular and renal effects, and we propose an integrated model of calcineurin inhibitor?induced hypertension. Twit Text FOAVip Pathogenesis of calcineurin inhibitor induced hypertension ????J Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=22573529 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=22573529 #FOAvip English Wikipedia <ref>{{Cite pmid|22573529}}</ref> Pathogenesis of calcineurin inhibitor?induced hypertension #MMPMID22573529 Hoorn EJ; Walsh SB; McCormick JA; Zietse R; Unwin RJ; Ellison DH J Nephrol 2012[May]; 25 (3): 269-75 PMID22573529show ga This article reviews the current understanding of the mechanisms of calcineurin inhibitor?induced hypertension. Already early after the introduction of cyclosporine in the 1980s, vasoconstriction, sympathetic excitation and sodium retention by the kidney had been shown to play a role in this form of hypertension. The vasoconstrictive effects of calcineurin inhibitors are related to interference with the balance of vasoactive substances, including endothelin and nitric oxide. Until recently, the renal site of the sodium-retaining effect of calcineurin inhibitors was unknown. We and others have shown that calcineurin inhibitors increase the activity of the thiazide-sensitive sodium chloride cotransporter through an effect on the kinases WNK and SPAK. Here, we review the pertinent literature on the hypertensinogenic effects of calcineurin inhibitors, including neural, vascular and renal effects, and we propose an integrated model of calcineurin inhibitor?induced hypertension. äPathogenesis of calcineurin inhibitor?induced hypertension (epmc).pdf DeepDyve Pubget Overpricing