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10.1152/ajprenal.00132.2016 http://scihub22266oqcxt.onion/10.1152/ajprenal.00132.2016 C4935775!4935775!27076645     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 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Physiol+Renal+Physiol 2016 ; 310 (11): F1389-96 Nephropedia Template TP {{tp|p=27076645|t=2016. The CUL3/KLHL3-WNK-SPAK/OSR1 pathway as a target for antihypertensive therapy |pdf=|usr=}}{{27076645}} gab.com Text The CUL3/KLHL3-WNK-SPAK/OSR1 pathway as a target for antihypertensive therapy JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=27076645 #FOAvip Chronic high blood pressure (hypertension) is the most common disease in the Unites States. While several classes of drugs exist to treat it, many patients (up to 10 million Americans) respond poorly to therapy, even when multiple classes are used. Recent evidence suggests that a significant portion of patients will always remain hypertensive despite maximum therapy with the drugs currently available. Therefore, there is a pressing need to develop novel antihypertensive agents. One limitation has been the identification of new targets, a limitation that has been overcome by recent insights into the mechanisms underlying monogenic forms of hypertension. The disease familial hyperkalemic hypertension is caused by mutations in with-no-lysine (WNK) kinases 1 and 4 and in cullin-3 and kelch-like 3, components of an E3 ubiquitin ligase complex that promotes WNK kinase degradation. The study of the mechanisms by which this pathway regulates blood pressure has identified several candidates for the development of new antihypertensive agents. This pathway is particularly attractive since its inhibition may not only reduce renal sodium reabsorption along multiple segments but may also reduce vascular tone. Here, we will describe the mechanisms by which this pathway regulate blood pressure and discuss the potential of targeting it to develop new antihypertensive drugs. Twit Text FOAVip The CUL3/KLHL3-WNK-SPAK/OSR1 pathway as a target for antihypertensive therapy ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=27076645 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27076645 #FOAvip English Wikipedia <ref>{{Cite pmid|27076645}}</ref> The CUL3/KLHL3-WNK-SPAK/OSR1 pathway as a target for antihypertensive therapy #MMPMID27076645 Ferdaus MZ; McCormick JA Am J Physiol Renal Physiol 2016[Jun]; 310 (11): F1389-96 PMID27076645show ga Chronic high blood pressure (hypertension) is the most common disease in the Unites States. While several classes of drugs exist to treat it, many patients (up to 10 million Americans) respond poorly to therapy, even when multiple classes are used. Recent evidence suggests that a significant portion of patients will always remain hypertensive despite maximum therapy with the drugs currently available. Therefore, there is a pressing need to develop novel antihypertensive agents. One limitation has been the identification of new targets, a limitation that has been overcome by recent insights into the mechanisms underlying monogenic forms of hypertension. The disease familial hyperkalemic hypertension is caused by mutations in with-no-lysine (WNK) kinases 1 and 4 and in cullin-3 and kelch-like 3, components of an E3 ubiquitin ligase complex that promotes WNK kinase degradation. The study of the mechanisms by which this pathway regulates blood pressure has identified several candidates for the development of new antihypertensive agents. This pathway is particularly attractive since its inhibition may not only reduce renal sodium reabsorption along multiple segments but may also reduce vascular tone. Here, we will describe the mechanisms by which this pathway regulate blood pressure and discuss the potential of targeting it to develop new antihypertensive drugs. äThe CUL3/KLHL3-WNK-SPAK/OSR1 pathway as a target for antihypertensive (epmc).pdf DeepDyve Pubget Overpricing